PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2497752-2	1989	HepG2-secreted cholesteryl ester transfer activity is associated with apoprotein (apo) A-I (58%) as well as apo A-II (55%), and is not associated with apo B or E. In contrast, our previous studies have shown that most (88%) cholesteryl ester transfer activity in human plasma is associated with apo A-I whereas very little (7%) is associated with apo A-II.	Cholesterol Esters	15-32	NLR family pyrin domain containing 3	Homo sapiens	112-116
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	lys-gly-val-asp-val-tyr-ala-val	127-158	NLR family pyrin domain containing 3	Homo sapiens	75-78
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	Hydrogen	201-203	NLR family pyrin domain containing 3	Homo sapiens	75-78
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	Phosphates	235-244	NLR family pyrin domain containing 3	Homo sapiens	75-78
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	Tromethamine	248-252	NLR family pyrin domain containing 3	Homo sapiens	75-78
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	Hydrochloric Acid	253-256	NLR family pyrin domain containing 3	Homo sapiens	75-78
2481315-1	1989	The potential binding of angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) (AII) to a peptide encoded by its complementary RNA (Lys-Gly-Val-Asp-Val-Tyr-Ala-Val) (IIA) has been studied by monitoring the 1H NMR spectrum of IIA in aqueous phosphate or Tris.HCl buffer (2H2O) as it is titrated with AII.	2h2o	265-269	NLR family pyrin domain containing 3	Homo sapiens	75-78
2497752-2	1989	HepG2-secreted cholesteryl ester transfer activity is associated with apoprotein (apo) A-I (58%) as well as apo A-II (55%), and is not associated with apo B or E. In contrast, our previous studies have shown that most (88%) cholesteryl ester transfer activity in human plasma is associated with apo A-I whereas very little (7%) is associated with apo A-II.	Cholesterol Esters	15-32	NLR family pyrin domain containing 3	Homo sapiens	351-355
2542871-3	1989	The effect of GDF on plasma lipids and apolipoproteins was investigated by following the concentrations of triglycerides, cholesterol, and apolipoproteins A-I, A-II, B, C-I, C-II, C-III, and E. Growth caught up significantly or remained in the normal range in 14 patients.	GDF	14-17	NLR family pyrin domain containing 3	Homo sapiens	139-172
2549116-2	1989	The present study has been designed in order to see if A II could modify in vitro spontaneous and ACTH-induced corticosterone (B) release from both fasciculata-reticularis enriched and total adrenal cells.	Corticosterone	111-125	NLR family pyrin domain containing 3	Homo sapiens	55-59
2549116-7	1989	Finally, 10(-10) to 10(-6) M A II and 22 pM ACTH stimulated aldosterone output from total adrenal cells; while, fasciculata-reticularis enriched cells did not secrete any measurable amount of aldosterone under basal condition and after incubation with A II.	Aldosterone	60-71	NLR family pyrin domain containing 3	Homo sapiens	29-33
2653621-4	1989	Fenofibrate also affected the structure and composition of some of the major classes of lipoproteins: increases in apolipoproteins (apo) AI and AII and decreases in apo B and apo E were consistent with reductions in TG, VLDL, and LDL and increases in HDL.	Fenofibrate	0-11	NLR family pyrin domain containing 3	Homo sapiens	144-147
2913054-8	1989	Induction studies in cell lines that similarly express only the AII isozyme indicated that its activity could be enhanced severalfold by exposure to elevated arginine levels.	Arginine	158-166	NLR family pyrin domain containing 3	Homo sapiens	64-67
3288099-3	1988	The primary effect of AII is activation of phospholipase C, which increases both calcium release from intracellular stores and calcium flux across the cell membrane and activates protein kinase C. Potassium depolarizes the membrane, thereby activating calcium flow through voltage-dependent calcium channels.	Calcium	81-88	NLR family pyrin domain containing 3	Homo sapiens	22-25
2503807-6	1989	Alcohol consumption was directly associated with apo A-I and A-II levels in both sexes; adiposity was inversely associated with apo A-I levels in both sexes but with apo A-II only in women.	Alcohols	0-7	NLR family pyrin domain containing 3	Homo sapiens	61-65
2503807-7	1989	Triglyceride levels showed an inverse association with apo A-II in women.	Triglycerides	0-12	NLR family pyrin domain containing 3	Homo sapiens	59-63
2452924-6	1988	The dose-dependent mean BP rises induced by AII were slightly blunted during nifedipine treatment, whereas the PRA decreases and the PA rises after the peak infusion were not significantly different before and during nifedipine administration.	Nifedipine	77-87	NLR family pyrin domain containing 3	Homo sapiens	44-47
3288099-3	1988	The primary effect of AII is activation of phospholipase C, which increases both calcium release from intracellular stores and calcium flux across the cell membrane and activates protein kinase C. Potassium depolarizes the membrane, thereby activating calcium flow through voltage-dependent calcium channels.	Calcium	127-134	NLR family pyrin domain containing 3	Homo sapiens	22-25
3288099-3	1988	The primary effect of AII is activation of phospholipase C, which increases both calcium release from intracellular stores and calcium flux across the cell membrane and activates protein kinase C. Potassium depolarizes the membrane, thereby activating calcium flow through voltage-dependent calcium channels.	Calcium	127-134	NLR family pyrin domain containing 3	Homo sapiens	22-25
3106036-10	1987	Analysis of the relative amounts of various apolipoproteins in the 125I-HDL bound to ABAE cells demonstrates a decrease in the relative amount of iodinated A-II concomitant with increase in the relative amounts of the other iodinated apolipoproteins, when compared to the composition of the native 125I-HDL.	abae	85-89	NLR family pyrin domain containing 3	Homo sapiens	156-160
3106756-6	1987	Thus, CS-514 reduces atherogenic lipoproteins and apolipoprotein B, and increases HDL and apolipoprotein A-I and A-II, and appears to be a useful drug for heterozygous familial hypercholesterolemia.	Cesium	6-8	NLR family pyrin domain containing 3	Homo sapiens	113-117
2822525-5	1987	In goldfish, the angiotensin-converting enzyme inhibitor captopril, which inhibits the conversion of AI to AII, was not able to block sAI-stimulated ACTH release.	Captopril	57-66	NLR family pyrin domain containing 3	Homo sapiens	107-110
2822525-7	1987	This hypothesis was supported by the observation that sarcosine analogs of AII, which block AII-stimulated ACTH release in mammals, failed to block hAII-stimulated ACTH release in goldfish.	Sarcosine	54-63	NLR family pyrin domain containing 3	Homo sapiens	75-78
3111539-6	1987	The uptake of HDL cholesteryl ester by intact adipocytes as monitored by [3H]cholesteryl ether labeled HDL3, was also significantly reduced (about 35% reduction, P less than 0.005) by substituting apolipoprotein A-II for A-I in HDL3.	Cholesterol Esters	18-35	NLR family pyrin domain containing 3	Homo sapiens	212-216
3585907-2	1987	Incorporation of hexafluorovaline into angiotensin resulted in [Sar1,Hfv8]AII and [Sar1,D-Hfv8]AII.	hexafluorovaline	17-33	NLR family pyrin domain containing 3	Homo sapiens	74-77
3585907-2	1987	Incorporation of hexafluorovaline into angiotensin resulted in [Sar1,Hfv8]AII and [Sar1,D-Hfv8]AII.	hexafluorovaline	17-33	NLR family pyrin domain containing 3	Homo sapiens	95-98
3033389-1	1987	It has been suggested that AII-mediated renal mechanisms limit the efficacy of moderate sodium restriction in the lowering of blood pressure (BP) in hypertension.	Sodium	88-94	NLR family pyrin domain containing 3	Homo sapiens	27-30
3106550-6	1987	BALB/c apoA-II contains one residue each of histidine and arginine, neither of which are found in the human A-II protein.	Histidine	44-53	NLR family pyrin domain containing 3	Homo sapiens	10-14
3106550-6	1987	BALB/c apoA-II contains one residue each of histidine and arginine, neither of which are found in the human A-II protein.	Arginine	58-66	NLR family pyrin domain containing 3	Homo sapiens	10-14
3038417-3	1987	In NM the renal vascular response to AII is blunted when the subjects are on a high-salt diet, but appropriate when they are on a low-salt diet.	Salts	84-88	NLR family pyrin domain containing 3	Homo sapiens	37-40
3038417-3	1987	In NM the renal vascular response to AII is blunted when the subjects are on a high-salt diet, but appropriate when they are on a low-salt diet.	Salts	134-138	NLR family pyrin domain containing 3	Homo sapiens	37-40
2856549-11	1987	Raising the level of endogenous AII by intravenous administration of its precursor renin has similar effects, and these are prevented if captopril is administered previously (Koller et al, 1979).	Captopril	137-146	NLR family pyrin domain containing 3	Homo sapiens	32-35
2856549-12	1987	Also, chronic oral treatment with captopril produces changes of brain renin angiotensin system parameters which suggest inhibition of AII biosyntheses in the brain (Scholkens et al, 1983).	Captopril	34-43	NLR family pyrin domain containing 3	Homo sapiens	134-137
2856549-13	1987	It is conceivable therefore, that our findings with prolonged administration of captopril are exerted through reduced formation of AII.	Captopril	80-89	NLR family pyrin domain containing 3	Homo sapiens	131-134
3533926-0	1986	Deletion of the propeptide from human preproapolipoprotein A-II redirects cotranslational processing by signal peptidase.	propeptide	16-26	NLR family pyrin domain containing 3	Homo sapiens	59-63
3583682-4	1987	A second isozyme, designated AII (or A4), has a neutral pI, is located in the mitochondrial matrix, and is thought to be involved primarily in the production of ornithine as a precursor of proline and glutamate.	Proline	189-196	NLR family pyrin domain containing 3	Homo sapiens	29-32
3583682-4	1987	A second isozyme, designated AII (or A4), has a neutral pI, is located in the mitochondrial matrix, and is thought to be involved primarily in the production of ornithine as a precursor of proline and glutamate.	Glutamic Acid	201-210	NLR family pyrin domain containing 3	Homo sapiens	29-32
3583682-4	1987	A second isozyme, designated AII (or A4), has a neutral pI, is located in the mitochondrial matrix, and is thought to be involved primarily in the production of ornithine as a precursor of proline and glutamate.	Ornithine	161-170	NLR family pyrin domain containing 3	Homo sapiens	29-32
2862635-2	1985	The dendritic morphology of the DAPI-labelled cells was defined by iontophoretic injection of Lucifer yellow under direct microscopic control: all the filled cells had the narrow-field bistratified morphology that is distinctive of the AII amacrine cells previously described from Golgi-stained retinae.	DAPI	32-36	NLR family pyrin domain containing 3	Homo sapiens	236-239
3100848-0	1986	[Effect of daily intake of carbohydrate, protein and fat on serum levels of HDL cholesterol and apolipoproteins A-I and A-II].	Carbohydrates	27-39	NLR family pyrin domain containing 3	Homo sapiens	96-125
2931988-4	1985	Both ethinyl estradiol/levonorgestrel and ethinyl estradiol/desogestrel increased apolipoproteins A (14%), A-I (20% to 30%), and A-II (25% to 35%) significantly.	Ethinyl Estradiol	5-22	NLR family pyrin domain containing 3	Homo sapiens	129-133
2931988-4	1985	Both ethinyl estradiol/levonorgestrel and ethinyl estradiol/desogestrel increased apolipoproteins A (14%), A-I (20% to 30%), and A-II (25% to 35%) significantly.	Levonorgestrel	23-37	NLR family pyrin domain containing 3	Homo sapiens	129-133
2931988-4	1985	Both ethinyl estradiol/levonorgestrel and ethinyl estradiol/desogestrel increased apolipoproteins A (14%), A-I (20% to 30%), and A-II (25% to 35%) significantly.	Ethinyl Estradiol	42-59	NLR family pyrin domain containing 3	Homo sapiens	129-133
2931988-4	1985	Both ethinyl estradiol/levonorgestrel and ethinyl estradiol/desogestrel increased apolipoproteins A (14%), A-I (20% to 30%), and A-II (25% to 35%) significantly.	Desogestrel	60-71	NLR family pyrin domain containing 3	Homo sapiens	129-133
3796815-5	1986	Three types of non-pyramidal layer II cells that project ipsilaterally from AI to the second auditory cortical field, AII, possibly accumulate gamma-aminobutyric acid; 3 types of commissural non-pyramidal cells of origin linking AI to AI appear to be labeled by gamma-aminobutyric acid.	gamma-Aminobutyric Acid	143-166	NLR family pyrin domain containing 3	Homo sapiens	118-121
3017059-8	1986	These changes in renal handling of salt and water are primarily caused by decreased AII.	Salts	35-39	NLR family pyrin domain containing 3	Homo sapiens	84-87
3017059-8	1986	These changes in renal handling of salt and water are primarily caused by decreased AII.	Water	44-49	NLR family pyrin domain containing 3	Homo sapiens	84-87
3999973-3	1985	Carbohydrate intake correlated negatively with HDL3 concentrations, and alcohol intake correlated positively with serum concentrations of HDL3 and apolipoproteins A-I, A-II, and D.	Alcohols	72-79	NLR family pyrin domain containing 3	Homo sapiens	147-179
3907298-2	1985	Gemfibrozil also produces increases in both Apo AI and AII, and in kininogen and prekallikrein.	Gemfibrozil	0-11	NLR family pyrin domain containing 3	Homo sapiens	55-58
2985608-0	1985	Binding of apolipoprotein A-I and A-II after recombination with phospholipid vesicles to the high density lipoprotein receptor of luteinized rat ovary.	Phospholipids	64-76	NLR family pyrin domain containing 3	Homo sapiens	34-38
2985608-2	1985	Both 125I-apo-A-I.DMPC and 125I-apo-A-II.DMPC were shown to bind to ovarian membranes with Kd = 2.87 and 5.70 micrograms of protein/ml, respectively.	Dimyristoylphosphatidylcholine	41-45	NLR family pyrin domain containing 3	Homo sapiens	36-40
2985608-10	1985	An examination of the equilibrium dissociation constant and binding capacity for 125I-apo-A-I.DMPC and 125I-apo-A-II.DMPC after human chorionic gonadotropin treatment revealed that the increase in binding activity was due to an increase in the number of binding sites rather than a change in the binding affinity.	Dimyristoylphosphatidylcholine	117-121	NLR family pyrin domain containing 3	Homo sapiens	112-116
2983412-3	1985	Despite appropriate correction for cross-reaction of AI with the AII antibody, one of the techniques gave consistently higher AII and lower AI levels in plasma of subjects treated with enalapril.	Enalapril	185-194	NLR family pyrin domain containing 3	Homo sapiens	65-68
2983412-3	1985	Despite appropriate correction for cross-reaction of AI with the AII antibody, one of the techniques gave consistently higher AII and lower AI levels in plasma of subjects treated with enalapril.	Enalapril	185-194	NLR family pyrin domain containing 3	Homo sapiens	126-129
6427534-0	1984	Acute effects of a glucose load on plasma apolipoproteins A-I, A-II, C-II, and C-III in normal and non-insulin-dependent diabetic men.	Glucose	19-26	NLR family pyrin domain containing 3	Homo sapiens	63-67
6427214-1	1984	Micellar, discoidal complexes of human apolipoproteins A-I, A-II, C-I, C-II, C-III-1, and C-III-2 with egg phosphatidylcholine (egg-PC) and cholesterol were prepared by the cholate dialysis method.	Phosphatidylcholines	107-126	NLR family pyrin domain containing 3	Homo sapiens	39-69
6427214-1	1984	Micellar, discoidal complexes of human apolipoproteins A-I, A-II, C-I, C-II, C-III-1, and C-III-2 with egg phosphatidylcholine (egg-PC) and cholesterol were prepared by the cholate dialysis method.	(3-Hexadecanoyloxy-2-nonadecanoyloxypropyl) 2-(trimethylazaniumyl)ethyl phosphate	128-134	NLR family pyrin domain containing 3	Homo sapiens	39-69
6427214-1	1984	Micellar, discoidal complexes of human apolipoproteins A-I, A-II, C-I, C-II, C-III-1, and C-III-2 with egg phosphatidylcholine (egg-PC) and cholesterol were prepared by the cholate dialysis method.	Cholesterol	140-151	NLR family pyrin domain containing 3	Homo sapiens	39-69
6427214-1	1984	Micellar, discoidal complexes of human apolipoproteins A-I, A-II, C-I, C-II, C-III-1, and C-III-2 with egg phosphatidylcholine (egg-PC) and cholesterol were prepared by the cholate dialysis method.	Cholates	173-180	NLR family pyrin domain containing 3	Homo sapiens	39-69
6427214-6	1984	In decreasing order of reactivity were the complexes with A-I, C-I, C-III-1, C-III-2, C-II, and A-II.	Carbon	63-64	NLR family pyrin domain containing 3	Homo sapiens	96-100
6742406-3	1984	The 125I-labeled angiotensins prepared by this method were bound by antibodies (AI) and adrenal receptors (AII, Saralasin) to an extent similar to angiotensins prepared by DEAE-Sephadex A-25 chromatography.	Iodine-125	4-8	NLR family pyrin domain containing 3	Homo sapiens	107-110
6427214-6	1984	In decreasing order of reactivity were the complexes with A-I, C-I, C-III-1, C-III-2, C-II, and A-II.	Carbon	68-69	NLR family pyrin domain containing 3	Homo sapiens	96-100
6403042-5	1983	Nicotinic acid selectively raised the plasma apolipoprotein A-I/A-II ratio by increasing the proportion of (AI)HDL particles.	Niacin	0-14	NLR family pyrin domain containing 3	Homo sapiens	64-68
6345360-6	1983	The pressor effect of AII increased in pregnant rabbits after the administration of meclofenamate and parturition but was not changed by volume expansion.	Meclofenamic Acid	84-97	NLR family pyrin domain containing 3	Homo sapiens	22-25
6418648-4	1983	Human AII (10(-6) M) produced a similar response in summer frogs that had been treated with 0.1% NaCl for 14 days.	Sodium Chloride	97-101	NLR family pyrin domain containing 3	Homo sapiens	6-9
6403535-8	1983	Apolipoproteins A-I, A-II, C-I, and E, in contrast, have a secondary structure that contains a high percentage of residues in an alpha-helical configuration and undergo major changes in structure at low concentrations of guanidinium chloride.	Guanidine	221-241	NLR family pyrin domain containing 3	Homo sapiens	0-25
6403535-9	1983	Highly flexible proteins, such as apolipoproteins A-I, A-II, and C-I, absorb rapidly and reversibly to air-water interfaces, whereas more rigid proteins, such as the classical globular proteins, interact with the interface more slowly and irreversibly.	Water	107-112	NLR family pyrin domain containing 3	Homo sapiens	34-59
6349867-6	1983	In the group given thiopentone there was no significant overall change in blood pressure but an increase in AII.	Thiopental	19-30	NLR family pyrin domain containing 3	Homo sapiens	108-111
6615245-4	1983	Propranolol treatment was associated with consistent and significant decreases in HDL-cholesterol, apoA-I and A-II levels, whereas these changes during the other treatments were neither significant nor consistent.	Propranolol	0-11	NLR family pyrin domain containing 3	Homo sapiens	110-114
7039897-2	1982	A depressor effect of Captopril was observed even in patients with AII-A unresponsive dialysis resistant hypertension.	Captopril	22-31	NLR family pyrin domain containing 3	Homo sapiens	67-70
7150617-3	1982	The addition of purified human plasma apolipoprotein A-I, A-II, E, C-I or C-III2 (containing 2 mol of sialic acid) to HDL2 caused inhibition of hepatic lipase activity.	N-Acetylneuraminic Acid	102-113	NLR family pyrin domain containing 3	Homo sapiens	58-70
6804585-9	1982	Chylomicron apoA-I/triglyceride and apoA-II/triglyceride mass ratios were lower in polyunsaturated fat-fed animals (A-I/TG = 1.56 x 10(-3); A-II/TG = 1.47 x 10(-3)) vs. saturated fat-fed animals (A-I/TG = 2.58 x 10(-3); A-II/TG = 2.77 x 10(-3)).	polyunsaturated fat	83-102	NLR family pyrin domain containing 3	Homo sapiens	39-43
6804585-9	1982	Chylomicron apoA-I/triglyceride and apoA-II/triglyceride mass ratios were lower in polyunsaturated fat-fed animals (A-I/TG = 1.56 x 10(-3); A-II/TG = 1.47 x 10(-3)) vs. saturated fat-fed animals (A-I/TG = 2.58 x 10(-3); A-II/TG = 2.77 x 10(-3)).	polyunsaturated fat	83-102	NLR family pyrin domain containing 3	Homo sapiens	140-144
6804585-10	1982	It was concluded that: (1) dietary polyunsaturated fat significantly lowered plasma cholesterol, HDL, and apoA-I concentrations relative to saturated fat; (2) the HDL-lowering effect of the dietary polyunsaturated fat may be due to the combined effects of decreased apoprotein production by the intestine and increased HDL catabolism; and (3) in the blood, chylomicron apoA-I and A-II differ in their metabolic fates.-Parks, J. S., and L. L. Rudel.	polyunsaturated fat	35-54	NLR family pyrin domain containing 3	Homo sapiens	380-384
6804585-10	1982	It was concluded that: (1) dietary polyunsaturated fat significantly lowered plasma cholesterol, HDL, and apoA-I concentrations relative to saturated fat; (2) the HDL-lowering effect of the dietary polyunsaturated fat may be due to the combined effects of decreased apoprotein production by the intestine and increased HDL catabolism; and (3) in the blood, chylomicron apoA-I and A-II differ in their metabolic fates.-Parks, J. S., and L. L. Rudel.	saturated fat	41-54	NLR family pyrin domain containing 3	Homo sapiens	380-384
6794096-7	1981	Meclofenamate (10(-7)M) pretreatment of strips subjected to dose-response studies using PGF2 alpha, PGE2, bradykinin (B K) and angiotensin II (AII) revealed a significant reduction in tension developed to both BK and AII.	Meclofenamic Acid	0-13	NLR family pyrin domain containing 3	Homo sapiens	210-220
7200346-6	1982	The data confirm the hypothesis that the principal determinant of pressor responsiveness to A II during pregnancy is arteriolar response; this seems to be modulated by alterations in the sodium content of the vessel wall.	Sodium	187-193	NLR family pyrin domain containing 3	Homo sapiens	92-96
7135667-6	1982	The apo A-II concentration was significantly correlated to the ratio between homo-gamma-linolenic and arachidonic acid in all serum lipid esters.	homo-gamma-linolenic	77-97	NLR family pyrin domain containing 3	Homo sapiens	8-12
7135667-6	1982	The apo A-II concentration was significantly correlated to the ratio between homo-gamma-linolenic and arachidonic acid in all serum lipid esters.	Arachidonic Acid	102-118	NLR family pyrin domain containing 3	Homo sapiens	8-12
7135667-6	1982	The apo A-II concentration was significantly correlated to the ratio between homo-gamma-linolenic and arachidonic acid in all serum lipid esters.	lipid esters	132-144	NLR family pyrin domain containing 3	Homo sapiens	8-12
6167515-9	1981	In addition, postjunctional pressor responses to AI, AII, and NE were also significantly inhibited by chronic captopril treatment.	Captopril	110-119	NLR family pyrin domain containing 3	Homo sapiens	53-56
6167515-11	1981	However, the combination of pretreatment of indomethacin and infusion of AII completely restored sympathetic function in SHR receiving captopril.	Captopril	135-144	NLR family pyrin domain containing 3	Homo sapiens	73-76
6167515-14	1981	Since, under appropriate conditions, the inhibition can be reversed by AII infusion but not nephrectomy, it is suggested that this inhibition occurs at the vascular level by inhibition of local AII formation by captopril, a site not accessible to teprotide or saralasin.	Captopril	211-220	NLR family pyrin domain containing 3	Homo sapiens	194-197
6776144-14	1980	By analogy to the apo(E--A-II) complex, which also occurs in human HDL, this mixed disulfide complex was designated as the apo(A-Icys--A-II) complex.	Disulfides	83-92	NLR family pyrin domain containing 3	Homo sapiens	25-29
7010929-11	1981	Apoprotein A-I remained unchanged, but A-II increased by 20% during gemfibrozil treatment.	Gemfibrozil	68-79	NLR family pyrin domain containing 3	Homo sapiens	39-43
7220655-2	1981	This dose of AII is well within that given experimentally by various workers, and was without such effect when initially given in the absence of PGE2 infusion.	Dinoprostone	145-149	NLR family pyrin domain containing 3	Homo sapiens	13-16
6776144-14	1980	By analogy to the apo(E--A-II) complex, which also occurs in human HDL, this mixed disulfide complex was designated as the apo(A-Icys--A-II) complex.	Disulfides	83-92	NLR family pyrin domain containing 3	Homo sapiens	135-139
7002566-3	1980	Both AIIA had agonistic pressor activities in subjects on high and regular sodium diets, [Sar, Ile]-AII being more potent than [Sar, Ala]-AII.	Sodium	75-81	NLR family pyrin domain containing 3	Homo sapiens	5-8
7002566-5	1980	Both AIIA strongly antagonized the rise in BP, the increase in PAC and the reduction of Ccr induced by AII administration in subjects on all three sodium diets.	Sodium	147-153	NLR family pyrin domain containing 3	Homo sapiens	5-8
228682-1	1979	This study on 4 type II hyperlipoproteinaemic subjects examines the effects of pharmacologic doses (8 g twice daily) of the bile acid sequestrant cholestyramine on the plasma distribution and chemical composition of the high density lipoprotein subfractions, HDL2 and HDL3, and describes the influence of the drug on the metabolism of the major HDL aporoteins, apolipoprotein A-I and A-II.	Cholestyramine Resin	146-160	NLR family pyrin domain containing 3	Homo sapiens	384-388
7362696-4	1980	With clofibrate, HDL cholesterol increased by 16 +/- 20% from baseline (mean +/- SD) (P less than 0.05), A-I by 11 +/- 13% (P less than 0.05) and A-II by 39 +/- 17% (P less than 0.01).	Clofibrate	5-15	NLR family pyrin domain containing 3	Homo sapiens	146-150
7362696-5	1980	During oxandrolone HDL cholesterol declined by 36 +/- 20% from baseline (P less than 0.01), A-I by 21 +/- 13% (P less than 0.01), and A-II by 16 +/- 11% (P less than 0.025).	Oxandrolone	7-18	NLR family pyrin domain containing 3	Homo sapiens	134-138
7350924-11	1980	Our results suggest that fragment A-II may be very useful as a model peptide to study the actions and mechanism of naturally occurring sometomedins.	sometomedins	135-147	NLR family pyrin domain containing 3	Homo sapiens	34-38
229069-2	1979	Ultraviolet irradiation generated the nitrene which led to crosslinking with the two main apolipoproteins AI and AII.	phenylnitrene	38-45	NLR family pyrin domain containing 3	Homo sapiens	90-116
6774752-0	1980	Reassembly of human apoproteins A-I and A-II with unilamellar phosphatidylcholine-cholesterol liposomes.	Phosphatidylcholines	62-81	NLR family pyrin domain containing 3	Homo sapiens	40-44
6774752-0	1980	Reassembly of human apoproteins A-I and A-II with unilamellar phosphatidylcholine-cholesterol liposomes.	Cholesterol	82-93	NLR family pyrin domain containing 3	Homo sapiens	40-44
6774752-5	1980	Under all incubation conditions the apoprotein A-II associates more readily with cholesterol-DMPC vesicles than apoprotein A-I, as the kinetics are faster and the complex yield larger.	Cholesterol	81-92	NLR family pyrin domain containing 3	Homo sapiens	47-51
6774752-5	1980	Under all incubation conditions the apoprotein A-II associates more readily with cholesterol-DMPC vesicles than apoprotein A-I, as the kinetics are faster and the complex yield larger.	Dimyristoylphosphatidylcholine	93-97	NLR family pyrin domain containing 3	Homo sapiens	47-51
6774752-7	1980	The apoprotein A-I/lipid association seems restricted to this narrow range for the temperature and the cholesterol/DMPC ratio, while the apoprotein A-II still associates with vesicles containing 20 mol% cholesterol and at temperatures up to 32 degrees C. The lipid-apoprotein complexes were isolated by gradient ultracentrifugation and by gel chromatography.	Cholesterol	203-214	NLR family pyrin domain containing 3	Homo sapiens	148-152
6774752-8	1980	According to these data the apoprotein A-II associates more readily than apoprotein A-I with cholesterol-DMPC vesicles to form protein-rich complexes, whilst the optimal apoprotein A-I-lipid association requires a more disordered lipid structure.	Dimyristoylphosphatidylcholine	105-109	NLR family pyrin domain containing 3	Homo sapiens	39-43
6773532-3	1980	The concentration of HDL cholesterol was significantly lower and that of apoprotein A-II significantly higher in the individuals treated with clofibrate than in the controls.	Clofibrate	142-152	NLR family pyrin domain containing 3	Homo sapiens	84-88
6773532-4	1980	On the other hand, the levels of both HDL cholesterol and apoprotein A-I were lower in the men treated with probucol than in the controls, whereas that of A-II was within the control limits.	Probucol	108-116	NLR family pyrin domain containing 3	Homo sapiens	155-159
113608-4	1979	Observations from the pharmacodynamic investigations have shown that saralasin is a specific competitive antagonist of the vascular, renal, adrenal, cardiac, and central nervous system actions of AII.	Saralasin	69-78	NLR family pyrin domain containing 3	Homo sapiens	196-199
837929-7	1977	Different techniques used to solubilise RNA polymerase activity from nucleoli are shown to give rise to different proportions of the two form A RNA polymerase species (AI and AII, as defined by their differential elution from phosphocellulose): whereas low-ionic-strength extraction gives rise to form AII, high-salt, sonication extracts contain predominantly the form AI enzyme.	phosphocellulose	226-242	NLR family pyrin domain containing 3	Homo sapiens	168-178
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	carbamino	56-65	NLR family pyrin domain containing 3	Homo sapiens	191-210
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	Amines	88-94	NLR family pyrin domain containing 3	Homo sapiens	191-210
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	pco2	120-124	NLR family pyrin domain containing 3	Homo sapiens	191-210
32935-4	1978	The mole fraction, Z, of carbamino adduct form of AII or BK shows a maximum variation in going from metabolic alkalosis, Z congruent to 0.30, to metabolic acidosis, Z congruent to 0.02, with Z near 0.2 for normal acid-base conditions.	carbamino	25-34	NLR family pyrin domain containing 3	Homo sapiens	50-53
194920-8	1977	The ability of Tangier apoprotein A-II to bind phospholipid was demonstrated by in vitro reconstitution experiments and morphological and chemical analysis of lipid-protein complexes.	Phospholipids	47-59	NLR family pyrin domain containing 3	Homo sapiens	34-38
194921-3	1977	A-II correlated significantly with apolipoprotein A-I (A-I) (r = 0.71) and high density lipoprotein (HDL) cholesterol (men, r = 0.64; women, r = 0.49).	Cholesterol	106-117	NLR family pyrin domain containing 3	Homo sapiens	0-4
194921-4	1977	The A-I/A-II ratio was significantly related to HDL cholesterol (men, r = 0.29; women, r = 0.44).	Cholesterol	52-63	NLR family pyrin domain containing 3	Homo sapiens	8-12
361487-6	1978	Of the 14C incorporated into the d less than 1.006 fraction, 10.8, 7.2, and 7.1% were specifically precipitated by rabbit antihuman apoproteins A-I, A-II, and B, respectively.	Carbon-14	7-10	NLR family pyrin domain containing 3	Homo sapiens	144-160
837929-7	1977	Different techniques used to solubilise RNA polymerase activity from nucleoli are shown to give rise to different proportions of the two form A RNA polymerase species (AI and AII, as defined by their differential elution from phosphocellulose): whereas low-ionic-strength extraction gives rise to form AII, high-salt, sonication extracts contain predominantly the form AI enzyme.	phosphocellulose	226-242	NLR family pyrin domain containing 3	Homo sapiens	175-178
1131700-4	1975	In other experiments L-[4-5-3-H]leucine was injected into the cortex of AI, AII and SF and its transport to the MGB was studied by autoradiography.	l-[4-5-3-h]leucine	21-39	NLR family pyrin domain containing 3	Homo sapiens	76-79
182183-20	1976	A-II had a molecular weight of about 10,000, contained no half cystine and had alanine as the C-terminal amino acid.	Alanine	79-86	NLR family pyrin domain containing 3	Homo sapiens	0-4
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	NLR family pyrin domain containing 3	Homo sapiens	27-39
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	NLR family pyrin domain containing 3	Homo sapiens	35-39
1185036-5	1975	Significant increments of PRA and A II on either sodium intake occurred within 5 to 20 minutes; the peak values occurred within 90 minutes and tended to plateau until the end of the study (240 minutes).	Sodium	49-55	NLR family pyrin domain containing 3	Homo sapiens	34-38
167864-16	1975	The serum apolipoproteins and their constitutive polypeptides (A-I, A-II, B, C-I, C-II, C-III, D and arginine-rich apolipoprotein) reacted negatively with antibodies to intact or EDTA-extracted ghosts.	Edetic Acid	179-183	NLR family pyrin domain containing 3	Homo sapiens	68-80
952970-2	1976	It was found: (1) In the presence of benzyl viologen as electron acceptor and with water as natural electron donor trypsin, incubation leads to a complete suppression of the absorption changes of the electrochromic effect and of chlorophyll aI and chlorophyll aII.	Water	83-88	NLR family pyrin domain containing 3	Homo sapiens	260-263
182183-20	1976	A-II had a molecular weight of about 10,000, contained no half cystine and had alanine as the C-terminal amino acid.	Cystine	63-70	NLR family pyrin domain containing 3	Homo sapiens	0-4
1177406-6	1975	Infusion of A II-amide increased extraction of A II.	Amides	17-22	NLR family pyrin domain containing 3	Homo sapiens	12-16
1177406-6	1975	Infusion of A II-amide increased extraction of A II.	Amides	17-22	NLR family pyrin domain containing 3	Homo sapiens	47-51
1177406-9	1975	Sodium depletion increased arterial and venous concentrations of A II and H.	Sodium	0-6	NLR family pyrin domain containing 3	Homo sapiens	65-75
1177406-10	1975	During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion.	Amides	34-39	NLR family pyrin domain containing 3	Homo sapiens	82-92
1177406-10	1975	During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion.	Sodium	155-161	NLR family pyrin domain containing 3	Homo sapiens	82-92
1177406-13	1975	The augmented extraction extraction of A II observed during infusion of angiotensin II-amide suggest an overproportional increase of the metabolism of A II under the latter condition.	Amides	87-92	NLR family pyrin domain containing 3	Homo sapiens	39-43
1177406-13	1975	The augmented extraction extraction of A II observed during infusion of angiotensin II-amide suggest an overproportional increase of the metabolism of A II under the latter condition.	Amides	87-92	NLR family pyrin domain containing 3	Homo sapiens	151-155
33677310-0	2021	Total glucosides of paeony protects THP-1 macrophages against monosodium urate-induced inflammation via MALAT1/miR-876-5p/NLRP3 signaling cascade in gouty arthritis.	Glucosides	6-16	NLR family pyrin domain containing 3	Homo sapiens	122-127
4357738-1	1973	Interaction of the cyanogen bromide fragments from apolipoprotein glutamine II (A-II) with phosphatidylcholine.	Cyanogen Bromide	19-35	NLR family pyrin domain containing 3	Homo sapiens	51-84
4357738-1	1973	Interaction of the cyanogen bromide fragments from apolipoprotein glutamine II (A-II) with phosphatidylcholine.	Phosphatidylcholines	91-110	NLR family pyrin domain containing 3	Homo sapiens	51-84
33845232-0	2021	Discovery of chalcone analogues as novel NLRP3 inflammasome inhibitors with potent anti-inflammation activities.	Chalcone	13-21	NLR family pyrin domain containing 3	Homo sapiens	41-46
33845232-4	2021	Further mechanistic study indicated that compound 40 inhibited the NLRP3 inflammasome activation via suppressing ROS production.	ros	113-116	NLR family pyrin domain containing 3	Homo sapiens	67-72
34036391-6	2021	Then, the therapeutic effect of the selective P2X7R antagonist, A740003, on P3X7R, NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome and IL-1beta alterations in HNECs was explored using enzyme-linked immunosorbent assay, WB and PCR.	(N-(1-(((cyanoimino)(5-quinolinylamino) methyl) amino)-2,2-dimethylpropyl)-2-(3,4-dimethoxyphenyl)acetamide)	64-71	NLR family pyrin domain containing 3	Homo sapiens	128-133
34036391-7	2021	It was found that P2X7R was overexpressed in CRSwNP, especially in eosinophilic CRSwNP, the expression of P2X7R, NLRP3 and IL-1beta were upregulated in HNECs after induction by LPS combined with BzATP; but the expression of NLRP3 and IL-1beta were downregulated after stimulation with A740003.	3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate	195-200	NLR family pyrin domain containing 3	Homo sapiens	113-118
34036391-7	2021	It was found that P2X7R was overexpressed in CRSwNP, especially in eosinophilic CRSwNP, the expression of P2X7R, NLRP3 and IL-1beta were upregulated in HNECs after induction by LPS combined with BzATP; but the expression of NLRP3 and IL-1beta were downregulated after stimulation with A740003.	(N-(1-(((cyanoimino)(5-quinolinylamino) methyl) amino)-2,2-dimethylpropyl)-2-(3,4-dimethoxyphenyl)acetamide)	285-292	NLR family pyrin domain containing 3	Homo sapiens	113-118
33485222-0	2021	A tandem activation of NLRP3 inflammasome induced by copper oxide nanoparticles and dissolved copper ion in J774A.1 macrophage.	cupric oxide	53-65	NLR family pyrin domain containing 3	Homo sapiens	23-28
33485222-0	2021	A tandem activation of NLRP3 inflammasome induced by copper oxide nanoparticles and dissolved copper ion in J774A.1 macrophage.	Copper	53-59	NLR family pyrin domain containing 3	Homo sapiens	23-28
33485222-1	2021	For the first time, we reported that CuONPs exposure induced interleukin (IL)-1beta-mediated inflammation via NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome in J774A.1 macrophage.	cuonps	37-43	NLR family pyrin domain containing 3	Homo sapiens	110-158
33485222-1	2021	For the first time, we reported that CuONPs exposure induced interleukin (IL)-1beta-mediated inflammation via NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome in J774A.1 macrophage.	cuonps	37-43	NLR family pyrin domain containing 3	Homo sapiens	160-165
33485222-5	2021	Consequently, the released copper ions significantly induced cellular oxidative stress and further mediated the activation of NLRP3 inflammasomes.	Copper	27-33	NLR family pyrin domain containing 3	Homo sapiens	126-131
33677310-8	2021	Overexpression of NLRP3 or MALAT1 reversed the protective effects of TGP in MSU-induced THP-1 macrophages.	tgp	69-72	NLR family pyrin domain containing 3	Homo sapiens	18-23
33677310-8	2021	Overexpression of NLRP3 or MALAT1 reversed the protective effects of TGP in MSU-induced THP-1 macrophages.	Uric Acid	76-79	NLR family pyrin domain containing 3	Homo sapiens	18-23
33677310-11	2021	TGP suppressed MSU-induced inflammation in THP-1 macrophages through regulating MALAT1/miR-876-5p/NLRP3 axis.	Uric Acid	15-18	NLR family pyrin domain containing 3	Homo sapiens	98-103
33677310-0	2021	Total glucosides of paeony protects THP-1 macrophages against monosodium urate-induced inflammation via MALAT1/miR-876-5p/NLRP3 signaling cascade in gouty arthritis.	Uric Acid	73-78	NLR family pyrin domain containing 3	Homo sapiens	122-127
33677310-12	2021	TGP suppressed MSU-induced activation of TLR4/MyD88/NF-kappaB pathway through regulating MALAT1/miR-876-5p/NLRP3 axis.	Uric Acid	15-18	NLR family pyrin domain containing 3	Homo sapiens	107-112
33848919-7	2021	It is known that melatonin prevents the activation of NLRP3 inflammasome.	Melatonin	17-26	NLR family pyrin domain containing 3	Homo sapiens	54-59
33857491-0	2021	Ganoderic acid A exerted antidepressant-like action through FXR modulated NLRP3 inflammasome and synaptic activity.	ganoderic acid A	0-16	NLR family pyrin domain containing 3	Homo sapiens	74-79
33864951-4	2021	Ceramides may be key players in promoting an obesity-induced inflammatory environment due to their ability to activate key pathways such as Toll-like receptor 4 (TLR4) and NLR pyrin domain containing receptor 3 (Nlrp3), while studies have shown that inhibition of ceramide synthesis gives rise to an anti-inflammatory environment.	Ceramides	0-9	NLR family pyrin domain containing 3	Homo sapiens	212-217
33915328-8	2021	A438079 promoted apoptosis via the Bcl-2/caspase9/caspase3 pathway and inhibited pyroptosis through the NLRP3/caspase1 pathway by inhibiting P2X7R in vitro and in vivo.	3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridine	0-7	NLR family pyrin domain containing 3	Homo sapiens	104-109
33848919-8	2021	In light of these findings, we think that melatonin treatment during COVID-19 or periodontal diseases may prevent the damage seen in periodontal tissues by preventing the activation of NLRP3 inflammasome.	Melatonin	42-51	NLR family pyrin domain containing 3	Homo sapiens	185-190
34058229-0	2021	VDAC1 regulates mitophagy in NLRP3 inflammasome activation in retinal capillary endothelial cells under high-glucose conditions.	Glucose	109-116	NLR family pyrin domain containing 3	Homo sapiens	29-34
33907835-8	2021	The expression of GOLPH3 and NLRP3 was associated with the expression of the proliferative marker Ki-67 in tissues, and associated with poor survival, tumor stage, degree of differentiation, depth of invasion, carbohydrate antigen 19-9 and C-reactive protein levels in patients with GBC.	Carbohydrates	210-222	NLR family pyrin domain containing 3	Homo sapiens	29-34
34059097-1	2021	BACKGROUND: Cryopyrin-associated periodic syndrome (CAPS) is a life-long, autoinflammatory disease associated with a gain-of-function mutation in the nucleotide-binding domain, leucine-rich repeat family, pyrin domain containing 3 (NLRP3) gene, which result in uncontrolled production of IL-1beta and chronic inflammation.	Leucine	177-184	NLR family pyrin domain containing 3	Homo sapiens	12-21
34059097-1	2021	BACKGROUND: Cryopyrin-associated periodic syndrome (CAPS) is a life-long, autoinflammatory disease associated with a gain-of-function mutation in the nucleotide-binding domain, leucine-rich repeat family, pyrin domain containing 3 (NLRP3) gene, which result in uncontrolled production of IL-1beta and chronic inflammation.	Leucine	177-184	NLR family pyrin domain containing 3	Homo sapiens	232-237
34053376-4	2021	EXPERT OPINION: Advances in molecular biology reveal that at the base of the inflammatory cascade, stimulated by MSU or CPP crystals, there are many complex cellular mechanisms mainly involving the NLRP3 inflammasome, the hallmark of autoinflammatory syndromes.	Uric Acid	113-116	NLR family pyrin domain containing 3	Homo sapiens	198-203
34048091-1	2021	The NMDA receptors (NMDARs) expressed by AII and A17 amacrine cells, the two main inhibitory interneurons of the rod pathway microcircuit in the mammalian retina, are exclusively extrasynaptic, activated by ambient levels of glutamate, and molecularly distinct, with AII and A17 amacrines expressing GluN2B- and GluN2A-containing receptors, respectively.	Glutamic Acid	225-234	NLR family pyrin domain containing 3	Homo sapiens	41-44
34048091-1	2021	The NMDA receptors (NMDARs) expressed by AII and A17 amacrine cells, the two main inhibitory interneurons of the rod pathway microcircuit in the mammalian retina, are exclusively extrasynaptic, activated by ambient levels of glutamate, and molecularly distinct, with AII and A17 amacrines expressing GluN2B- and GluN2A-containing receptors, respectively.	Glutamic Acid	225-234	NLR family pyrin domain containing 3	Homo sapiens	267-270
34048091-5	2021	Pre-incubation of retina with bafilomycin A1 (an inhibitor of neurotransmitter uptake into synaptic vesicles) abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a vesicular source of glutamate activates AII NMDARs, whereas a non-vesicular source activates A17 NMDARs.	bafilomycin A1	30-44	NLR family pyrin domain containing 3	Homo sapiens	144-147
34048091-5	2021	Pre-incubation of retina with bafilomycin A1 (an inhibitor of neurotransmitter uptake into synaptic vesicles) abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a vesicular source of glutamate activates AII NMDARs, whereas a non-vesicular source activates A17 NMDARs.	bafilomycin A1	30-44	NLR family pyrin domain containing 3	Homo sapiens	225-228
34048091-6	2021	Pre-incubation of retina with L-methionine-sulfoximine (an inhibitor of glutamine synthetase) also abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a neuronal source of glutamate activates AII NMDARs, whereas a glial source activates A17 NMDARs.	L-Methionine sulfoximine	30-54	NLR family pyrin domain containing 3	Homo sapiens	133-136
34048091-6	2021	Pre-incubation of retina with L-methionine-sulfoximine (an inhibitor of glutamine synthetase) also abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a neuronal source of glutamate activates AII NMDARs, whereas a glial source activates A17 NMDARs.	L-Methionine sulfoximine	30-54	NLR family pyrin domain containing 3	Homo sapiens	213-216
34048091-6	2021	Pre-incubation of retina with L-methionine-sulfoximine (an inhibitor of glutamine synthetase) also abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a neuronal source of glutamate activates AII NMDARs, whereas a glial source activates A17 NMDARs.	Glutamine	72-81	NLR family pyrin domain containing 3	Homo sapiens	133-136
34048091-7	2021	Enzymatic breakdown of D-serine reduced NMDAR-mediated noise in AII, but not A17 amacrines, suggesting D-serine is the endogenous co-agonist at AII, but not A17 NMDARs.	Serine	25-31	NLR family pyrin domain containing 3	Homo sapiens	64-67
34048091-7	2021	Enzymatic breakdown of D-serine reduced NMDAR-mediated noise in AII, but not A17 amacrines, suggesting D-serine is the endogenous co-agonist at AII, but not A17 NMDARs.	Serine	25-31	NLR family pyrin domain containing 3	Homo sapiens	144-147
34059091-4	2021	The NLRP3 inflammasome is a complex with multiple components, including an NAIP, CIITA, HET-E, and TP1 (NACHT) domain; apoptosis-associated speck-like protein containing a CARD (ASC); and a leucine-rich repeat (LRR) domain.	Leucine	190-197	NLR family pyrin domain containing 3	Homo sapiens	4-9
34058186-0	2021	Pharmacological inhibition of fatty acid oxidation reduces atherosclerosis progression by suppression of macrophage NLRP3 inflammasome activation.	Fatty Acids	30-40	NLR family pyrin domain containing 3	Homo sapiens	116-121
34058186-3	2021	Fatty acid oxidation (FAO) was previously demonstrated to interact with the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) pathway which is required for mature IL-1beta secretion.	Fatty Acids	0-10	NLR family pyrin domain containing 3	Homo sapiens	76-124
34058186-3	2021	Fatty acid oxidation (FAO) was previously demonstrated to interact with the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) pathway which is required for mature IL-1beta secretion.	Fatty Acids	0-10	NLR family pyrin domain containing 3	Homo sapiens	126-131
34058186-11	2021	CONCLUSION: Overall, we therefore suggest that the main mechanism of reducing inflammation of trimetazidine and FAO inhibition is the reduction of the NLRP-3 activation leading to reduced levels of the proinflammatory cytokine IL-1beta.	Trimetazidine	94-107	NLR family pyrin domain containing 3	Homo sapiens	151-157
34037470-0	2021	MiR-494-3p alleviates acute lung injury through regulating NLRP3 activation by targeting CMPK2.	mir-494-3p	0-10	NLR family pyrin domain containing 3	Homo sapiens	59-64
34044014-9	2021	Similarly, in the inflammatory model, we found that different concentrations of kaempferol reduced the LPS-induced M1 polarization and NLRP3 inflammasome activation.	kaempferol	80-90	NLR family pyrin domain containing 3	Homo sapiens	135-140
34052623-7	2021	By using a mouse infection model, we also found that ATP exacerbated clinical signs and death of mice infected by PRV in a NLRP3-dependent manner.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	123-128
34052623-8	2021	These results indicate that ATP facilitates activation of NLRP3 inflammasome and enhances the pathogenicity of PRV in mice during its acute infection.	Adenosine Triphosphate	28-31	NLR family pyrin domain containing 3	Homo sapiens	58-63
34031983-2	2021	In this paper, we aim to investigate whether verapamil, an antagonist of TXNIP, inhibits early ALF through suppressing the NLRP3 inflammasome pathway.	Verapamil	45-54	NLR family pyrin domain containing 3	Homo sapiens	123-128
34044014-11	2021	In conclusion, we found that kaempferol can inhibit the activation of NLRP3 inflammasomes by inducing autophagy, thus inhibiting macrophage polarization, and ultimately alleviating corneal transplantation rejection.	kaempferol	29-39	NLR family pyrin domain containing 3	Homo sapiens	70-75
34024891-7	2021	Cardamonin reversed the effect of IL-1beta on cell viability, cell apoptosis, pro-inflammatory cytokines, MMPs, Collage II, NLRP3 inflammasome levels.	cardamonin	0-10	NLR family pyrin domain containing 3	Homo sapiens	124-129
34058500-0	2021	Biotransformation of soluble-insoluble lanthanum species and its induced NLRP3 inflammasome activation and chronic fibrosis.	Lanthanum	39-48	NLR family pyrin domain containing 3	Homo sapiens	73-78
34058500-4	2021	Insoluble La(III) species could adhere to extracellular membrane or be internalized into cells, capable of activating a nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome.	la(iii)	10-17	NLR family pyrin domain containing 3	Homo sapiens	181-186
34058500-4	2021	Insoluble La(III) species could adhere to extracellular membrane or be internalized into cells, capable of activating a nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome.	Leucine	150-157	NLR family pyrin domain containing 3	Homo sapiens	181-186
34024891-10	2021	Cardamonin inhibited IL-1beta-induced injury by inhibition of NLRP3 inflammasome via activating Nrf2/NQO1 signaling pathway in chondrocyte.	cardamonin	0-10	NLR family pyrin domain containing 3	Homo sapiens	62-67
34024891-0	2021	Cardamonin Inhibited IL-1beta-induced Injury by Inhibition of NLRP3 Inflammasome via Activating Nrf2/NQO1 Signaling Pathway in Chondrocyte.	cardamonin	0-10	NLR family pyrin domain containing 3	Homo sapiens	62-67
34011928-0	2021	Alternative polyadenylation trans-factor FIP1 exacerbates UUO/IRI-induced kidney injury and contributes to AKI-CKD transition via ROS-NLRP3 axis.	ros	130-133	NLR family pyrin domain containing 3	Homo sapiens	134-139
34011327-0	2021	Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy.	rhodioloside	0-11	NLR family pyrin domain containing 3	Homo sapiens	93-98
34011327-12	2021	SAL also attenuated LPS-induced activation of NLRP3 inflammasome, reduced the protein expression of NLRP3-related proteins, including ASC and caspase-1.	rhodioloside	0-3	NLR family pyrin domain containing 3	Homo sapiens	46-51
34011327-12	2021	SAL also attenuated LPS-induced activation of NLRP3 inflammasome, reduced the protein expression of NLRP3-related proteins, including ASC and caspase-1.	rhodioloside	0-3	NLR family pyrin domain containing 3	Homo sapiens	100-105
34011327-13	2021	Autophagy inhibition by 3-MA markedly reversed SAL-modulated changes in cell viability and NLRP3 expression in LPS-stimulated HUVECs.	3-methyladenine	24-28	NLR family pyrin domain containing 3	Homo sapiens	91-96
34011327-13	2021	Autophagy inhibition by 3-MA markedly reversed SAL-modulated changes in cell viability and NLRP3 expression in LPS-stimulated HUVECs.	rhodioloside	47-50	NLR family pyrin domain containing 3	Homo sapiens	91-96
34011327-14	2021	CONCLUSION: SAL protects endothelial cells against LPS-induced injury through inhibition of NLRP3 pathways and enhancing autophagy.	rhodioloside	12-15	NLR family pyrin domain containing 3	Homo sapiens	92-97
34054813-5	2021	Notably, excessive mitochondrial ROS (mtROS) was observed to trigger pyroptosis by activating the NLRP3 inflammasome, which was ameliorated by Mito-TEMPO treatment, indicating that the anti-pyroptotic role of PRX3 relies on its powerful ability to regulate mtROS.	Reactive Oxygen Species	33-36	NLR family pyrin domain containing 3	Homo sapiens	98-103
34008185-7	2022	The multivariate regression model showed that periodontitis (p = 0.029) and HDL-cholesterol (p = 0.012) were significant predictors of serum NLRP3 concentrations while periodontitis (p = 0.036) and CRP (p = 0.012) were significant predictors of salivary NLRP3.	Cholesterol	80-91	NLR family pyrin domain containing 3	Homo sapiens	141-146
34003636-3	2021	Herein, we report the design, synthesis, and application of a novel photoaffinity alkyne-tagged probe for MCC950 (IMP2070) which shows direct engagement with NLRP3 and inhibition of inflammasome activation in macrophages.	Alkynes	82-88	NLR family pyrin domain containing 3	Homo sapiens	158-163
34022434-5	2021	Mitochondrial dysfunction and subsequent accumulation of mitochondrial reactive oxygen species, mitochondrial deoxyribonucleic acid, and other mitochondria-associated proteins and lipids play vital roles in the instigation of the NLRP3 inflammasome.	Reactive Oxygen Species	71-94	NLR family pyrin domain containing 3	Homo sapiens	230-235
34054813-5	2021	Notably, excessive mitochondrial ROS (mtROS) was observed to trigger pyroptosis by activating the NLRP3 inflammasome, which was ameliorated by Mito-TEMPO treatment, indicating that the anti-pyroptotic role of PRX3 relies on its powerful ability to regulate mtROS.	MitoTEMPO	143-153	NLR family pyrin domain containing 3	Homo sapiens	98-103
34054813-6	2021	Overall, PRX3 regulates NLRP3-dependent pyroptosis in APAP-induced liver injury by targeting mitochondrial oxidative stress.	Acetaminophen	54-58	NLR family pyrin domain containing 3	Homo sapiens	24-29
32523112-0	2021	Ticagrelor inhibits the NLRP3 inflammasome to protect against inflammatory disease independent of the P2Y12 signaling pathway.	Ticagrelor	0-10	NLR family pyrin domain containing 3	Homo sapiens	24-29
32523112-7	2021	Importantly, oral administration of ticagrelor rapidly and strongly inhibited NLRP3 inflammasome activation in peripheral blood mononuclear cells from patients with acute coronary syndrome.	Ticagrelor	36-46	NLR family pyrin domain containing 3	Homo sapiens	78-83
32523112-4	2021	In this study, we systematically examined the effects of ticagrelor on the NLRP3 inflammasome and found that ticagrelor inhibits NLRP3 inflammasome activation in macrophages independent of its classic inhibitory effect on the P2Y12 signaling pathway.	Ticagrelor	109-119	NLR family pyrin domain containing 3	Homo sapiens	129-134
32523112-8	2021	Overall, our study reveals a novel pharmacological function of ticagrelor in addition to its classic antiplatelet properties, which suggests that ticagrelor may serve as a potential therapeutic agent for use in NLRP3-associated diseases.	Ticagrelor	63-73	NLR family pyrin domain containing 3	Homo sapiens	211-216
32523112-8	2021	Overall, our study reveals a novel pharmacological function of ticagrelor in addition to its classic antiplatelet properties, which suggests that ticagrelor may serve as a potential therapeutic agent for use in NLRP3-associated diseases.	Ticagrelor	146-156	NLR family pyrin domain containing 3	Homo sapiens	211-216
33417223-0	2021	NLRP3 Inflammasome Blockade Reduces Cocaine-Induced Microglial Activation and Neuroinflammation.	Cocaine	36-43	NLR family pyrin domain containing 3	Homo sapiens	0-5
33145969-0	2021	Bafilomycin A1 enhances NLRP3 inflammasome activation in human monocytes independent of lysosomal acidification.	bafilomycin A1	0-14	NLR family pyrin domain containing 3	Homo sapiens	24-29
33145969-3	2021	Here we report that pharmacological inhibition of V-ATPase with bafilomycin A1 exacerbated LPS-induced NLRP3 inflammasome activation in primary human monocytes.	bafilomycin A1	64-78	NLR family pyrin domain containing 3	Homo sapiens	103-108
33159713-0	2021	Exposure to mono (2-ethylhexyl) phthalate facilitates apoptosis and pyroptosis of human endometrial microvascular endothelial cells through NLRP3 inflammasome.	mono-(2-ethylhexyl)phthalate	12-41	NLR family pyrin domain containing 3	Homo sapiens	140-145
33159713-15	2021	NLRP3 knockdown markedly ameliorated the increase in LDH release and apoptosis induced by MEHP exposure in HEMECs.	mono-(2-ethylhexyl)phthalate	90-94	NLR family pyrin domain containing 3	Homo sapiens	0-5
33159713-16	2021	Our findings suggested that exposure to MEHP facilitates apoptosis and pyroptosis of HEMECs through NLRP3 inflammasome.	mono-(2-ethylhexyl)phthalate	40-44	NLR family pyrin domain containing 3	Homo sapiens	100-105
33417223-9	2021	Furthermore, cortical brain tissues of chronic cocaine-dependent humans also exhibited upregulated expression of the NLRP3 pathway mediators compared with non-cocaine dependent controls.	Cocaine	47-54	NLR family pyrin domain containing 3	Homo sapiens	117-122
33417223-9	2021	Furthermore, cortical brain tissues of chronic cocaine-dependent humans also exhibited upregulated expression of the NLRP3 pathway mediators compared with non-cocaine dependent controls.	Cocaine	159-166	NLR family pyrin domain containing 3	Homo sapiens	117-122
33417223-10	2021	Collectively, these findings suggest that cocaine activates microglia involving the NLRP3 inflammasome pathway, thereby contributing to neuroinflammation.	Cocaine	42-49	NLR family pyrin domain containing 3	Homo sapiens	84-89
33417223-3	2021	Based on the premise that cocaine induces both reactive oxygen species (ROS) as well as microglial activation, we hypothesized that cocaine-mediated microglial activation involves both ROS and NLRP3 signaling pathways.	Cocaine	26-33	NLR family pyrin domain containing 3	Homo sapiens	193-198
33417223-11	2021	NLRP3 can thus be considered as a potential therapeutic target for alleviating cocaine-mediated neuroinflammation.	Cocaine	79-86	NLR family pyrin domain containing 3	Homo sapiens	0-5
33417223-3	2021	Based on the premise that cocaine induces both reactive oxygen species (ROS) as well as microglial activation, we hypothesized that cocaine-mediated microglial activation involves both ROS and NLRP3 signaling pathways.	Cocaine	132-139	NLR family pyrin domain containing 3	Homo sapiens	193-198
33417223-5	2021	We found that microglia exposed to cocaine exhibited significant induction of NLRP3 and mature IL-1beta expression.	Cocaine	35-42	NLR family pyrin domain containing 3	Homo sapiens	78-83
33417223-6	2021	Intriguingly, blockade of ROS (Tempol) attenuated cocaine-mediated priming of NLRP3 and microglial activation (CD11b).	Reactive Oxygen Species	26-29	NLR family pyrin domain containing 3	Homo sapiens	78-83
33417223-6	2021	Intriguingly, blockade of ROS (Tempol) attenuated cocaine-mediated priming of NLRP3 and microglial activation (CD11b).	Cocaine	50-57	NLR family pyrin domain containing 3	Homo sapiens	78-83
33417223-7	2021	Blockade of NLRP3 by both pharmacological (MCC950) as well as gene silencing (siNLRP3) approaches underpinned the critical role of NLRP3 in cocaine-mediated activation of inflammasome and microglial activation.	Cocaine	140-147	NLR family pyrin domain containing 3	Homo sapiens	12-17
33417223-7	2021	Blockade of NLRP3 by both pharmacological (MCC950) as well as gene silencing (siNLRP3) approaches underpinned the critical role of NLRP3 in cocaine-mediated activation of inflammasome and microglial activation.	Cocaine	140-147	NLR family pyrin domain containing 3	Homo sapiens	80-85
33004259-3	2021	Recent work revealed that HBL binds to the mammalian surface receptors LITAF and CDIP1 and that both HBL and NHE induce potassium efflux and activate the NLRP3 inflammasome, leading to pyroptosis.	Potassium	120-129	NLR family pyrin domain containing 3	Homo sapiens	154-159
33416933-8	2021	Studies indicate that one of the possible anti-inflammatory mechanisms of chloroquine and hydroxychloroquine is inhibition of the activity of NLRP3 inflammasome.	Chloroquine	74-85	NLR family pyrin domain containing 3	Homo sapiens	142-147
33416933-8	2021	Studies indicate that one of the possible anti-inflammatory mechanisms of chloroquine and hydroxychloroquine is inhibition of the activity of NLRP3 inflammasome.	Hydroxychloroquine	90-108	NLR family pyrin domain containing 3	Homo sapiens	142-147
33561510-2	2021	In the brain ethanol can be detrimental to memory formation, through inducing the integrated stress response/endoplasmic reticulum stress/unfolded protein response and the molecular mechanisms linking stress to other events such as NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammation and autophagy.	Ethanol	13-20	NLR family pyrin domain containing 3	Homo sapiens	232-280
33561510-2	2021	In the brain ethanol can be detrimental to memory formation, through inducing the integrated stress response/endoplasmic reticulum stress/unfolded protein response and the molecular mechanisms linking stress to other events such as NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammation and autophagy.	Ethanol	13-20	NLR family pyrin domain containing 3	Homo sapiens	282-287
33561510-3	2021	This literature review aims to provide an overview of our current understanding of the molecular mechanisms involved in ethanol-induced damage with endoplasmic reticulum stress, integrated stress response, NLRP3 inflammation and autophagy, while discussing the impact of neurosteroids and oxysterols, including allopregnanolone, 25-hydroxycholesterol and 24S-hydroxycholesterol, on the central nervous system.	Ethanol	120-127	NLR family pyrin domain containing 3	Homo sapiens	206-211
33740502-0	2021	ATP exposure stimulates glutathione efflux as a necessary switch for NLRP3 inflammasome activation.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	69-74
33740502-0	2021	ATP exposure stimulates glutathione efflux as a necessary switch for NLRP3 inflammasome activation.	Glutathione	24-35	NLR family pyrin domain containing 3	Homo sapiens	69-74
33740502-4	2021	We demonstrate here that ATP exposure evoked a sharp decrease in glutathione (GSH) levels in macrophages, which led to NLRP3 inflammasome activation.	Adenosine Triphosphate	25-28	NLR family pyrin domain containing 3	Homo sapiens	119-124
33740502-4	2021	We demonstrate here that ATP exposure evoked a sharp decrease in glutathione (GSH) levels in macrophages, which led to NLRP3 inflammasome activation.	Glutathione	65-76	NLR family pyrin domain containing 3	Homo sapiens	119-124
33740502-4	2021	We demonstrate here that ATP exposure evoked a sharp decrease in glutathione (GSH) levels in macrophages, which led to NLRP3 inflammasome activation.	Glutathione	78-81	NLR family pyrin domain containing 3	Homo sapiens	119-124
33740502-7	2021	Also, exogenous GSH or GSSG strongly inhibited NLRP3 inflammasome activation in vitro and in vivo.	Glutathione	16-19	NLR family pyrin domain containing 3	Homo sapiens	47-52
33740502-7	2021	Also, exogenous GSH or GSSG strongly inhibited NLRP3 inflammasome activation in vitro and in vivo.	Glutathione Disulfide	23-27	NLR family pyrin domain containing 3	Homo sapiens	47-52
33740502-8	2021	These data suggest that GSH efflux controls NLRP3 inflammasome activation, which may lead to development of novel therapeutic strategies for NLRP3 inflammasome-associated disorders.	Glutathione	24-27	NLR family pyrin domain containing 3	Homo sapiens	44-49
33740502-8	2021	These data suggest that GSH efflux controls NLRP3 inflammasome activation, which may lead to development of novel therapeutic strategies for NLRP3 inflammasome-associated disorders.	Glutathione	24-27	NLR family pyrin domain containing 3	Homo sapiens	141-146
33995345-6	2021	Blockages of EIII-induced platelet signaling using the competitive inhibitor chondroitin sulfate B or selective Nlrp3 inflammasome inhibitors OLT1177 and Z-WHED-FMK markedly ameliorated DENV- and EIII-induced thrombocytopenia, platelet activation, and cell death.	z-whed-fmk	154-164	NLR family pyrin domain containing 3	Homo sapiens	112-117
33926523-15	2021	CONCLUSIONS: As synthetic hydroxyapatite, human calcifications were able to induce an inflammatory response resulting in the production of IL-1beta after NF-kB activation and through NLRP3 inflammasome.	Durapatite	26-40	NLR family pyrin domain containing 3	Homo sapiens	183-188
33996748-0	2021	Development of Fluorescent and Biotin Probes Targeting NLRP3.	Biotin	31-37	NLR family pyrin domain containing 3	Homo sapiens	55-60
33909257-0	2021	Bavachin enhances NLRP3 inflammasome activation induced by ATP or nigericin and causes idiosyncratic hepatotoxicity.	bavachin	0-8	NLR family pyrin domain containing 3	Homo sapiens	18-23
33909257-0	2021	Bavachin enhances NLRP3 inflammasome activation induced by ATP or nigericin and causes idiosyncratic hepatotoxicity.	Adenosine Triphosphate	59-62	NLR family pyrin domain containing 3	Homo sapiens	18-23
33909257-0	2021	Bavachin enhances NLRP3 inflammasome activation induced by ATP or nigericin and causes idiosyncratic hepatotoxicity.	Nigericin	66-75	NLR family pyrin domain containing 3	Homo sapiens	18-23
33909257-4	2021	This paper reports that bavachin isolated from PF enhances the specific stimuli-induced activation of the NLRP3 inflammasome and leads to hepatotoxicity.	bavachin	24-32	NLR family pyrin domain containing 3	Homo sapiens	106-111
33909257-7	2021	Mechanistically, bavachin specifically increases the production of nigericin-induced mitochondrial reactive oxygen species among the most important upstream events in the activation of the NLRP3 inflammasome.	bavachin	17-25	NLR family pyrin domain containing 3	Homo sapiens	189-194
33909257-7	2021	Mechanistically, bavachin specifically increases the production of nigericin-induced mitochondrial reactive oxygen species among the most important upstream events in the activation of the NLRP3 inflammasome.	Nigericin	67-76	NLR family pyrin domain containing 3	Homo sapiens	189-194
33909257-7	2021	Mechanistically, bavachin specifically increases the production of nigericin-induced mitochondrial reactive oxygen species among the most important upstream events in the activation of the NLRP3 inflammasome.	Reactive Oxygen Species	99-122	NLR family pyrin domain containing 3	Homo sapiens	189-194
33909257-11	2021	Moreover, bavachin and PF should be evaded among patients with diseases linked to the ATP- or nigericin-mediated activation of the NLRP3 inflammasome, which may be a dangerous factor for liver injury.	bavachin	10-18	NLR family pyrin domain containing 3	Homo sapiens	131-136
33909257-11	2021	Moreover, bavachin and PF should be evaded among patients with diseases linked to the ATP- or nigericin-mediated activation of the NLRP3 inflammasome, which may be a dangerous factor for liver injury.	pf	23-25	NLR family pyrin domain containing 3	Homo sapiens	131-136
33909257-11	2021	Moreover, bavachin and PF should be evaded among patients with diseases linked to the ATP- or nigericin-mediated activation of the NLRP3 inflammasome, which may be a dangerous factor for liver injury.	Adenosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	131-136
33909257-11	2021	Moreover, bavachin and PF should be evaded among patients with diseases linked to the ATP- or nigericin-mediated activation of the NLRP3 inflammasome, which may be a dangerous factor for liver injury.	Nigericin	94-103	NLR family pyrin domain containing 3	Homo sapiens	131-136
33902703-10	2021	This MSU-induced IL-1beta secretion from CIRP-primed neutrophils was accompanied by the induction of cleaved IL-1beta (p17), which was inhibited by the pretreatment of MCC950, a specific inhibitor for NLRP3.	Uric Acid	5-8	NLR family pyrin domain containing 3	Homo sapiens	201-206
33902703-13	2021	CONCLUSIONS: Our data indicate that CIRP, an endogenous stress molecule, triggers uric acid-induced mature IL-1beta induction as a priming stimulus for NLRP3 inflammasome in human neutrophils.	Uric Acid	82-91	NLR family pyrin domain containing 3	Homo sapiens	152-157
33901504-4	2021	The nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome is the best understood in terms of molecular mechanisms, and is a promising therapeutic target in immune-related disorders.	Leucine	46-53	NLR family pyrin domain containing 3	Homo sapiens	97-102
33968092-0	2021	Corrigendum: Immunomodulatory Effects of Diterpenes and Their Derivatives Through NLRP3 Inflammasome Pathway: A Review.	Diterpenes	41-51	NLR family pyrin domain containing 3	Homo sapiens	82-87
33968934-2	2021	The anti-inflammatory action of colchicine seems to result from irreversible inhibition of tubulin polymerization and microtubule (MT) assembly by binding to the tubulin heterodimer, avoiding the signal transduction required to the activation of the entire NLRP3 inflammasome.	Colchicine	32-42	NLR family pyrin domain containing 3	Homo sapiens	257-262
33996748-7	2021	The initial characterizations of NLRP3-targeting probes highlighted the coumarin probe 2 as a suitable tool compound for the cellular and biochemical analysis of the NLRP3 inflammasome.	coumarin	72-80	NLR family pyrin domain containing 3	Homo sapiens	33-38
33996748-7	2021	The initial characterizations of NLRP3-targeting probes highlighted the coumarin probe 2 as a suitable tool compound for the cellular and biochemical analysis of the NLRP3 inflammasome.	coumarin	72-80	NLR family pyrin domain containing 3	Homo sapiens	166-171
33967625-12	2021	In vitro experiments revealed that Xi Lei San could repress apoptosis as well as ROS and inflammatory cytokine production in TNF-alpha-induced CACO2 cells by reducing the activity of NLRP3 inflammasomes and autophagy.	ros	81-84	NLR family pyrin domain containing 3	Homo sapiens	183-188
33967813-0	2021	Corrigendum: Hydroxysafflor Yellow A Protects Against Myocardial Ischemia/Reperfusion Injury via Suppressing NLRP3 Inflammasome and Activating Autophagy.	hydroxysafflor yellow A	13-36	NLR family pyrin domain containing 3	Homo sapiens	109-114
33894359-5	2021	It also generates excessive Reactive oxygen species (ROS) and releases mtDNA into the cytoplasm, which causes induction of NLRP3 inflammasome and apoptosis.	Reactive Oxygen Species	28-51	NLR family pyrin domain containing 3	Homo sapiens	123-128
33894359-5	2021	It also generates excessive Reactive oxygen species (ROS) and releases mtDNA into the cytoplasm, which causes induction of NLRP3 inflammasome and apoptosis.	Reactive Oxygen Species	53-56	NLR family pyrin domain containing 3	Homo sapiens	123-128
33967625-12	2021	In vitro experiments revealed that Xi Lei San could repress apoptosis as well as ROS and inflammatory cytokine production in TNF-alpha-induced CACO2 cells by reducing the activity of NLRP3 inflammasomes and autophagy.	caco2	143-148	NLR family pyrin domain containing 3	Homo sapiens	183-188
33892379-0	2021	Brevilin A inhibits NLRP3 inflammasome activation in vivo and in vitro by acting on the upstream of NLRP3-induced ASC oligomerization.	brevilin A	0-10	NLR family pyrin domain containing 3	Homo sapiens	20-25
33892379-0	2021	Brevilin A inhibits NLRP3 inflammasome activation in vivo and in vitro by acting on the upstream of NLRP3-induced ASC oligomerization.	brevilin A	0-10	NLR family pyrin domain containing 3	Homo sapiens	100-105
33892379-4	2021	Here, we found that BA significantly attenuates the activation of caspase-1 and the subsequent secretion of the interleukin-1beta (IL-1beta) in mouse macrophages and human THP-1 cells, showing the inhibitory effect of BA on the NLRP3 inflammasome activation.	brevilin A	20-22	NLR family pyrin domain containing 3	Homo sapiens	228-233
33892379-6	2021	Research on the mechanism found BA inhibits NLRP3 inflammasome activation by blocking the upstream of ASC oligomerization.	brevilin A	32-34	NLR family pyrin domain containing 3	Homo sapiens	44-49
33892379-7	2021	Importantly, in vivo experiments showed that BA markedly reduces the secretion of IL-1beta to suppress NLRP3 inflammasome in the LPS-induced inflammation and MSU-challenged peritonitis model.	brevilin A	45-47	NLR family pyrin domain containing 3	Homo sapiens	103-108
33892379-8	2021	In conclusion, our experiments show that BA is an effective NLRP3 inflammasome inhibitor and can be regarded as a drug candidate for NLRP3 inflammasome-driven diseases.	brevilin A	41-43	NLR family pyrin domain containing 3	Homo sapiens	60-65
33892379-8	2021	In conclusion, our experiments show that BA is an effective NLRP3 inflammasome inhibitor and can be regarded as a drug candidate for NLRP3 inflammasome-driven diseases.	brevilin A	41-43	NLR family pyrin domain containing 3	Homo sapiens	133-138
33592257-8	2021	Furthermore, Cd caused mitochondrial dysfunction and fragmentation by inhibiting the AMPK-PGC-1alpha-NRF1/2 signaling pathway and reduced the expression of mitochondrial-related regulatory factors OPA1, TFAM and mtDNA, resulting in the increase of NLRP3 inflammasome.	Cadmium	13-15	NLR family pyrin domain containing 3	Homo sapiens	248-253
33994056-11	2021	HJ105 decreased TXNIP expression, suppressing NLRP3 inflammasome activation in the hippocampus, which in turn counteracted the upregulation of IL-1beta and TNF-alpha.	hj105	0-5	NLR family pyrin domain containing 3	Homo sapiens	46-51
33935726-9	2021	The abundance of the NLRP3 inflammasome and cytokines was significantly increased after RAW264.7 macrophages were treated with MSU (p < 0.01, respectively), while that of miR-223 was significantly reduced (p < 0.01).	Uric Acid	127-130	NLR family pyrin domain containing 3	Homo sapiens	21-26
33861800-6	2021	Using a combination of siRNA knockdowns in monocyte derived macrophages (MDMs) of different TLRs and NLRs as well as chemical inhibition, it was demonstrated that HIV Vpu could trigger inflammasome activation via TLR4/NLRP3 leading to IL-1beta/IL-18 secretion.	VPU	167-170	NLR family pyrin domain containing 3	Homo sapiens	218-223
32893669-0	2021	Cpt1a promoted ROS-induced oxidative stress and inflammation in liver injury via the Nrf2/HO-1 and NLRP3 inflammasome signaling pathway.	Reactive Oxygen Species	15-18	NLR family pyrin domain containing 3	Homo sapiens	99-104
32893669-6	2021	In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway.	Reactive Oxygen Species	52-55	NLR family pyrin domain containing 3	Homo sapiens	119-184
32893669-6	2021	In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway.	Reactive Oxygen Species	52-55	NLR family pyrin domain containing 3	Homo sapiens	186-191
33592257-6	2021	Our results revealed that Cd caused cerebral histopathology lesions, inducing cerebral pyroptosis and the mass generation of inflammatory cytokines, as indicated by the increased NLRP3 inflammasome activation (NLRP3, Cas1 and ASC) and the upregulation of inflammation factors IL-2, IL-6, IL-7 and inhibition of IL-10.	Cadmium	26-28	NLR family pyrin domain containing 3	Homo sapiens	179-184
33592257-6	2021	Our results revealed that Cd caused cerebral histopathology lesions, inducing cerebral pyroptosis and the mass generation of inflammatory cytokines, as indicated by the increased NLRP3 inflammasome activation (NLRP3, Cas1 and ASC) and the upregulation of inflammation factors IL-2, IL-6, IL-7 and inhibition of IL-10.	Cadmium	26-28	NLR family pyrin domain containing 3	Homo sapiens	210-215
33847912-0	2021	Verapamil as an Adjunct Therapy to Reduce tPA Toxicity in Hyperglycemic Stroke: Implication of TXNIP/NLRP3 Inflammasome.	Verapamil	0-9	NLR family pyrin domain containing 3	Homo sapiens	101-106
33850279-0	2022	Correction: 1,2,4-Trimethoxybenzene selectively inhibits NLRP3 inflammasome activation and attenuates experimental autoimmune encephalomyelitis.	1,2,4-trimethoxybenzene	12-35	NLR family pyrin domain containing 3	Homo sapiens	57-62
33847912-9	2021	Importantly, verapamil strongly reversed tPA-induced TXNIP/NLRP3 (NOD-like receptor pyrin domain-containing-3) inflammasome activation and reduced infarct volume.	Verapamil	13-22	NLR family pyrin domain containing 3	Homo sapiens	59-64
33823789-0	2021	Dexmedetomidine attenuates myocardial ischemia-reperfusion injury in vitro by inhibiting NLRP3 Inflammasome activation.	Dexmedetomidine	0-15	NLR family pyrin domain containing 3	Homo sapiens	89-94
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	Nigericin	239-248	NLR family pyrin domain containing 3	Homo sapiens	18-54
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	Nigericin	239-248	NLR family pyrin domain containing 3	Homo sapiens	56-61
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	tributyltin	253-264	NLR family pyrin domain containing 3	Homo sapiens	18-54
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	tributyltin	253-264	NLR family pyrin domain containing 3	Homo sapiens	56-61
33917140-12	2021	Furthermore, phosphoramidon inhibited ER stress and the NLRP3 inflammasome in tubular epithelial cells.	phosphoramidon	13-27	NLR family pyrin domain containing 3	Homo sapiens	56-61
33849790-0	2021	Corrigendum to "Hydroxysafflor yellow A inhibits hypoxia/reoxygenation-induced cardiomyocyte injury via regulating the AMPK/NLRP3 inflammasome pathway" [Int.	hydroxysafflor yellow A	16-39	NLR family pyrin domain containing 3	Homo sapiens	124-129
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Acetates	0-3	NLR family pyrin domain containing 3	Homo sapiens	62-67
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Nigericin	85-94	NLR family pyrin domain containing 3	Homo sapiens	62-67
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Uric Acid	96-112	NLR family pyrin domain containing 3	Homo sapiens	62-67
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Uric Acid	114-117	NLR family pyrin domain containing 3	Homo sapiens	62-67
33823789-5	2021	Here, we investigated whether dexmedetomidine protects against MIRI by inhibiting the activation of the NLRP3 inflammasome in vitro.	Dexmedetomidine	30-45	NLR family pyrin domain containing 3	Homo sapiens	104-109
33823789-10	2021	The expression of the NLRP3 protein was significantly upregulated in cardiac fibroblasts but not in cardiomyocytes after H/R and was significantly attenuated by dexmedetomidine treatment.	Dexmedetomidine	161-176	NLR family pyrin domain containing 3	Homo sapiens	22-27
33823789-12	2021	NLRP3 inflammasome activation induced the increased expression of cleaved caspase1, mature IL-1beta and IL-18, while dexmedetomidine suppressed H/R-induced NLRP3 inflammasome activation in cardiac fibroblasts.	Dexmedetomidine	117-132	NLR family pyrin domain containing 3	Homo sapiens	0-5
33823789-12	2021	NLRP3 inflammasome activation induced the increased expression of cleaved caspase1, mature IL-1beta and IL-18, while dexmedetomidine suppressed H/R-induced NLRP3 inflammasome activation in cardiac fibroblasts.	Dexmedetomidine	117-132	NLR family pyrin domain containing 3	Homo sapiens	156-161
33823789-13	2021	In addition, dexmedetomidine reduced the expression of Bcl2 and BAX in cocultured cardiomyocytes by suppressing H/R-induced NLRP3 inflammasome activation in cardiac fibroblasts.	Dexmedetomidine	13-28	NLR family pyrin domain containing 3	Homo sapiens	124-129
33823789-14	2021	CONCLUSION: Dexmedetomidine treatment can suppress H/R-induced NLRP3 inflammasome activation in cardiac fibroblasts, thereby alleviating MIRI by inhibiting the inflammatory response.	Dexmedetomidine	12-27	NLR family pyrin domain containing 3	Homo sapiens	63-68
32901127-6	2021	RKIP-deficient mice showed increased sensitivity to Alum-induced peritonitis and Salmonella typhimurium-induced inflammation, indicating that RKIP inhibits NLRP3 and NLRC4 inflammasome activation in vivo.	aluminum sulfate	52-56	NLR family pyrin domain containing 3	Homo sapiens	156-161
33839695-0	2021	Melatonin attenuates smoking-induced atherosclerosis by activating the Nrf2 pathway via NLRP3 inflammasomes in endothelial cells.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	88-93
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Carbon	32-38	NLR family pyrin domain containing 3	Homo sapiens	211-216
33715208-3	2021	However, the mechanism underlying the effect of microRNAs on the NLRP3 inflammasome induced by Abeta remains poorly understood.	UNII-042A8N37WH	95-100	NLR family pyrin domain containing 3	Homo sapiens	65-70
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Reactive Oxygen Species	89-112	NLR family pyrin domain containing 3	Homo sapiens	211-216
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Reactive Oxygen Species	114-117	NLR family pyrin domain containing 3	Homo sapiens	211-216
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	25-44	NLR family pyrin domain containing 3	Homo sapiens	116-121
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	46-49	NLR family pyrin domain containing 3	Homo sapiens	116-121
32779379-9	2021	NLRP3 and Caspase-1 inhibitors (MCC950 and YVAD) significantly inhibited IL-1beta expression and NLRP3 activation, but not NLRP3 expression following exposure to BC +- pollen.	YVAD	43-47	NLR family pyrin domain containing 3	Homo sapiens	0-5
33529913-0	2021	Contribution of the NLRP3/IL-1beta axis to impaired vasodilation in sepsis through facilitation of eNOS proteolysis and the protective role of melatonin.	Melatonin	143-152	NLR family pyrin domain containing 3	Homo sapiens	20-25
33529913-10	2021	Notably, treatment with 30 mg/kg melatonin downregulated NLRP3 expression levels and decreased IL-1beta secretion, subsequently increasing the expression of eNOS and improving endothelium-dependent vascular relaxation.	Melatonin	33-42	NLR family pyrin domain containing 3	Homo sapiens	57-62
33529913-11	2021	In conclusion, the findings of the present study indicated that the NLRP3/IL-1beta axis may impair vasodilation by promoting the proteolysis of eNOS and melatonin may protect against sepsis-induced endothelial relaxation dysfunction by inhibiting the NLRP3/IL-1beta axis, suggesting its pharmacological potential in sepsis.	Melatonin	153-162	NLR family pyrin domain containing 3	Homo sapiens	68-73
32779379-9	2021	NLRP3 and Caspase-1 inhibitors (MCC950 and YVAD) significantly inhibited IL-1beta expression and NLRP3 activation, but not NLRP3 expression following exposure to BC +- pollen.	YVAD	43-47	NLR family pyrin domain containing 3	Homo sapiens	97-102
33529913-11	2021	In conclusion, the findings of the present study indicated that the NLRP3/IL-1beta axis may impair vasodilation by promoting the proteolysis of eNOS and melatonin may protect against sepsis-induced endothelial relaxation dysfunction by inhibiting the NLRP3/IL-1beta axis, suggesting its pharmacological potential in sepsis.	Melatonin	153-162	NLR family pyrin domain containing 3	Homo sapiens	251-256
32779379-9	2021	NLRP3 and Caspase-1 inhibitors (MCC950 and YVAD) significantly inhibited IL-1beta expression and NLRP3 activation, but not NLRP3 expression following exposure to BC +- pollen.	YVAD	43-47	NLR family pyrin domain containing 3	Homo sapiens	97-102
32779379-10	2021	CONCLUSION: These findings suggest that exposure to BC and pollen can exaggerate oxidative stress and significantly increase the expression of IL-1beta in hNECs, and that this may involve a pathway integrating ROS-NLRP3-Caspase-1-IL-1beta signaling.	Reactive Oxygen Species	210-213	NLR family pyrin domain containing 3	Homo sapiens	214-219
33537804-0	2021	Quercetin reverses TNF-alpha induced osteogenic damage to human periodontal ligament stem cells by suppressing the NF-kappaB/NLRP3 inflammasome pathway.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	125-130
33578174-0	2021	Progesterone and vitamin D downregulate the activation of the NLRP1/NLRP3 inflammasomes and TLR4-MyD88-NF-kappaB pathway in monocytes from pregnant women with preeclampsia.	Progesterone	0-12	NLR family pyrin domain containing 3	Homo sapiens	68-73
33578174-0	2021	Progesterone and vitamin D downregulate the activation of the NLRP1/NLRP3 inflammasomes and TLR4-MyD88-NF-kappaB pathway in monocytes from pregnant women with preeclampsia.	Vitamin D	17-26	NLR family pyrin domain containing 3	Homo sapiens	68-73
33578174-1	2021	This study evaluated the in vitro modulatory effect of progesterone (PG) and vitamin D (VD) on NLRP1/NLRP3 inflammasomes and TLR4/NF-kappaB pathway in monocytes from pregnant women with preeclampsia (PE).	Progesterone	55-67	NLR family pyrin domain containing 3	Homo sapiens	101-106
33578174-1	2021	This study evaluated the in vitro modulatory effect of progesterone (PG) and vitamin D (VD) on NLRP1/NLRP3 inflammasomes and TLR4/NF-kappaB pathway in monocytes from pregnant women with preeclampsia (PE).	Progesterone	69-71	NLR family pyrin domain containing 3	Homo sapiens	101-106
33578174-1	2021	This study evaluated the in vitro modulatory effect of progesterone (PG) and vitamin D (VD) on NLRP1/NLRP3 inflammasomes and TLR4/NF-kappaB pathway in monocytes from pregnant women with preeclampsia (PE).	Vitamin D	77-86	NLR family pyrin domain containing 3	Homo sapiens	101-106
33607128-0	2021	Involvement of TCF7L2 in generation of morphine-induced antinociceptive tolerance and hyperalgesia by modulating TLR4/ NF-kappaB/NLRP3 in microglia.	Morphine	39-47	NLR family pyrin domain containing 3	Homo sapiens	129-134
33492610-7	2021	Priming the activation of the NLRP3 inflammasome, mtDAMPs promote secretion of proinflammatory cytokines, including interleukin-1beta (IL-1beta), implicated in atherosclerotic lesions through vascular smooth muscle and fibroblast proliferation, arterial wall thickening, and plaque formation.	mtdamps	50-57	NLR family pyrin domain containing 3	Homo sapiens	30-35
33492610-8	2021	In this article we critically reviewed and discussed the central role of the NLRP3 inflammasome in mtDAMP-induced sterile inflammation in atherosclerosis with specific components including caspase-1, pregnane X receptor (PXR), adenosine monophosphate activated protein kinase (AMPK), protein phosphatase 2A (PP2A), thioredoxin-interacting protein (TXNIP), and downstream cytokines including IL-1beta and IL-18 as potential mediators of atherosclerosis.	mtdamp	99-105	NLR family pyrin domain containing 3	Homo sapiens	77-82
33607128-7	2021	In this study, we found that morphine tolerance led to the upregulation of TCF7L2 in the spinal cord, and also led to the upregulation of TCF7L2 expression in glial cells, which promoted inflammation related signal, and activated TLR4 / NF-kappaB/NLRP3 pathway.	Morphine	29-37	NLR family pyrin domain containing 3	Homo sapiens	247-252
33607128-10	2021	We therefore suggested that TCF7L2 regulates the activation of TLR4/ NF-kappaB/NLRP3 pathway in microglia, and is involved in the formation of morphine tolerance.	Morphine	143-151	NLR family pyrin domain containing 3	Homo sapiens	79-84
33328588-8	2021	Elevated levels of extracellular ATP induced by SARS-CoV-2 infection may trigger hyperactivation of P2X7 receptors leading to NLRP3 inflammasome stimulation as a key mediator of neuroinvasion and consequent neuroinflammatory processes, as observed in psychiatric disorders and neurodegenerative diseases.	Adenosine Triphosphate	33-36	NLR family pyrin domain containing 3	Homo sapiens	126-131
33404978-0	2021	Telmisartan Inhibits the NLRP3 Inflammasome by Activating the PI3K Pathway in Neural Stem Cells Injured by Oxygen-Glucose Deprivation.	Telmisartan	0-11	NLR family pyrin domain containing 3	Homo sapiens	25-30
33404978-0	2021	Telmisartan Inhibits the NLRP3 Inflammasome by Activating the PI3K Pathway in Neural Stem Cells Injured by Oxygen-Glucose Deprivation.	Glucose	114-121	NLR family pyrin domain containing 3	Homo sapiens	25-30
33404978-2	2021	In the present study, the effects of the ARB telmisartan on the NLRP3 inflammasome induced by oxygen-glucose deprivation (OGD) in neural stem cells (NSCs) were investigated, as well as their possible association with the activation of the PI3K pathway.	Telmisartan	45-56	NLR family pyrin domain containing 3	Homo sapiens	64-69
33404978-10	2021	In particular, telmisartan attenuated OGD-dependent expression of the NLRP3 inflammasome and its related signaling proteins.	Telmisartan	15-26	NLR family pyrin domain containing 3	Homo sapiens	70-75
33404978-12	2021	Together, these results indicate that telmisartan attenuated the activation of the NLRP3 inflammasome by triggering the PI3K pathway, thereby contributing to neuroprotection.	Telmisartan	38-49	NLR family pyrin domain containing 3	Homo sapiens	83-88
33677475-6	2021	In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3.	Chlorides	34-42	NLR family pyrin domain containing 3	Homo sapiens	196-201
33855019-8	2021	When additionally stimulating macrophages with the ionophore nigericin, we observed an enhanced formation of the NLRP3 inflammasome, increased levels of cell death, and higher secreted protein levels of IL-1beta and IL-6 on compliant substrates.	Nigericin	61-70	NLR family pyrin domain containing 3	Homo sapiens	113-118
33729569-0	2021	Protective mechanisms of Taiwanese green propolis toward high glucose-induced inflammation via NLRP3 inflammasome signaling pathway in human gingival fibroblasts.	Glucose	62-69	NLR family pyrin domain containing 3	Homo sapiens	95-100
33607929-6	2021	Critical Issues: Combining H2S physiology and currently available knowledge of COVID-19, H2S is hypothesized to target three main vulnerabilities of SARS-CoV-2: 1) cell entry through interfering with functional host receptors, 2) viral replication through acting on RNA-dependent RNA-polymerase (RdRp), and 3) the escalation of inflammation to a potentially lethal hyperinflammatory cytokine storm (TLR4 pathway and NLRP3 inflammasome).	Deuterium	27-30	NLR family pyrin domain containing 3	Homo sapiens	416-421
33607929-6	2021	Critical Issues: Combining H2S physiology and currently available knowledge of COVID-19, H2S is hypothesized to target three main vulnerabilities of SARS-CoV-2: 1) cell entry through interfering with functional host receptors, 2) viral replication through acting on RNA-dependent RNA-polymerase (RdRp), and 3) the escalation of inflammation to a potentially lethal hyperinflammatory cytokine storm (TLR4 pathway and NLRP3 inflammasome).	Deuterium	89-92	NLR family pyrin domain containing 3	Homo sapiens	416-421
33781745-3	2021	Previous work has demonstrated that inhibiting the ATPase activity of the Nucleotide-Binding Oligomerization Domain, Leucine-Rich Repeat and Pyrin Domain (NLR) containing protein 3 (NLRP3) disrupts inflammasome assembly and function.	Leucine	117-124	NLR family pyrin domain containing 3	Homo sapiens	182-187
33781745-8	2021	We also validated the active pharmacophore shared among all the NLRP3 inhibitors, and through computational docking, we clarify key structural features for compound positioning within the inflammasome ATP binding site.	Adenosine Triphosphate	201-204	NLR family pyrin domain containing 3	Homo sapiens	64-69
33729569-10	2021	RESULTS: High glucose could induce IL-1beta-driven inflammatory responses in HGFs via the activation of NLRP3 inflammasome regulated by TLR2/TLR4 coupled ROS in NF-kappaB-dependent manner.	Glucose	14-21	NLR family pyrin domain containing 3	Homo sapiens	104-109
33729569-10	2021	RESULTS: High glucose could induce IL-1beta-driven inflammatory responses in HGFs via the activation of NLRP3 inflammasome regulated by TLR2/TLR4 coupled ROS in NF-kappaB-dependent manner.	ros	154-157	NLR family pyrin domain containing 3	Homo sapiens	104-109
33729569-12	2021	CONCLUSION: Taiwanese green propolis could elicit protective effects against IL-1beta-driven inflammation in high glucose-exposed HGFs through TLR2/TLR4 combined ROS/NF-kappaB/NLRP3 inflammasome pathway.	Glucose	114-121	NLR family pyrin domain containing 3	Homo sapiens	176-181
33720048-6	2021	Mechanistically, caspase-1 activation closely correlated with the inflammatory marker expression and was shown to occur through NLRP3 inflammasome activation driven by virus-dependent and/or -independent ROS production, while caspase-3 activation in CD4+ T cells was more closely related to T cell activation status.	ros	204-207	NLR family pyrin domain containing 3	Homo sapiens	128-133
33724611-9	2021	Subsequently, we found that TRIM24 negatively regulated NLRP3/Caspase-1/IL-1beta-mediated pyroptosis and cell migration of hESC, and CY-09, the specific inhibitor of NLRP3, could reverse the promoted pyroptosis and cell migration induced by siTRIM24.	CY5.5 cyanine dye	133-138	NLR family pyrin domain containing 3	Homo sapiens	166-171
33724611-9	2021	Subsequently, we found that TRIM24 negatively regulated NLRP3/Caspase-1/IL-1beta-mediated pyroptosis and cell migration of hESC, and CY-09, the specific inhibitor of NLRP3, could reverse the promoted pyroptosis and cell migration induced by siTRIM24.	sitrim24	241-249	NLR family pyrin domain containing 3	Homo sapiens	56-61
33724611-9	2021	Subsequently, we found that TRIM24 negatively regulated NLRP3/Caspase-1/IL-1beta-mediated pyroptosis and cell migration of hESC, and CY-09, the specific inhibitor of NLRP3, could reverse the promoted pyroptosis and cell migration induced by siTRIM24.	sitrim24	241-249	NLR family pyrin domain containing 3	Homo sapiens	166-171
33691120-0	2021	Jack-of-all-trades: itaconate tolerizes NLRP3 inflammasome activation.	itaconic acid	20-29	NLR family pyrin domain containing 3	Homo sapiens	40-45
33691097-0	2021	Itaconate confers tolerance to late NLRP3 inflammasome activation.	itaconic acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	36-41
33683342-6	2021	Unexpectedly, the CD66b+CD16dim granulocytes had decreased nigericin-triggered caspase-1 activation potential associated with an increased percentage of NLRP3 inflammasome impaired immature neutrophils and a loss of eosinophils in the blood.	Nigericin	59-68	NLR family pyrin domain containing 3	Homo sapiens	153-158
33747105-13	2021	It was found that GLGZG could inhibit OGD/R-induced cell apoptosis, increase neuronal cell viability, decrease the production of IL-18 and IL-1beta, and downregulate the expression levels of pyroptosis markers (NLRP3, ASC, and caspase-1).	glgzg	18-23	NLR family pyrin domain containing 3	Homo sapiens	211-216
33691097-3	2021	We show that endogenous itaconate is a key regulator of the signal 2 of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation after long lipopolysaccharide (LPS) priming, which establishes tolerance to late NLRP3 inflammasome activation.	itaconic acid	24-33	NLR family pyrin domain containing 3	Homo sapiens	72-108
33691097-3	2021	We show that endogenous itaconate is a key regulator of the signal 2 of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation after long lipopolysaccharide (LPS) priming, which establishes tolerance to late NLRP3 inflammasome activation.	itaconic acid	24-33	NLR family pyrin domain containing 3	Homo sapiens	110-115
33691097-3	2021	We show that endogenous itaconate is a key regulator of the signal 2 of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation after long lipopolysaccharide (LPS) priming, which establishes tolerance to late NLRP3 inflammasome activation.	itaconic acid	24-33	NLR family pyrin domain containing 3	Homo sapiens	222-227
33747919-4	2021	Recent studies have shown a potential role of EMP1, CASP1, and NLRP3 genes in prednisolone response.	Prednisolone	78-90	NLR family pyrin domain containing 3	Homo sapiens	63-68
33691120-3	2021	(2021) demonstrate that itaconate and iNOS collaborate to tolerize the NLRP3 inflammasome, thereby limiting cytokine secretion and cell death.	itaconic acid	24-33	NLR family pyrin domain containing 3	Homo sapiens	71-76
33653970-0	2021	Interruption of Helicobacter pylori-Induced NLRP3 Inflammasome Activation by Chalcone Derivatives.	Chalcone	77-85	NLR family pyrin domain containing 3	Homo sapiens	44-49
33663554-9	2021	NAC improved HTM cell viability, inhibited the activation of the NLRP3 inflammasome axis, and HTM cell contraction by scavenging ROS.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	65-70
33653970-2	2021	To identify useful compounds against H. pylori-associated gastric disorders, the effect of chalcone derivatives to activate the nucleotide-binding oligomerization domain (NOD)-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome was examined in an H. pylori-infected human monocytic THP-1 cell line in this study.	Chalcone	91-99	NLR family pyrin domain containing 3	Homo sapiens	225-230
33653970-3	2021	Among the five synthetic structurally-related chalcone derivatives examined, 2"-hydroxy-4",6"-dimethoxychalcone (8) and 2"-hydroxy-3,4,5- trimethoxychalcone (12) strongly blocked the NLRP3 inflammasome in H. pylori-infected THP-1 cells.	Chalcone	46-54	NLR family pyrin domain containing 3	Homo sapiens	183-188
33653970-3	2021	Among the five synthetic structurally-related chalcone derivatives examined, 2"-hydroxy-4",6"-dimethoxychalcone (8) and 2"-hydroxy-3,4,5- trimethoxychalcone (12) strongly blocked the NLRP3 inflammasome in H. pylori-infected THP-1 cells.	2"-hydroxy-4",6"-dimethoxychalcone	77-111	NLR family pyrin domain containing 3	Homo sapiens	183-188
33653970-3	2021	Among the five synthetic structurally-related chalcone derivatives examined, 2"-hydroxy-4",6"-dimethoxychalcone (8) and 2"-hydroxy-3,4,5- trimethoxychalcone (12) strongly blocked the NLRP3 inflammasome in H. pylori-infected THP-1 cells.	2"-hydroxy-3,4,5- trimethoxychalcone	120-156	NLR family pyrin domain containing 3	Homo sapiens	183-188
33653970-7	2021	These results show for the first time that certain chalcones could interrupt the activation of the NLRP3 inflammasome in H. pylori-infected THP-1 cells.	Chalcones	51-60	NLR family pyrin domain containing 3	Homo sapiens	99-104
33434563-4	2021	Correlations were sought with functional single nucleotide polymorphisms in the NLRP3 inflammasone pathway and severity of the endophenotypes.	inflammasone	86-98	NLR family pyrin domain containing 3	Homo sapiens	80-85
33746978-6	2021	In bone marrow-derived macrophages, THP-1 and U937 cells, we found that the MSU crystal-induced secretion of IL-1beta and activation of NLRP3 were suppressed by both DcR3.Fc and HBD.Fc.	Uric Acid	76-79	NLR family pyrin domain containing 3	Homo sapiens	136-141
33746978-7	2021	The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta.	Uric Acid	23-26	NLR family pyrin domain containing 3	Homo sapiens	35-40
33746978-7	2021	The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta.	Uric Acid	23-26	NLR family pyrin domain containing 3	Homo sapiens	297-302
33746978-7	2021	The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta.	Reactive Oxygen Species	152-175	NLR family pyrin domain containing 3	Homo sapiens	35-40
33746978-7	2021	The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta.	Reactive Oxygen Species	177-180	NLR family pyrin domain containing 3	Homo sapiens	35-40
33883451-6	2022	Cholesterol-induced sterile inflammation is thought to be central to this process via activation of a protein complex called the NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	129-134
33651308-5	2021	The NLRP3 inflammasome is considered a novel target of melatonin.	Melatonin	55-64	NLR family pyrin domain containing 3	Homo sapiens	4-9
33651308-8	2021	By inhibiting NLRP3, melatonin diminishes inflammation and influences various molecular pathways, such as SIRT1, microRNA, long non-coding RNA, and Wnt/beta-catenin.	Melatonin	21-30	NLR family pyrin domain containing 3	Homo sapiens	14-19
33651308-9	2021	Here, we discuss these molecular pathways and suggest that melatonin-induced inhibition of NLRP3 should be advanced in disease therapy.	Melatonin	59-68	NLR family pyrin domain containing 3	Homo sapiens	91-96
33231721-8	2021	NLRP3-inflammasome activation induced by reswelling, nigericin, and ATP was also blocked when AQP3 was inhibited or silenced.	Nigericin	53-62	NLR family pyrin domain containing 3	Homo sapiens	0-5
32335773-0	2021	Knockdown of TRIM22 Relieves Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis and Inflammation Through Inhibition of NF-kappaB/NLRP3 Axis.	Oxygen	29-35	NLR family pyrin domain containing 3	Homo sapiens	137-142
32335773-9	2021	Furthermore, inhibition of NF-kappaB by pyrrolidine dithiocarbamate inhibited OGD/R-induced NLRP3 inflammasome activation in HCN-2 cells.	pyrrolidine dithiocarbamic acid	40-67	NLR family pyrin domain containing 3	Homo sapiens	92-97
33231721-8	2021	NLRP3-inflammasome activation induced by reswelling, nigericin, and ATP was also blocked when AQP3 was inhibited or silenced.	Adenosine Triphosphate	68-71	NLR family pyrin domain containing 3	Homo sapiens	0-5
33187650-8	2021	DBDPE not only induced cytotoxicity and reactive oxygen species (ROS) generation in HAECs but also caused HAECs pyroptosis, which was evidenced by the elevated expression of Nod-like receptor protein -3 (NLRP3), ASC, and caspase-1 in DBDPE-treated group.	decabromodiphenyl ethane	0-5	NLR family pyrin domain containing 3	Homo sapiens	204-209
33433347-5	2021	Simultaneously, Mo or/and Cd upregulated ASC, NLRP3, NEK7, Caspase-1, GSDMA, GSDME, IL-18 and IL-1beta mRNA levels and Caspase-1 p20, NLRP3, ASC, GSDMD protein levels, increased the percentage of pyroptotic cells, LDH, NO, IL-18 and IL-1beta releases as well as relative conductivity.	Cadmium	26-28	NLR family pyrin domain containing 3	Homo sapiens	46-51
33433347-5	2021	Simultaneously, Mo or/and Cd upregulated ASC, NLRP3, NEK7, Caspase-1, GSDMA, GSDME, IL-18 and IL-1beta mRNA levels and Caspase-1 p20, NLRP3, ASC, GSDMD protein levels, increased the percentage of pyroptotic cells, LDH, NO, IL-18 and IL-1beta releases as well as relative conductivity.	Cadmium	26-28	NLR family pyrin domain containing 3	Homo sapiens	134-139
33433347-6	2021	Moreover, NLRP3 inhibitor MCC950 and ROS scavenger BHA could ameliorate the above changed factors induced by Mo and Cd co-exposure.	Cadmium	116-118	NLR family pyrin domain containing 3	Homo sapiens	10-15
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Uric Acid	89-98	NLR family pyrin domain containing 3	Homo sapiens	0-5
33571641-7	2021	Knock-down of TNXIP rescued the endothelial cells from CIH-induced apoptosis, indicating that activation of the TXNIP/NLRP3/IL-1beta pathway mediated the CIH-induced endothelial apoptosis.	cih	55-58	NLR family pyrin domain containing 3	Homo sapiens	118-123
33571641-7	2021	Knock-down of TNXIP rescued the endothelial cells from CIH-induced apoptosis, indicating that activation of the TXNIP/NLRP3/IL-1beta pathway mediated the CIH-induced endothelial apoptosis.	cih	154-157	NLR family pyrin domain containing 3	Homo sapiens	118-123
33571641-8	2021	Administration of the mitochondria-targeted antioxidant mito-TEMPO improved mitochondrial function and suppressed upregulation of the TXNIP/NLRP3/IL-1beta pathway, thereby alleviating CIH-induced endothelial apoptosis.	cih	184-187	NLR family pyrin domain containing 3	Homo sapiens	140-145
33571641-10	2021	The results imply that CIH-induced mitochondrial dysfunction mediates endothelial injury implication of TXNIP/NLRP3/IL-1beta signaling pathway.	cih	23-26	NLR family pyrin domain containing 3	Homo sapiens	110-115
33508701-1	2021	INF39 is a nontoxic, irreversible, acrylate-based NLRP3 inhibitor and a further optimization of ethyl 2-((2-chlorophenyl) hydroxyl) methyl) acrylate (INF4E).	acrylic acid	35-43	NLR family pyrin domain containing 3	Homo sapiens	50-55
33422385-12	2021	CONCLUSION: We make the novel observation that the NLRP3 inflammasome activity is correlated with certain metabolites (Isoleucine, GABA, Carnitine and PC34:2) and hypothesize that they could trigger increased NLRP3 Inflammasome activity in MetS.	Isoleucine	119-129	NLR family pyrin domain containing 3	Homo sapiens	51-56
33422385-12	2021	CONCLUSION: We make the novel observation that the NLRP3 inflammasome activity is correlated with certain metabolites (Isoleucine, GABA, Carnitine and PC34:2) and hypothesize that they could trigger increased NLRP3 Inflammasome activity in MetS.	Isoleucine	119-129	NLR family pyrin domain containing 3	Homo sapiens	209-214
33422385-12	2021	CONCLUSION: We make the novel observation that the NLRP3 inflammasome activity is correlated with certain metabolites (Isoleucine, GABA, Carnitine and PC34:2) and hypothesize that they could trigger increased NLRP3 Inflammasome activity in MetS.	gamma-Aminobutyric Acid	131-135	NLR family pyrin domain containing 3	Homo sapiens	51-56
33422385-12	2021	CONCLUSION: We make the novel observation that the NLRP3 inflammasome activity is correlated with certain metabolites (Isoleucine, GABA, Carnitine and PC34:2) and hypothesize that they could trigger increased NLRP3 Inflammasome activity in MetS.	Carnitine	137-146	NLR family pyrin domain containing 3	Homo sapiens	51-56
32531835-2	2021	Distinctiveness of the nucleotide-binding oligomerization (NOD), Leucine-rich repeat (LRR)-containing protein (NLRP3) inflammasome resides in the diversity of molecules that induce its activation, indicating a certain intricacy.	Leucine	65-72	NLR family pyrin domain containing 3	Homo sapiens	111-116
33605079-11	2021	Furthermore, LPZ deteriorated cisplatin-induced inflammation, as revealed by the increased mRNA expression of pro-inflammatory factors including, NLRP3, IL-1beta, TNF-alpha and caspase 1, as well as neutrophil infiltration.	Lansoprazole	13-16	NLR family pyrin domain containing 3	Homo sapiens	146-151
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Uric Acid	89-98	NLR family pyrin domain containing 3	Homo sapiens	243-248
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Aspartic Acid	172-185	NLR family pyrin domain containing 3	Homo sapiens	0-5
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Aspartic Acid	172-185	NLR family pyrin domain containing 3	Homo sapiens	243-248
32072190-0	2021	Physcion 8-O-beta-glucopyranoside mediates the NLRP3-associated pyroptosis and cell metastasis in the human osteosarcoma cells via ER stress activation.	6''-O-glucopyranoside	9-33	NLR family pyrin domain containing 3	Homo sapiens	47-52
32072190-9	2021	However, inhibition of NLPR3 and the ER stress maker CHOP restored the effect of PG on pyroptosis and cell metastasis, suggesting that the PG-induced antitumor effects on the HOS and the SAOS-2 cells were mediated by the ER stress-activated NLRP3 inflammasome.	physcione	139-141	NLR family pyrin domain containing 3	Homo sapiens	241-246
33524445-1	2021	Activation of NLRP3 inflammasome is implicated in varieties of pathologies, the aim of the present study is to characterize the effect and mechanism of mitochondrial uncouplers on NLRP3 inflammasome activation by using three types of uncouplers, niclosamide, CCCP and BAM15.	Niclosamide	246-257	NLR family pyrin domain containing 3	Homo sapiens	14-19
33383234-0	2021	Reduced intracellular antioxidant capacity in platelets contributes to primary immune thrombocytopenia via ROS-NLRP3-caspase-1 pathway.	ros	107-110	NLR family pyrin domain containing 3	Homo sapiens	111-116
33383234-9	2021	H2O2 supplementation elevated the expression of NLRP3 inflammasome and increased IL-1beta secretion in ITP platelets.	Hydrogen Peroxide	0-4	NLR family pyrin domain containing 3	Homo sapiens	48-53
33383234-11	2021	Pretreating ITP platelets with NLRP3 inhibitor MCC950 or caspase-1 inhibitor Z-YVAD-FMK significantly reduced the proportion of pyroptotic cells in H2O2-treated ITP platelets and suppressed IL-1beta secretion in supernatants.	Hydrogen Peroxide	148-152	NLR family pyrin domain containing 3	Homo sapiens	31-36
33524445-1	2021	Activation of NLRP3 inflammasome is implicated in varieties of pathologies, the aim of the present study is to characterize the effect and mechanism of mitochondrial uncouplers on NLRP3 inflammasome activation by using three types of uncouplers, niclosamide, CCCP and BAM15.	Niclosamide	246-257	NLR family pyrin domain containing 3	Homo sapiens	180-185
33524445-1	2021	Activation of NLRP3 inflammasome is implicated in varieties of pathologies, the aim of the present study is to characterize the effect and mechanism of mitochondrial uncouplers on NLRP3 inflammasome activation by using three types of uncouplers, niclosamide, CCCP and BAM15.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	259-263	NLR family pyrin domain containing 3	Homo sapiens	14-19
33524445-1	2021	Activation of NLRP3 inflammasome is implicated in varieties of pathologies, the aim of the present study is to characterize the effect and mechanism of mitochondrial uncouplers on NLRP3 inflammasome activation by using three types of uncouplers, niclosamide, CCCP and BAM15.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	259-263	NLR family pyrin domain containing 3	Homo sapiens	180-185
33524445-2	2021	Niclosamide, CCCP and BAM15 inhibited LPS plus ATP-induced increases of NLRP3 protein and IL-1beta mRNA levels in RAW264.7 macrophages and THP-1 derived macrophages.	Niclosamide	0-11	NLR family pyrin domain containing 3	Homo sapiens	72-77
33524445-2	2021	Niclosamide, CCCP and BAM15 inhibited LPS plus ATP-induced increases of NLRP3 protein and IL-1beta mRNA levels in RAW264.7 macrophages and THP-1 derived macrophages.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	13-17	NLR family pyrin domain containing 3	Homo sapiens	72-77
33524445-2	2021	Niclosamide, CCCP and BAM15 inhibited LPS plus ATP-induced increases of NLRP3 protein and IL-1beta mRNA levels in RAW264.7 macrophages and THP-1 derived macrophages.	Adenosine Triphosphate	47-50	NLR family pyrin domain containing 3	Homo sapiens	72-77
33524445-5	2021	In conclusion, chemical mitochondrial uncouplers niclosamide, CCCP and BAM15 share common inhibitory effect on NLRP3 inflammasome activation through inhibiting NFkappaB nuclear translocation.	Niclosamide	49-60	NLR family pyrin domain containing 3	Homo sapiens	111-116
33524445-5	2021	In conclusion, chemical mitochondrial uncouplers niclosamide, CCCP and BAM15 share common inhibitory effect on NLRP3 inflammasome activation through inhibiting NFkappaB nuclear translocation.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	62-66	NLR family pyrin domain containing 3	Homo sapiens	111-116
33524445-5	2021	In conclusion, chemical mitochondrial uncouplers niclosamide, CCCP and BAM15 share common inhibitory effect on NLRP3 inflammasome activation through inhibiting NFkappaB nuclear translocation.	BAM 15	71-76	NLR family pyrin domain containing 3	Homo sapiens	111-116
33714286-0	2021	Astragaloside IV attenuates TGF-beta-mediated epithelial-mesenchymal transition of pulmonary fibrosis via suppressing NLRP3 expression in vitro.	astragaloside	0-13	NLR family pyrin domain containing 3	Homo sapiens	118-123
33630211-0	2021	Arginine Regulates NLRP3 Inflammasome Activation Through SIRT1 in Vascular Endothelial Cells.	Arginine	0-8	NLR family pyrin domain containing 3	Homo sapiens	19-24
33630211-3	2021	In this study, we aimed to confirm the modulatory effect of Arg on NLRP3 inflammasome and the underlying mechanisms in vascular endothelial cells (ECs).	Arginine	60-63	NLR family pyrin domain containing 3	Homo sapiens	67-72
33630211-4	2021	Arg suppressed NLRP3 inflammasome activation in ECs stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP).	Arginine	0-3	NLR family pyrin domain containing 3	Homo sapiens	15-20
33630211-4	2021	Arg suppressed NLRP3 inflammasome activation in ECs stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP).	Adenosine	97-106	NLR family pyrin domain containing 3	Homo sapiens	15-20
33630211-4	2021	Arg suppressed NLRP3 inflammasome activation in ECs stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP).	Adenosine Triphosphate	121-124	NLR family pyrin domain containing 3	Homo sapiens	15-20
33630211-6	2021	Importantly, knockdown of SIRT1 abolished the inhibitory potential of Arg on the activation of NLRP3 inflammasome.	Arginine	70-73	NLR family pyrin domain containing 3	Homo sapiens	95-100
33630211-8	2021	In addition, Arg may regulate NLRP3 inflammasome activation partly through suppression of ROS production.	Arginine	13-16	NLR family pyrin domain containing 3	Homo sapiens	30-35
33630211-8	2021	In addition, Arg may regulate NLRP3 inflammasome activation partly through suppression of ROS production.	Reactive Oxygen Species	90-93	NLR family pyrin domain containing 3	Homo sapiens	30-35
33630211-9	2021	In combination, we speculate that Arg exerts an inhibitory effect on the activation of NLRP3 inflammasome in ECs, which may be partly mediated by SIRT1 and ROS.	Arginine	34-37	NLR family pyrin domain containing 3	Homo sapiens	87-92
33630211-9	2021	In combination, we speculate that Arg exerts an inhibitory effect on the activation of NLRP3 inflammasome in ECs, which may be partly mediated by SIRT1 and ROS.	Reactive Oxygen Species	156-159	NLR family pyrin domain containing 3	Homo sapiens	87-92
33714286-3	2021	This study was designed to elucidate the regulatory effect of ASV on PF via NLRP3.	astragaloside A	62-65	NLR family pyrin domain containing 3	Homo sapiens	76-81
33626512-4	2021	Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1beta, IL-18, and gasdermin D.	Nicotine	54-62	NLR family pyrin domain containing 3	Homo sapiens	201-206
33626512-4	2021	Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1beta, IL-18, and gasdermin D.	Reactive Oxygen Species	173-176	NLR family pyrin domain containing 3	Homo sapiens	201-206
33626512-10	2021	Therefore, targeting the TXNIP/NLRP3-mediated pyroptotic pathway in macrophages may ameliorate nicotine-induced endothelial damage.	Nicotine	95-103	NLR family pyrin domain containing 3	Homo sapiens	31-36
33546399-10	2021	Finally, studies revealing the role of glucose concentration in the activation of NLRP3 inflammasome are analyzed.	Glucose	39-46	NLR family pyrin domain containing 3	Homo sapiens	82-87
33053467-0	2021	Amorphous silica nanoparticles induce inflammation via activation of NLRP3 inflammasome and HMGB1/TLR4/MYD88/NF-kb signaling pathway in HUVEC cells.	Silicon Dioxide	10-16	NLR family pyrin domain containing 3	Homo sapiens	69-74
33053467-5	2021	In addition, SiO2 NPs were found to promote the translocation and release of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm, which was demonstrated to be regulated by ROS and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome.	Reactive Oxygen Species	180-183	NLR family pyrin domain containing 3	Homo sapiens	233-238
33673188-2	2021	The NACHT, leucine-rich repeat (LRR), and pyrin domain (PYD)-containing protein 3 (NLRP3) inflammasome is a protein complex that functions as a platform for rapid induction of the inflammatory response to infection or sterile injury.	Leucine	11-18	NLR family pyrin domain containing 3	Homo sapiens	83-88
33547278-0	2021	Sensing soluble uric acid by Naip1-Nlrp3 platform.	Uric Acid	16-25	NLR family pyrin domain containing 3	Homo sapiens	35-40
33547278-4	2021	Through structural modelling predictions and transcriptome and functional analyses, we found that murine Naip1 expression in human macrophages induces IL-1beta expression, fatty acid production and an inflammation-related response upon sUA stimulation, a process reversed by the pharmacological and genetic inhibition of Nlrp3.	sua	236-239	NLR family pyrin domain containing 3	Homo sapiens	321-326
33355638-5	2021	In this mini-review, we present a brief summary of the current knowledge about how different ionic flows (including K+, sodium ion, Ca2+, magnesium ion, manganese ion, zinc ion, iron ion, and Cl-) are involved in regulating the NLRP3 inflammasome activation in macrophages.	Magnesium	138-147	NLR family pyrin domain containing 3	Homo sapiens	228-233
33636340-3	2021	The nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP3) inflammasome is the most well characterised inflammasome, and its aberrant activation is implicated in many inflammatory diseases.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	90-95
33679687-5	2020	In the present study, we used LPS and ATP to induce the intracellular formation of the NLRP3 inflammasome.	Adenosine Triphosphate	38-41	NLR family pyrin domain containing 3	Homo sapiens	87-92
33418063-0	2021	Discovery of Carbon-11 Labeled Sulfonamide Derivative: A PET Tracer for Imaging Brain NLRP3 Inflammasome.	Carbon-11	13-22	NLR family pyrin domain containing 3	Homo sapiens	86-91
33418063-0	2021	Discovery of Carbon-11 Labeled Sulfonamide Derivative: A PET Tracer for Imaging Brain NLRP3 Inflammasome.	Sulfonamides	31-42	NLR family pyrin domain containing 3	Homo sapiens	86-91
33418063-2	2021	Our recent medicinal chemistry campaign on developing sulfonamide-based NLRP3 inhibitors led to an analog, 1, with a methoxy substituent amenable to labeling with carbon-11.	Sulfonamides	54-65	NLR family pyrin domain containing 3	Homo sapiens	72-77
33418063-2	2021	Our recent medicinal chemistry campaign on developing sulfonamide-based NLRP3 inhibitors led to an analog, 1, with a methoxy substituent amenable to labeling with carbon-11.	Carbon-11	163-172	NLR family pyrin domain containing 3	Homo sapiens	72-77
33573688-14	2021	The findings suggest that Icariside I or EF should be avoided in patients with diseases related to ATP or nigericin-induced NLRP3 inflammasome activation, which may be risk factors for IDILI.	Nigericin	106-115	NLR family pyrin domain containing 3	Homo sapiens	124-129
33633700-0	2021	Progesterone Suppresses Neisseria gonorrhoeae-Induced Inflammation Through Inhibition of NLRP3 Inflammasome Pathway in THP-1 Cells and Murine Models.	Progesterone	0-12	NLR family pyrin domain containing 3	Homo sapiens	89-94
33613529-4	2020	Method: The effect of Caspase 1 inhibitor (VX765) and combination of LPS/Nigericin on NLRP3 inflammasome activity was analyzed in A549 (lung cancer), MCF-7 (breast cancer), PC3 (prostate cancer), SH-SY5Y (neuroblastoma), and U138MG (glioblastoma) cells.	Nigericin	73-82	NLR family pyrin domain containing 3	Homo sapiens	86-91
33613529-6	2020	The effect of VX765 and LPS/Nigericin on NLRP3 expression was analyzed using western blot, while IL-1beta and IL-18 secretion was detected by ELISA.	Nigericin	28-37	NLR family pyrin domain containing 3	Homo sapiens	41-46
33613529-18	2020	Discussion: Our data suggest that NLRP3 activation using Nigericin could be a novel therapeutic approach to control the growth of tumors producing a low level of IL-1beta and IL-18.	Nigericin	57-66	NLR family pyrin domain containing 3	Homo sapiens	34-39
33546151-0	2021	Green Synthesis of Silver Nanoparticles Using Annona muricata Extract as an Inducer of Apoptosis in Cancer Cells and Inhibitor for NLRP3 Inflammasome via Enhanced Autophagy.	Silver	19-25	NLR family pyrin domain containing 3	Homo sapiens	131-136
33159581-7	2021	Furthermore, SA/Col loaded with hUC-MSCs significantly lowered the expression of NLRP3 inflammasome-related proteins (p < 0.05).	Alginates	13-15	NLR family pyrin domain containing 3	Homo sapiens	81-86
33546151-12	2021	In addition, AgNP-induced autophagy reduced the levels of IL-1beta and NLRP3 inflammasome activation.	agnp	13-17	NLR family pyrin domain containing 3	Homo sapiens	71-76
33022793-9	2021	We demonstrated that bacterial components and eHsp70 activate NLRP3 inflammasome and increase ATP secretion.	Adenosine Triphosphate	94-97	NLR family pyrin domain containing 3	Homo sapiens	62-67
32396707-11	2021	Interestingly, we also found that the anti-proliferative and anti-metastatic effects of RB were alleviated by the blockade of pyroptosis using NLRP3 inhibitor MCC950.	bufogenin	88-90	NLR family pyrin domain containing 3	Homo sapiens	143-148
33159581-8	2021	Taken together, our results suggest that SA/Col loaded with hUC-MSCs promotes skin wound healing via partly inhibiting NLRP3 pathway, which has potential to the treatment of skin wounds.	Alginates	41-43	NLR family pyrin domain containing 3	Homo sapiens	119-124
32966618-11	2021	In contrast, the miR-223 mimic significantly inhibited the NLRP3/CASP1 inflammasome pathway activation induced by ATP plus LPS compared to the ATP plus LPS-induced group (p<0.05).	Adenosine Triphosphate	114-117	NLR family pyrin domain containing 3	Homo sapiens	59-64
33181351-5	2021	Other endogenous molecules (e.g. TNF, ATP, serum amyloid A), as well as dysbiosis, can induce peripheral or central inflammation and thereby promote microglial NLRP3 inflammasome signalling and resultant AD.	Adenosine Triphosphate	38-41	NLR family pyrin domain containing 3	Homo sapiens	160-165
33171231-0	2021	Inhibition of NLRP3-inflammasome mediated IL-1beta release by phenylpropanoic acid derivatives: in-silico and in-vitro approach.	3-phenylpropionic acid	62-82	NLR family pyrin domain containing 3	Homo sapiens	14-19
33171231-3	2021	The study was carried out to test the ability of phenylpropanoic acid derivatives to inhibit the NLRP3 inflammasome pathway and IL-1beta release.	3-phenylpropionic acid	49-69	NLR family pyrin domain containing 3	Homo sapiens	97-102
33171231-11	2021	Based on the above results, phenylpropanoic acid derivatives have potential to be developed as specific NLRP3-inflammasome inhibitors.	3-phenylpropionic acid	28-48	NLR family pyrin domain containing 3	Homo sapiens	104-109
32966618-10	2021	The miR-223 inhibitor further promoted ATP plus LPS-induced NLRP3/CASP1 inflammasome pathway activation compared to the ATP plus LPS-induced group (p<0.05).	Adenosine Triphosphate	39-42	NLR family pyrin domain containing 3	Homo sapiens	60-65
33416115-6	2021	LPS upregulated the expression of inflammatory cytokines and NLRP3, inhibited the expression of autophagy-related and osteogenesis-related proteins, promoted apoptosis and altered the cell cycle, which was partially inhibited by NEAT1 overexpression and promoted by bexarotene.	Bexarotene	266-276	NLR family pyrin domain containing 3	Homo sapiens	61-66
33603947-0	2021	Propionibacterium acnes Accelerates Intervertebral Disc Degeneration by Inducing Pyroptosis of Nucleus Pulposus Cells via the ROS-NLRP3 Pathway.	Reactive Oxygen Species	126-129	NLR family pyrin domain containing 3	Homo sapiens	130-135
33470533-9	2021	In the Langendorff model, PD98059 inhibited ERK1/2 and up-regulated the expression of NOX4, NLRP3, caspase-1 and IL-1beta, which exacerbated oxidative stress and inflammation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	26-33	NLR family pyrin domain containing 3	Homo sapiens	92-97
33259938-9	2021	These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-kappaB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.	Vitamin D	26-35	NLR family pyrin domain containing 3	Homo sapiens	133-138
33259938-9	2021	These data suggested that vitamin D/VDR could alleviate cisplatin-induced acute renal injury partly by inhibiting NF-kappaB-mediated NLRP3/Caspase-1/GSDMD pyroptosis.	Cisplatin	56-65	NLR family pyrin domain containing 3	Homo sapiens	133-138
32712773-7	2021	Finally, we transfected miR-1301-3p inhibitor to MPP+-induced SH-SY5Y cells following si-NEAT1, and found that downregulation of NEAT1 repressed alpha-syn-mediated the activation of NLRP3 inflammasome through regulating miR-1301-3p/GJB1 signaling pathway.	mangion-purified polysaccharide (Candida albicans)	49-53	NLR family pyrin domain containing 3	Homo sapiens	182-187
33603947-7	2021	Therefore, P. acnes induces NPC pyroptosis via the ROS-NLRP3 signaling pathway, and the pyroptotic NPCs cause an IVD degeneration cascade.	Reactive Oxygen Species	51-54	NLR family pyrin domain containing 3	Homo sapiens	55-60
33522150-4	2021	The VTPA is composed of an organosilica coated iron oxide nanoparticle core and spiky manganese dioxide protrusions, which can readily accumulate in tumor after systemic administration, facilitate the tumor intracellular lysosomal rupture, and be degraded by tumor over-expressed intracellular glutathione (GSH) to release Mn ions and iron oxide nanoparticles (IONPs) for the synergetic activation of nucleotide binding oligomerization domain-like receptors protein 3 (NLRP3) inflammasomes.	vtpa	4-8	NLR family pyrin domain containing 3	Homo sapiens	469-474
32797724-4	2021	The most investigated is the NLRP3 inflammasome, which can be activated by various stimuli, such as the recognition of extracellular ATP by the P2X7 receptor.	Adenosine Triphosphate	133-136	NLR family pyrin domain containing 3	Homo sapiens	29-34
33352465-6	2021	In addition, treatment with NATx0 prevented NLRP3 inflammasome activation after LPS/ATP stimulation in macrophages in vitro.	Adenosine Triphosphate	84-87	NLR family pyrin domain containing 3	Homo sapiens	44-49
33522150-5	2021	Consequently, the activation of NLRP3 inflammasomes and the release of lactate dehydrogenase of tumor cells are observed after the treatment of VTPA, resulting in a specific pyroptotic cell death.	vtpa	144-148	NLR family pyrin domain containing 3	Homo sapiens	32-37
33584673-0	2020	Extracellular Adenosine Triphosphate (eATP) and Its Metabolite, Extracellular Adenosine (eAdo), as Opposing "Yin-Yang" Regulators of Nlrp3 Inflammasome in the Trafficking of Hematopoietic Stem/Progenitor Cells.	eado	89-93	NLR family pyrin domain containing 3	Homo sapiens	133-138
33584673-0	2020	Extracellular Adenosine Triphosphate (eATP) and Its Metabolite, Extracellular Adenosine (eAdo), as Opposing "Yin-Yang" Regulators of Nlrp3 Inflammasome in the Trafficking of Hematopoietic Stem/Progenitor Cells.	Adenosine	14-23	NLR family pyrin domain containing 3	Homo sapiens	133-138
33584673-6	2020	Importantly, the Nlrp3 inflammasome responds to mediators of purinergic signaling, and while extracellular adenosine triphosphate (eATP) activates this protein complex, its metabolite extracellular adenosine (eAdo) has the opposite effect.	Adenosine	107-116	NLR family pyrin domain containing 3	Homo sapiens	17-22
33584673-6	2020	Importantly, the Nlrp3 inflammasome responds to mediators of purinergic signaling, and while extracellular adenosine triphosphate (eATP) activates this protein complex, its metabolite extracellular adenosine (eAdo) has the opposite effect.	eatp	131-135	NLR family pyrin domain containing 3	Homo sapiens	17-22
33584673-0	2020	Extracellular Adenosine Triphosphate (eATP) and Its Metabolite, Extracellular Adenosine (eAdo), as Opposing "Yin-Yang" Regulators of Nlrp3 Inflammasome in the Trafficking of Hematopoietic Stem/Progenitor Cells.	eatp	38-42	NLR family pyrin domain containing 3	Homo sapiens	133-138
33584673-0	2020	Extracellular Adenosine Triphosphate (eATP) and Its Metabolite, Extracellular Adenosine (eAdo), as Opposing "Yin-Yang" Regulators of Nlrp3 Inflammasome in the Trafficking of Hematopoietic Stem/Progenitor Cells.	Adenosine	78-87	NLR family pyrin domain containing 3	Homo sapiens	133-138
33584673-6	2020	Importantly, the Nlrp3 inflammasome responds to mediators of purinergic signaling, and while extracellular adenosine triphosphate (eATP) activates this protein complex, its metabolite extracellular adenosine (eAdo) has the opposite effect.	Adenosine	198-207	NLR family pyrin domain containing 3	Homo sapiens	17-22
33584673-6	2020	Importantly, the Nlrp3 inflammasome responds to mediators of purinergic signaling, and while extracellular adenosine triphosphate (eATP) activates this protein complex, its metabolite extracellular adenosine (eAdo) has the opposite effect.	eado	209-213	NLR family pyrin domain containing 3	Homo sapiens	17-22
33471105-2	2021	P2X7 is a highly polymorphic gene encoding an ATP-gated cationic pore, widely expressed on immune cells and the brain, and regulating the NLRP3 inflammasome, as well as diverse neural functions.	Adenosine Triphosphate	46-49	NLR family pyrin domain containing 3	Homo sapiens	138-143
33509217-8	2021	Quercetin suppresses the NLRP3 inflammasome by affecting these regulators.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	25-30
33504771-12	2021	ATP activated the NLRP3 inflammasome in renal tubular epithelial cells, which were blunted by transient silence of P2X7 receptor, as well as by P2X7 receptor blocking with A438079.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	18-23
33504771-12	2021	ATP activated the NLRP3 inflammasome in renal tubular epithelial cells, which were blunted by transient silence of P2X7 receptor, as well as by P2X7 receptor blocking with A438079.	3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridine	172-179	NLR family pyrin domain containing 3	Homo sapiens	18-23
33504771-14	2021	Extracellular ATP/P2X7 receptor axis blocking may protect renal tubular epithelial cells from ischemia-reperfusion injury through the regulation of NLRP3 inflammasome.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	148-153
33530480-0	2021	KMU-1170, a Novel Multi-Protein Kinase Inhibitor, Suppresses Inflammatory Signal Transduction in THP-1 Cells and Human Osteoarthritic Fibroblast-Like Synoviocytes by Suppressing Activation of NF-kappaB and NLRP3 Inflammasome Signaling Pathway.	kmu-1170	0-8	NLR family pyrin domain containing 3	Homo sapiens	206-211
33530480-4	2021	Moreover, KMU-1170 suppressed LPS-induced upregulation of proinflammatory cytokines such as IL-1beta, TNF-alpha, and IL-6, and, notably, inhibited LPS-induced upregulation of the NLRP3 inflammasome in THP-1 cells.	kmu-1170	10-18	NLR family pyrin domain containing 3	Homo sapiens	179-184
33000169-0	2021	Albiflorin Attenuates Mood Disorders Under Neuropathic Pain State By Suppressing The Hippocampal NLRP3 Inflammasome Activation During Chronic Constriction Injury.	albiflorin	0-10	NLR family pyrin domain containing 3	Homo sapiens	97-102
33000169-6	2021	Albiflorin (AF), a monoterpene glycoside, may be a potential regulator of the NLRP3 inflammasome, but it is not clear whether AF relates to NLRP3 inflammasome activation.	albiflorin	0-10	NLR family pyrin domain containing 3	Homo sapiens	78-83
33469482-0	2021	Effects of quercetin on diabetic retinopathy and its association with NLRP3 inflammasome and autophagy.	Quercetin	11-20	NLR family pyrin domain containing 3	Homo sapiens	70-75
33469482-1	2021	AIM: To investigate the effects of quercetin on diabetic retinopathy (DR) and its association with nucleotide-binding oligomerization domain-like receptors 3 (NLRP3) inflammasome and autophagy using retinal endothelial cell as an experimental model.	Quercetin	35-44	NLR family pyrin domain containing 3	Homo sapiens	159-164
33469482-7	2021	Quercetin inhibited angiogenesis of HRMECs as well as the expressions of NLRP3, ASC, Caspase-1, IL-1beta, IL-18, LC3, Beclin-1, and autophagy of HRMECs under a HG condition.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	73-78
33469482-8	2021	The inhibitory effects of quercetin on angiogenesis, NLRP3 inflammasome and autophagy increased with the increase of its concentration.	Quercetin	26-35	NLR family pyrin domain containing 3	Homo sapiens	53-58
33520966-10	2020	Conclusion: Enriched miR-100-5p in hucMSC-exo suppressed FOXO3 expression to inhibit NLRP3 inflammasome activation and suppress cytokine release and, therefore, protected cardiomyocytes from H/R-induced pyroptosis and injury.	mir-100-5p	21-31	NLR family pyrin domain containing 3	Homo sapiens	85-90
33157513-0	2021	Inhibition of ROS/NLRP3/Caspase-1 mediated pyroptosis alleviates excess molybdenum-induced apoptosis in duck renal tubular epithelial cells.	Molybdenum	72-82	NLR family pyrin domain containing 3	Homo sapiens	18-23
33527027-11	2021	Proteasome inhibitor MG132 abolished PARK2 overexpression-induced down-regulation of NLRP3 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	NLR family pyrin domain containing 3	Homo sapiens	85-90
33332136-3	2021	In this study, we discovered and synthesized a series of tetrahydroquinoline inhibitors of NLRP3 inflammasome.	1,2,3,4-tetrahydroquinoline	57-76	NLR family pyrin domain containing 3	Homo sapiens	91-96
33436541-0	2021	DHA/AA alleviates LPS-induced Kupffer cells pyroptosis via GPR120 interaction with NLRP3 to inhibit inflammasome complexes assembly.	Docosahexaenoic Acids	0-3	NLR family pyrin domain containing 3	Homo sapiens	83-88
33440945-0	2021	Berberine Directly Targets the NEK7 Protein to Block the NEK7-NLRP3 Interaction and Exert Anti-inflammatory Activity.	Berberine	0-9	NLR family pyrin domain containing 3	Homo sapiens	62-67
33441928-2	2021	Inflammation in DE might be mediated by the NLRP3 inflammasome, which activated by exposure to reactive oxygen species (ROS).	Reactive Oxygen Species	95-118	NLR family pyrin domain containing 3	Homo sapiens	44-49
33441928-2	2021	Inflammation in DE might be mediated by the NLRP3 inflammasome, which activated by exposure to reactive oxygen species (ROS).	Reactive Oxygen Species	120-123	NLR family pyrin domain containing 3	Homo sapiens	44-49
33441928-6	2021	These findings indicate that combined CMC + alpha-MSH treatment could ameliorate lesions and restore ocular surface function in patients with DE through reduction of ROS level and inhibition of NLRP3 signalling.	Carboxymethylcellulose Sodium	38-41	NLR family pyrin domain containing 3	Homo sapiens	194-199
33436541-4	2021	The present study demonstrated that DHA and AA ameliorated lipopolysaccharide (LPS)-induced Kupffer cells pyroptosis by reversing the increased expression of NLRP3 inflammasome complex, GSDMD, IL-1beta, IL-18, and PI-stained positive rate.	Docosahexaenoic Acids	36-39	NLR family pyrin domain containing 3	Homo sapiens	158-163
33436541-7	2021	Furthermore, co-immunoprecipitation showed that DHA and AA promoted the interaction between GPR120 and NLRP3 in LPS-exposed Kupffer cells, thus inhibiting the self-assembly of NLRP3 inflammasome complex.	Docosahexaenoic Acids	48-51	NLR family pyrin domain containing 3	Homo sapiens	103-108
33436541-7	2021	Furthermore, co-immunoprecipitation showed that DHA and AA promoted the interaction between GPR120 and NLRP3 in LPS-exposed Kupffer cells, thus inhibiting the self-assembly of NLRP3 inflammasome complex.	Docosahexaenoic Acids	48-51	NLR family pyrin domain containing 3	Homo sapiens	176-181
33436541-9	2021	The findings indicated that DHA and AA alleviated LPS-induced Kupffer cells pyroptosis via GPR120 interaction with NLRP3, it might become a potential therapeutic approach hepatic injury.	Docosahexaenoic Acids	28-31	NLR family pyrin domain containing 3	Homo sapiens	115-120
33435142-1	2021	NLRP3 inflammasome is one of the multimeric protein complexes of the nucleotide-binding domain, leucine-rich repeat (NLR)-containing pyrin and HIN domain family (PYHIN).	Leucine	96-103	NLR family pyrin domain containing 3	Homo sapiens	0-5
33430114-6	2021	The present study aims to investigate the potential effect of alpha-lipoic acid (ALA) on NALP-3 and ER-beta expression using a western blot analysis, NALP-3-induced cytokines production by ELISA, migration and invasion of immortalized epithelial (12Z) and stromal endometriotic cells (22B) using a 3D culture invasion assay, and matrix-metalloprotease (MMPs) activity using gelatin zymography.	Thioctic Acid	62-79	NLR family pyrin domain containing 3	Homo sapiens	89-95
33430114-6	2021	The present study aims to investigate the potential effect of alpha-lipoic acid (ALA) on NALP-3 and ER-beta expression using a western blot analysis, NALP-3-induced cytokines production by ELISA, migration and invasion of immortalized epithelial (12Z) and stromal endometriotic cells (22B) using a 3D culture invasion assay, and matrix-metalloprotease (MMPs) activity using gelatin zymography.	Thioctic Acid	81-84	NLR family pyrin domain containing 3	Homo sapiens	89-95
33430114-7	2021	ALA significantly reduces ER-beta, NALP-3 protein expression/activity and the secretion of IL-1beta and IL-18 in both 12Z and 22B cells.	Thioctic Acid	0-3	NLR family pyrin domain containing 3	Homo sapiens	35-41
33505807-10	2021	SK and its derivatives inhibited the activation of nucleotide binding oligomerization domain-like receptors (NLRP3) inflammasome and NF-kappaB signaling pathway, thereby relieving the DSS-induced disruption of epithelial tight junction (TJ) in colonic tissues.	shikonin	0-2	NLR family pyrin domain containing 3	Homo sapiens	109-114
33430226-0	2021	Indoxyl Sulfate Mediates the Low Inducibility of the NLRP3 Inflammasome in Hemodialysis Patients.	Indican	0-15	NLR family pyrin domain containing 3	Homo sapiens	53-58
33505807-10	2021	SK and its derivatives inhibited the activation of nucleotide binding oligomerization domain-like receptors (NLRP3) inflammasome and NF-kappaB signaling pathway, thereby relieving the DSS-induced disruption of epithelial tight junction (TJ) in colonic tissues.	Dextran Sulfate	184-187	NLR family pyrin domain containing 3	Homo sapiens	109-114
33505510-0	2021	Cichoric Acid Ameliorates Monosodium Urate-Induced Inflammatory Response by Reducing NLRP3 Inflammasome Activation via Inhibition of NF-kB Signaling Pathway.	chicoric acid	0-13	NLR family pyrin domain containing 3	Homo sapiens	85-90
33414419-4	2021	Mitochondrial reactive oxygen species (mtROS) driven by gefitinib stimulated the formation of the NLRP3 (NACHT, LRR and PYD-containing protein 3) inflammasome, leading to mature-IL-1beta release.	reactive oxygen	14-29	NLR family pyrin domain containing 3	Homo sapiens	98-103
33414419-4	2021	Mitochondrial reactive oxygen species (mtROS) driven by gefitinib stimulated the formation of the NLRP3 (NACHT, LRR and PYD-containing protein 3) inflammasome, leading to mature-IL-1beta release.	reactive oxygen	14-29	NLR family pyrin domain containing 3	Homo sapiens	105-144
33414419-4	2021	Mitochondrial reactive oxygen species (mtROS) driven by gefitinib stimulated the formation of the NLRP3 (NACHT, LRR and PYD-containing protein 3) inflammasome, leading to mature-IL-1beta release.	Gefitinib	56-65	NLR family pyrin domain containing 3	Homo sapiens	98-103
33414419-4	2021	Mitochondrial reactive oxygen species (mtROS) driven by gefitinib stimulated the formation of the NLRP3 (NACHT, LRR and PYD-containing protein 3) inflammasome, leading to mature-IL-1beta release.	Gefitinib	56-65	NLR family pyrin domain containing 3	Homo sapiens	105-144
33505510-0	2021	Cichoric Acid Ameliorates Monosodium Urate-Induced Inflammatory Response by Reducing NLRP3 Inflammasome Activation via Inhibition of NF-kB Signaling Pathway.	Uric Acid	26-42	NLR family pyrin domain containing 3	Homo sapiens	85-90
33505510-6	2021	Therefore, we infer that CA effectively alleviated MSU-induced inflammation by suppressing the degradation of IkappaBalpha, thereby reducing the activation of the NF-kappaB signaling pathway and the NLRP3 inflammasome.	Uric Acid	51-54	NLR family pyrin domain containing 3	Homo sapiens	199-204
31971103-8	2021	The development of NLRP3 inhibitors was described from the earliest glyburide in 2001 to the latest progress in 2019.	Glyburide	68-77	NLR family pyrin domain containing 3	Homo sapiens	19-24
33402173-0	2021	Isoliquiritin ameliorates depression by suppressing NLRP3-mediated pyroptosis via miRNA-27a/SYK/NF-kappaB axis.	neoisoliquiritin	0-13	NLR family pyrin domain containing 3	Homo sapiens	52-57
33402173-2	2021	Isoliquiritin is a phenolic flavonoid compound that has been demonstrated to suppress NLRP3-mediated pyroptosis.	neoisoliquiritin	0-13	NLR family pyrin domain containing 3	Homo sapiens	86-91
33402173-2	2021	Isoliquiritin is a phenolic flavonoid compound that has been demonstrated to suppress NLRP3-mediated pyroptosis.	Flavonoids	28-37	NLR family pyrin domain containing 3	Homo sapiens	86-91
33402173-3	2021	However, it is still unknown whether isoliquiritin could confer antidepressant activity via decreasing NLRP3-mediated pyroptosis by stimulating miRNA-27a.	neoisoliquiritin	37-50	NLR family pyrin domain containing 3	Homo sapiens	103-108
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	neoisoliquiritin	10-23	NLR family pyrin domain containing 3	Homo sapiens	106-111
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	neoisoliquiritin	10-23	NLR family pyrin domain containing 3	Homo sapiens	199-204
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	Adenosine	68-77	NLR family pyrin domain containing 3	Homo sapiens	106-111
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	Adenosine Triphosphate	92-95	NLR family pyrin domain containing 3	Homo sapiens	106-111
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	Adenosine Triphosphate	92-95	NLR family pyrin domain containing 3	Homo sapiens	199-204
33402173-18	2021	Taken together, these findings suggest that isoliquiritin possesses potent antidepressant property, which requires miRNA-27a/SYK/NF-kappaB axis controlled decrease of pyroptosis via NLRP3 cascade.	neoisoliquiritin	44-57	NLR family pyrin domain containing 3	Homo sapiens	182-187
33569466-10	2021	The potential mechanism of YZTM anti-VaD may be through inhibiting the NLRP3 inflammasome, TNF signaling pathway, and toll-like receptor signaling pathways.	yztm	27-31	NLR family pyrin domain containing 3	Homo sapiens	71-76
33569466-13	2021	Conclusions: YZTM may exert an anti-VaD effect through inhibition of the NLRP3 inflammasome.	yztm	13-17	NLR family pyrin domain containing 3	Homo sapiens	73-78
33099890-9	2021	Curcumin regulates several molecules in the intracellular signal transduction pathways involved in inflammation, including IBB, NF-kBERK1,2, AP-1, TGF-beta, TXNIP, STAT3, PPARgamma, JAK2-STAT3, NLRP3, p38MAPK, Nrf2, Notch-1, AMPK, TLR-4 and MyD-88.	Curcumin	0-8	NLR family pyrin domain containing 3	Homo sapiens	194-199
33407596-0	2021	Sialylated human milk oligosaccharides prevent intestinal inflammation by inhibiting toll like receptor 4/NLRP3 inflammasome pathway in necrotizing enterocolitis rats.	Oligosaccharides	22-38	NLR family pyrin domain containing 3	Homo sapiens	106-111
32852568-0	2021	The beneficial effects of reducing NLRP3 inflammasome activation in the cardiotoxicity and the anti-cancer effects of doxorubicin.	Doxorubicin	118-129	NLR family pyrin domain containing 3	Homo sapiens	35-40
32852568-6	2021	Recent studies have suggested that the Nucleotide-Binding Domain-Like Receptor Protein 3 (NLRP3) inflammasome is implicated in tumor progression and the chemoresistance of cancer cells to DOX.	Doxorubicin	188-191	NLR family pyrin domain containing 3	Homo sapiens	39-88
32852568-6	2021	Recent studies have suggested that the Nucleotide-Binding Domain-Like Receptor Protein 3 (NLRP3) inflammasome is implicated in tumor progression and the chemoresistance of cancer cells to DOX.	Doxorubicin	188-191	NLR family pyrin domain containing 3	Homo sapiens	90-95
32852568-7	2021	Of interest, reducing NLRP3 inflammasome activity alleviates DOX-induced cardiotoxicity.	Doxorubicin	61-64	NLR family pyrin domain containing 3	Homo sapiens	22-27
32852568-8	2021	Therefore, we postulate that strategies that target the NLRP3 inflammasome can help mitigate the cardiotoxic effects of DOX while maintaining and/or even enhancing its anti-cancer activity.	Doxorubicin	120-123	NLR family pyrin domain containing 3	Homo sapiens	56-61
32852568-9	2021	Herein, we review the current knowledge about the potential implication of the NLRP3 inflammasome in the anti-cancer and cardiotoxic effects of DOX.	Doxorubicin	144-147	NLR family pyrin domain containing 3	Homo sapiens	79-84
33160017-0	2021	The SGLT2 inhibitor Empagliflozin attenuates interleukin-17A-induced human aortic smooth muscle cell proliferation and migration by targeting TRAF3IP2/ROS/NLRP3/Caspase-1-dependent IL-1beta and IL-18 secretion.	empagliflozin	20-33	NLR family pyrin domain containing 3	Homo sapiens	155-160
33160017-6	2021	Importantly, SMC express SGLT2, and pre-treatment with EMPA attenuated IL-17A/TRAF3IP2-dependent oxidative stress, NLRP3 expression, caspase-1 activation, IL-1beta and IL-18 secretion, and SMC proliferation and migration.	empagliflozin	55-59	NLR family pyrin domain containing 3	Homo sapiens	115-120
32510626-7	2021	Introduction of miR-181b-5p could alleviate NLRP3 inflammasome-dependent pyroptosis.	mir-181b-5p	16-27	NLR family pyrin domain containing 3	Homo sapiens	44-49
33189612-4	2021	This study found that lipopolysaccharide + ATP upregulated Meg3, promoted microglia activation, Nlrp3/caspase1 activation and inflammation, and markedly reduced miR-7a-5p.	Adenosine Triphosphate	43-46	NLR family pyrin domain containing 3	Homo sapiens	96-101
33199234-6	2021	The cyclic stretch also induced the expression of caspase-1 and NLRP3 inflammasome, which could also be inhibited by apocynin.	acetovanillone	117-125	NLR family pyrin domain containing 3	Homo sapiens	64-69
32941940-5	2021	Inflammasome activation was determined in reconstituted HEK293T cells with NLRP3 inflammasome components, doxycycline-inducible NLRP3 macrophages, as well as PBMCs and biopsies from patients with NLRP3 variants.	Doxycycline	106-117	NLR family pyrin domain containing 3	Homo sapiens	128-133
32941940-5	2021	Inflammasome activation was determined in reconstituted HEK293T cells with NLRP3 inflammasome components, doxycycline-inducible NLRP3 macrophages, as well as PBMCs and biopsies from patients with NLRP3 variants.	Doxycycline	106-117	NLR family pyrin domain containing 3	Homo sapiens	128-133
33136175-12	2021	CONCLUSION: The results suggest that LTD4 could induce inflammatory response in human airway epithelial cell by activating NALP3 inflammasome.	Leukotriene D4	37-41	NLR family pyrin domain containing 3	Homo sapiens	123-128
33223465-0	2021	Shionone alleviates NLRP3 inflammasome mediated pyroptosis in interstitial cystitis injury.	shionone	0-8	NLR family pyrin domain containing 3	Homo sapiens	20-25
33223465-2	2021	The activation of NLRP3 inflammasome plays an important role in cystitis, and the effect of Shionone on NLRP3 inflammasome-dependent pyroptosis remains unclear.	shionone	92-100	NLR family pyrin domain containing 3	Homo sapiens	104-109
33223465-3	2021	In this study, we established an interstitial cystitis (IC) rat model and SV-HUC-1 cell model with CYP or LPS + ATP treatment to mimic inflammation response and induce NLRP3 inflammasome activation.	Adenosine Triphosphate	112-115	NLR family pyrin domain containing 3	Homo sapiens	168-173
33223465-5	2021	Moreover, Shionone reduced the expression of NF-kappaB, NLRP3, ASC, Pro-caspase-1, Caspase-1, GSDMD, GSDMD-N at the mRNA and protein levels both in rat and SV-HUC-1 cell model, demonstrating NLRP3 inflammasome pathway was blocked and pyroptosis degree was reduced.	shionone	10-18	NLR family pyrin domain containing 3	Homo sapiens	191-196
33223465-6	2021	These results indicated that Shionone could alleviate interstitial cystitis in Rat model and enhancing the viability of SV-HUC-1 cells via NF-kappaB/NLRP3/GSDMD-N pathway, which illustrated that Shionone could be used as a drug candidate for the treatment of interstitial cystitis.	shionone	29-37	NLR family pyrin domain containing 3	Homo sapiens	149-154
33223465-6	2021	These results indicated that Shionone could alleviate interstitial cystitis in Rat model and enhancing the viability of SV-HUC-1 cells via NF-kappaB/NLRP3/GSDMD-N pathway, which illustrated that Shionone could be used as a drug candidate for the treatment of interstitial cystitis.	shionone	195-203	NLR family pyrin domain containing 3	Homo sapiens	149-154
32579244-0	2021	Clinical and biological data on the use of hydroxychloroquine against SARS-CoV-2 could support the role of the NLRP3 inflammasome in the pathogenesis of respiratory disease.	Hydroxychloroquine	43-61	NLR family pyrin domain containing 3	Homo sapiens	111-116
33295020-8	2021	In conclusion, in this study the results suggested that AS-IV could inhibit monocrotaline-induced pulmonary arterial hypertension via the NLRP-3/calpain-1 pathway.	Monocrotaline	76-89	NLR family pyrin domain containing 3	Homo sapiens	138-144
33295020-0	2021	Astragaloside IV attenuates inflammatory response mediated by NLRP-3/calpain-1 is involved in the development of pulmonary hypertension.	astragaloside	0-13	NLR family pyrin domain containing 3	Homo sapiens	62-68
33130474-0	2021	Celastrol ameliorates Propionibacterium acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	142-147
32975056-0	2021	Nlrp3, Csf3, and Edn1 in Macrophage Response to Saturated Fatty Acids and Modified Low-Density Lipoprotein.	Fatty Acids	48-69	NLR family pyrin domain containing 3	Homo sapiens	0-5
33130474-3	2021	PURPOSE: This study aims to investigate whether the inhibition of NLRP3 inflammasome is engaged in the anti-inflammatory activities of celastrol and delineate the underlying mechanism.	celastrol	135-144	NLR family pyrin domain containing 3	Homo sapiens	66-71
33296813-8	2021	RESULTS: Oral administration of mogrol (5 mg/kg/daily) in vivo significantly attenuated pathological colonic damage, inhibited inflammatory infiltration and improved the abnormal expression of NLRP3 inflammasome in colonic mucosa via the AMPK and NF-kappaB signaling pathways.	MOGROL	32-38	NLR family pyrin domain containing 3	Homo sapiens	193-198
33130474-9	2021	Celastrol suppressed NLRP3 inflammasome activation and alleviated P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	21-26
33130474-10	2021	Mechanism study revealed that celastrol could interdict K63 deubiquitination of NLRP3, which may concern interaction of celastrol and BRCA1/BRCA2-containing complex subunit 3 (BRCC3), and thereby prohibited the formation of NLRP3, ASC and pro-caspase-1 complex to block the generation of mature IL-1beta.	celastrol	30-39	NLR family pyrin domain containing 3	Homo sapiens	80-85
33130474-10	2021	Mechanism study revealed that celastrol could interdict K63 deubiquitination of NLRP3, which may concern interaction of celastrol and BRCA1/BRCA2-containing complex subunit 3 (BRCC3), and thereby prohibited the formation of NLRP3, ASC and pro-caspase-1 complex to block the generation of mature IL-1beta.	celastrol	30-39	NLR family pyrin domain containing 3	Homo sapiens	224-229
33130474-11	2021	CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases.	celastrol	12-21	NLR family pyrin domain containing 3	Homo sapiens	33-38
33130474-11	2021	CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases.	celastrol	12-21	NLR family pyrin domain containing 3	Homo sapiens	171-176
33130474-11	2021	CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases.	celastrol	12-21	NLR family pyrin domain containing 3	Homo sapiens	171-176
33391544-0	2021	Tofacitinib restores the balance of gammadeltaTreg/gammadeltaT17 cells in rheumatoid arthritis by inhibiting the NLRP3 inflammasome.	tofacitinib	0-11	NLR family pyrin domain containing 3	Homo sapiens	113-118
33523841-6	2021	Deficiency of NLRP3 also reduced serum FSH and estradiol levels.	Estradiol	47-56	NLR family pyrin domain containing 3	Homo sapiens	14-19
33375031-7	2020	We found that NPs, by activating NPR-1/cGMP/PKG-I axis, lead to phosphorylation of NLRP3 at Ser295 and to inflammasome platform disassembly.	Cyclic GMP	39-43	NLR family pyrin domain containing 3	Homo sapiens	83-88
33565399-9	2021	CONCLUSIONS: iMSC-Exos successfully reversed the AM pyroptosis and inflammatory factor expression induced by LPS/ATP, which may be due to the targeted inhibition of NLRP3 inflammasome pathway, suggesting that iMSC-Exos can exert anti-inflammatory effects by inhibiting the pyrolysis of AM.	Adenosine Triphosphate	113-116	NLR family pyrin domain containing 3	Homo sapiens	165-170
33396676-6	2020	However, NLRP3 and cleaved caspase-1 complex formation increased with hyperglycemia and cytokine challenge but was inhibited by tonabersat treatment.	tonabersat	128-138	NLR family pyrin domain containing 3	Homo sapiens	9-14
33500734-7	2021	Results: Exposure to the PPARgamma agonist, rosiglitazone, during the second signal of NLRP3 inflammasome activation attenuated caspase-1 and IL-1beta maturation.	Rosiglitazone	44-57	NLR family pyrin domain containing 3	Homo sapiens	87-92
33500734-8	2021	Moreover, PPARgamma interfered with NLRP3 inflammasome formation by decreasing NLRP3-ASC and NLRP3-NLRP3 interactions as well as NLRP3-dependent ASC oligomerization, which is mediated through interaction between the PPARgamma DNA-binding domain and the nucleotide-binding and leucine-rich repeat domains of NLRP3.	Leucine	276-283	NLR family pyrin domain containing 3	Homo sapiens	36-41
33457411-0	2020	miR-1929-3p Overexpression Alleviates Murine Cytomegalovirus-Induced Hypertensive Myocardial Remodeling by Suppressing Ednra/NLRP3 Inflammasome Activation.	mir-1929-3p	0-11	NLR family pyrin domain containing 3	Homo sapiens	125-130
33456483-6	2020	To determine how aldosterone (Aldo) activated the mineralocorticoid receptor (MR) and then induced mesangial cell pyroptosis with NLRP3-caspase-1-IL-1beta pathway, human mesangial cells (HMCs) were treated with HJHR and eplerenone, which were examined to detect the expression of NLRP3 inflammasome-associated proteins following treatment with Aldo.	Aldosterone	30-34	NLR family pyrin domain containing 3	Homo sapiens	130-135
33456483-7	2020	Conclusion: These results suggest that HJHR and eplerenone suppressed HMC pyroptosis via the MR/NLRP3 pathway.	Eplerenone	48-58	NLR family pyrin domain containing 3	Homo sapiens	96-101
33414782-7	2020	Overexpression of Gm28309 or inhibition of miR-3068-5p repressed p65 phosphorylation and reduced NLRP3 inflammasome and IL-1beta and IL-18 secretion.	gm28309	18-25	NLR family pyrin domain containing 3	Homo sapiens	97-102
33414782-7	2020	Overexpression of Gm28309 or inhibition of miR-3068-5p repressed p65 phosphorylation and reduced NLRP3 inflammasome and IL-1beta and IL-18 secretion.	mir-3068	43-51	NLR family pyrin domain containing 3	Homo sapiens	97-102
33414782-11	2020	Conclusions: Our study demonstrates, for the first time, that LncRNAs are involved in regulating immune responses during Brucella infection, and Gm28309, an lncRNA, plays a crucial role in activating NF-kappaB/NLRP3 inflammasome signaling pathway.	gm28309	145-152	NLR family pyrin domain containing 3	Homo sapiens	210-215
33332241-6	2021	In this study, melatonin attenuated the expression of pyroptosis-related genes, including NLRP3, caspase-1 and IL-1beta, in human umbilical vein endothelial cells treated with oxidised low-density lipoprotein.	Melatonin	15-24	NLR family pyrin domain containing 3	Homo sapiens	90-95
33337127-3	2021	In particular, pre-clinical and clinical studies have contributed to increasing our knowledge on the role of interleukin (IL)-1 and NLRP3 (NACHT, leucine- rich repeat, and pyrin domain- containing protein 3) inflammasome.	Leucine	146-153	NLR family pyrin domain containing 3	Homo sapiens	132-137
33337127-6	2021	This pathway is confirmed indirectly by the beneficial effect of colchicine (an indirect NLRP3 inflammasome inhibitor) and IL-1 blockers in patients with recurrent pericarditis.	Colchicine	65-75	NLR family pyrin domain containing 3	Homo sapiens	89-94
33390969-6	2020	Among all the compounds, diterpenoids is the most promising candidates for inhibiting NLRP3 inflammasome activation and improving fibrosis, as they possess combined inhibitory effect on NLRP3 inflammasome assembly and NF-kappaB signaling pathway.	Diterpenes	25-37	NLR family pyrin domain containing 3	Homo sapiens	86-91
33390969-6	2020	Among all the compounds, diterpenoids is the most promising candidates for inhibiting NLRP3 inflammasome activation and improving fibrosis, as they possess combined inhibitory effect on NLRP3 inflammasome assembly and NF-kappaB signaling pathway.	Diterpenes	25-37	NLR family pyrin domain containing 3	Homo sapiens	186-191
33333846-6	2020	ROS play central roles in the activation of the NF-kappaB and NLRP3 signaling pathways via IkappaB (an inhibitor of NF-kappaB) and thioredoxin-interacting protein, respectively, thereby linking the molecular mechanisms of oxidative stress, inflammation and fibrosis.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	62-67
32583615-3	2020	Extracellular ATP contributed to the NLRP3 inflammasome-mediated IL-1beta release, which in turn was preferentially skewed toward Th17 differentiation via enhanced phosphorylation of STAT3.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	37-42
33257576-5	2020	In the present study, we analyzed the effect of pharmacological inhibition of the NLRP3 inflammasome using dapansutrile (OLT1177), an oral NLRP3-specific inhibitor that is safe in humans.	dapansutrile	107-119	NLR family pyrin domain containing 3	Homo sapiens	82-87
33424864-0	2020	Distinct Molecular Mechanisms Underlying Potassium Efflux for NLRP3 Inflammasome Activation.	Potassium	41-50	NLR family pyrin domain containing 3	Homo sapiens	62-67
33424864-2	2020	Potassium efflux has been reported to be essential for NLRP3 inflammasome activation by structurally diverse pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs).	Potassium	0-9	NLR family pyrin domain containing 3	Homo sapiens	55-60
33424864-3	2020	Thus, the molecular mechanisms underlying potassium efflux to activate NLRP3 inflammasome are under extensive investigation.	Potassium	42-51	NLR family pyrin domain containing 3	Homo sapiens	71-76
33424864-4	2020	Here, we review current knowledge about the distinction channels or pore-forming proteins underlying potassium efflux for NLRP3 inflammasome activation with canonical/non-canonical signaling or following caspase-8 induced pyroptosis.	Potassium	101-110	NLR family pyrin domain containing 3	Homo sapiens	122-127
33318544-7	2020	Furthermore, inhibition of caspase-1 and NLRP3 activation increased neutrophil ROS-production, phagocytosis and the ability of neutrophils to suppress UPEC growth.	ros	79-82	NLR family pyrin domain containing 3	Homo sapiens	41-46
33292150-4	2020	Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process.	Reactive Oxygen Species	100-103	NLR family pyrin domain containing 3	Homo sapiens	0-5
33292150-4	2020	Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process.	Reactive Oxygen Species	105-128	NLR family pyrin domain containing 3	Homo sapiens	0-5
33213267-5	2021	As a result, the accumulation of damaged, ROS-generating mitochondria leads to activation of the NLRP3 inflammasome, which induces abnormal soluble cytokines secretion, then promotes the differentiation and maturation of osteoclasts, and ultimately results in bone metastasis.	ros	42-45	NLR family pyrin domain containing 3	Homo sapiens	97-102
33213267-8	2021	The MAP2K/MEK inhibitor trametinib is sufficient to restore mitophagy function via upregulation of ULK1, leading to inhibition of NLRP3 inflammasome activation, thereby reduces bone metastasis.	trametinib	24-34	NLR family pyrin domain containing 3	Homo sapiens	130-135
32098511-0	2020	The protective effect of doxofylline against lipopolysaccharides (LPS)-induced activation of NLRP3 inflammasome is mediated by SIRT1 in human pulmonary bronchial epithelial cells.	doxofylline	25-36	NLR family pyrin domain containing 3	Homo sapiens	93-98
32098511-8	2020	Doxofylline inhibits LPS-induced NLRP3-TXNIP inflammasome activation as revealed by its inhibitive effect on NLRP3, caspase 1 (P10 unit), and TXNIP induction as well as weakened induction of IL-1beta and IL-18.	doxofylline	0-11	NLR family pyrin domain containing 3	Homo sapiens	33-38
32098511-8	2020	Doxofylline inhibits LPS-induced NLRP3-TXNIP inflammasome activation as revealed by its inhibitive effect on NLRP3, caspase 1 (P10 unit), and TXNIP induction as well as weakened induction of IL-1beta and IL-18.	doxofylline	0-11	NLR family pyrin domain containing 3	Homo sapiens	109-114
32098511-10	2020	The silencing of SIRT1 abolishes the inhibitory effect of doxofylline on NLRP3 inflammasome activation.	doxofylline	58-69	NLR family pyrin domain containing 3	Homo sapiens	73-78
33084415-11	2020	Additionally, anti-RA activity of icariin was restored by NLRP3 inhibitor MCC950 in miR-223-3p knockdown RA-FLS cells.	mir-223	84-91	NLR family pyrin domain containing 3	Homo sapiens	58-63
32098511-11	2020	Collectively, our study demonstrates that doxofylline mitigates epithelial inflammation via amelioration of multiple cellular pathways, including NLRP3-TXNIP inflammasome activation.	doxofylline	42-53	NLR family pyrin domain containing 3	Homo sapiens	146-151
33084415-11	2020	Additionally, anti-RA activity of icariin was restored by NLRP3 inhibitor MCC950 in miR-223-3p knockdown RA-FLS cells.	p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine	92-94	NLR family pyrin domain containing 3	Homo sapiens	58-63
33084415-12	2020	Icariin inhibits proliferation and inflammation, promotes apoptosis of RA-FLS cells by regulating miR-223-3p/NLRP3 signalling, which may serve as a potential therapeutic target to alleviate RA.	icariin	0-7	NLR family pyrin domain containing 3	Homo sapiens	109-114
33323459-2	2020	Recent studies suggest NIMA-related kinase 7 (NEK7) is necessary for NLRP3 inflammasome activation during potassium efflux.	Potassium	106-115	NLR family pyrin domain containing 3	Homo sapiens	69-74
33011160-7	2020	Reactive oxygen species (ROS) scavengers, p38 and FOXO1 inhibitors and TXNIP siRNA inhibited TXNIP protein upregulation and NLRP3 inflammasome assembly and activation.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	124-129
33011160-7	2020	Reactive oxygen species (ROS) scavengers, p38 and FOXO1 inhibitors and TXNIP siRNA inhibited TXNIP protein upregulation and NLRP3 inflammasome assembly and activation.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	124-129
33011160-8	2020	Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs.	rosmarinic acid	0-15	NLR family pyrin domain containing 3	Homo sapiens	91-96
33011160-8	2020	Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs.	rosmarinic acid	0-15	NLR family pyrin domain containing 3	Homo sapiens	110-115
33011160-8	2020	Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs.	Reactive Oxygen Species	217-220	NLR family pyrin domain containing 3	Homo sapiens	91-96
33011160-8	2020	Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs.	Reactive Oxygen Species	217-220	NLR family pyrin domain containing 3	Homo sapiens	110-115
33113418-10	2020	We present reports where ASX is shown to prevent against oxidative damage and attenuate exacerbation of the inflammatory responses by regulating signaling pathways like NF-kB, NLRP3 and JAK/STAT.	astaxanthine	25-28	NLR family pyrin domain containing 3	Homo sapiens	176-181
33130239-0	2020	Gallic and butyric acids modulated NLRP3 inflammasome markers in a co-culture model of intestinal inflammation.	gallic	0-6	NLR family pyrin domain containing 3	Homo sapiens	35-40
33254688-7	2020	In addition, increased NLRP3 aggregation and enhanced production of IL-1beta occurred after PFOA treatment.	perfluorooctanoic acid	92-96	NLR family pyrin domain containing 3	Homo sapiens	23-28
33254688-9	2020	Rapamycin alleviated PFOA-induced lipid accumulation and NLRP3 inflammasome activation by activating autophagic flux.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	57-62
33254688-10	2020	Conversely, chloroquine, an autophagic flux inhibitor, exacerbated PFOA-induced lipid accumulation and NLRP3 inflammasome activation.	Chloroquine	12-23	NLR family pyrin domain containing 3	Homo sapiens	103-108
33354512-0	2020	Erratum: Author correction to "Cardamonin from a medicinal herb protects against LPS-induced septic shock by suppressing NLRP3 inflammasome" [Acta Pharmaceutica Sinica B 9 (2019) 734-744].	cardamonin	31-41	NLR family pyrin domain containing 3	Homo sapiens	121-126
33130239-0	2020	Gallic and butyric acids modulated NLRP3 inflammasome markers in a co-culture model of intestinal inflammation.	Butyrates	11-24	NLR family pyrin domain containing 3	Homo sapiens	35-40
32805375-0	2020	Activation of NLRP3 inflammasome in hepatocytes after exposure to cobalt nanoparticles: The role of oxidative stress.	Cobalt	66-72	NLR family pyrin domain containing 3	Homo sapiens	14-19
32596762-0	2020	Paeoniflorin attenuates chronic constriction injury-induced neuropathic pain by suppressing spinal NLRP3 inflammasome activation.	peoniflorin	0-12	NLR family pyrin domain containing 3	Homo sapiens	99-104
33145937-0	2020	MiR-223-3p inhibits rTp17-induced inflammasome activation and pyroptosis by targeting NLRP3.	mir-223-3p	0-10	NLR family pyrin domain containing 3	Homo sapiens	86-91
33145937-6	2020	The biological function of miR-223-3p in the NLRP3 inflammasome and pyroptosis was evaluated in T pallidum-infected human umbilical vein endothelial cells (HUVECs).	mir-223-3p	27-37	NLR family pyrin domain containing 3	Homo sapiens	45-50
33145937-10	2020	Moreover, NLRP3 overexpression or knockdown largely blocked the effects of miR-223-3p on T pallidum-induced inflammasome activation and pyroptosis in HUVECs.	mir-223-3p	75-85	NLR family pyrin domain containing 3	Homo sapiens	10-15
32805375-7	2020	Using antioxidants to scavenge ROS and mtROS, we demonstrated that Nano-Co-induced mtROS generation was related to Nano-Co-induced NLRP3 inflammasome activation.	Reactive Oxygen Species	31-34	NLR family pyrin domain containing 3	Homo sapiens	131-136
32805375-8	2020	Our findings demonstrated that Nano-Co exposure may promote intracellular oxidative stress damage, and mtROS may mediate the activation of the NLRP3 inflammasome in hepatocytes exposed to Nano-Co, suggesting an important role of ROS/NLRP3 pathway in Nano-Co-induced hepatotoxicity.	Reactive Oxygen Species	105-108	NLR family pyrin domain containing 3	Homo sapiens	143-148
32805375-8	2020	Our findings demonstrated that Nano-Co exposure may promote intracellular oxidative stress damage, and mtROS may mediate the activation of the NLRP3 inflammasome in hepatocytes exposed to Nano-Co, suggesting an important role of ROS/NLRP3 pathway in Nano-Co-induced hepatotoxicity.	Reactive Oxygen Species	105-108	NLR family pyrin domain containing 3	Homo sapiens	233-238
33325366-2	2020	On one hand, extracellular ATP promotes inflammation through activating ATP receptor represented by P2X7 (P2 purinergic receptor) and downstream NLRP3 inflammasome assembly.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	145-150
33330501-4	2020	In conjunction with key binding partners Leucine rich repeat in the Flightless I interaction proteins (LRRFIP)1/2, Flightless I acts both synergistically and competitively to regulate a wide range of cellular signaling including interacting with two of the most important inflammatory pathways, the NLRP3 inflammasome and the MyD88-TLR4 pathways.	Leucine	41-48	NLR family pyrin domain containing 3	Homo sapiens	299-304
33131902-2	2020	Many triggers, including microbial pathogens (ie, bacteria and viruses) and other signals (ie, reactive oxygen species, adenosine triphosphate, urate, silicon, and asbestos), can stimulate the NLRP3 inflammasome.	Reactive Oxygen Species	95-118	NLR family pyrin domain containing 3	Homo sapiens	193-198
33131902-2	2020	Many triggers, including microbial pathogens (ie, bacteria and viruses) and other signals (ie, reactive oxygen species, adenosine triphosphate, urate, silicon, and asbestos), can stimulate the NLRP3 inflammasome.	Adenosine	120-129	NLR family pyrin domain containing 3	Homo sapiens	193-198
33131902-2	2020	Many triggers, including microbial pathogens (ie, bacteria and viruses) and other signals (ie, reactive oxygen species, adenosine triphosphate, urate, silicon, and asbestos), can stimulate the NLRP3 inflammasome.	Uric Acid	144-149	NLR family pyrin domain containing 3	Homo sapiens	193-198
33131902-2	2020	Many triggers, including microbial pathogens (ie, bacteria and viruses) and other signals (ie, reactive oxygen species, adenosine triphosphate, urate, silicon, and asbestos), can stimulate the NLRP3 inflammasome.	Silicon	151-158	NLR family pyrin domain containing 3	Homo sapiens	193-198
33324236-0	2020	Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	38-43
33324236-5	2020	Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	210-259
33324236-5	2020	Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	261-266
33324236-5	2020	Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	210-259
33324236-5	2020	Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	261-266
33255431-2	2020	P2X7 receptor (P2X7R) stimulation by extracellular ATP is best known to active the NLRP3 inflammasome and release IL-1beta, but stimulation also leads to release of other cytokines.	Adenosine Triphosphate	51-54	NLR family pyrin domain containing 3	Homo sapiens	83-88
33243234-0	2020	Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome.	Adenosine Triphosphate	18-21	NLR family pyrin domain containing 3	Homo sapiens	62-67
33243234-2	2020	ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	139-144
33243234-5	2020	RESULTS: We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome.	Adenosine Triphosphate	65-68	NLR family pyrin domain containing 3	Homo sapiens	113-118
33243234-6	2020	Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	81-86
33243234-7	2020	Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux.	Adenosine Triphosphate	94-97	NLR family pyrin domain containing 3	Homo sapiens	70-75
33243234-8	2020	Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment.	Adenosine Triphosphate	103-106	NLR family pyrin domain containing 3	Homo sapiens	75-80
33243234-9	2020	Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex.	Adenosine Triphosphate	23-26	NLR family pyrin domain containing 3	Homo sapiens	49-54
33243234-9	2020	Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex.	Adenosine Triphosphate	23-26	NLR family pyrin domain containing 3	Homo sapiens	160-165
33243234-12	2020	Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.	Adenosine Triphosphate	28-31	NLR family pyrin domain containing 3	Homo sapiens	76-81
33243234-12	2020	Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.	Adenosine Triphosphate	28-31	NLR family pyrin domain containing 3	Homo sapiens	147-152
33212483-8	2021	Furthermore, analysis of the association between NLRP3 inflammasome and CIT response using six CIT response datasets revealed the predictive value of NLRP3 inflammasome for immunotherapy response of patients in diverse cancers.	cit	72-75	NLR family pyrin domain containing 3	Homo sapiens	49-54
33212483-8	2021	Furthermore, analysis of the association between NLRP3 inflammasome and CIT response using six CIT response datasets revealed the predictive value of NLRP3 inflammasome for immunotherapy response of patients in diverse cancers.	cit	72-75	NLR family pyrin domain containing 3	Homo sapiens	150-155
33329557-0	2020	Computational Modeling of NLRP3 Identifies Enhanced ATP Binding and Multimerization in Cryopyrin-Associated Periodic Syndromes.	Adenosine Triphosphate	52-55	NLR family pyrin domain containing 3	Homo sapiens	26-31
33329557-0	2020	Computational Modeling of NLRP3 Identifies Enhanced ATP Binding and Multimerization in Cryopyrin-Associated Periodic Syndromes.	Adenosine Triphosphate	52-55	NLR family pyrin domain containing 3	Homo sapiens	87-96
33329557-6	2020	Bioinformatics tools and computational modeling revealed that NLRP3 mutations that are predicted to be structurally severely-disruptive localize around the ATP binding pocket and that specific proteo-structural changes to the ATP binding pocket lead to enhanced ATP binding affinity by altering hydrogen-bond and charge interactions.	Adenosine Triphosphate	156-159	NLR family pyrin domain containing 3	Homo sapiens	62-67
33329557-6	2020	Bioinformatics tools and computational modeling revealed that NLRP3 mutations that are predicted to be structurally severely-disruptive localize around the ATP binding pocket and that specific proteo-structural changes to the ATP binding pocket lead to enhanced ATP binding affinity by altering hydrogen-bond and charge interactions.	Adenosine Triphosphate	226-229	NLR family pyrin domain containing 3	Homo sapiens	62-67
33329557-6	2020	Bioinformatics tools and computational modeling revealed that NLRP3 mutations that are predicted to be structurally severely-disruptive localize around the ATP binding pocket and that specific proteo-structural changes to the ATP binding pocket lead to enhanced ATP binding affinity by altering hydrogen-bond and charge interactions.	Adenosine Triphosphate	226-229	NLR family pyrin domain containing 3	Homo sapiens	62-67
33329557-6	2020	Bioinformatics tools and computational modeling revealed that NLRP3 mutations that are predicted to be structurally severely-disruptive localize around the ATP binding pocket and that specific proteo-structural changes to the ATP binding pocket lead to enhanced ATP binding affinity by altering hydrogen-bond and charge interactions.	Hydrogen	295-303	NLR family pyrin domain containing 3	Homo sapiens	62-67
32866784-8	2020	Additionally, IL-1beta/IL-18 secretion from ATP + LPS stimulated THP-1-derived macrophages was RalA-dependently suppressed by levornidazole, suggesting that RalA might have an inhibitory effect on NLRP3 inflammasome activation.	Adenosine Triphosphate	44-47	NLR family pyrin domain containing 3	Homo sapiens	197-202
33188176-4	2020	In this study, scutellarin suppressed BLM-induced inflammation via NF-kappaB/NLRP3 pathway both in vivo and in vitro.	scutellarin	15-26	NLR family pyrin domain containing 3	Homo sapiens	77-82
33198300-9	2020	Treatment of PAMs with cell culture supernatants from macrophages subjected to NLRP3 inflammasome activation (via polyinosinic-polycytidylic acid (poly I:C) transfection), prior to PRRSV infection resulted in significantly reduced viral RNA levels compared to PAMs treated with cell culture supernatants from macrophages subjected to NLRP3 inflammasome inhibition (MCC950 treatment/poly I:C transfection).	Poly I-C	114-145	NLR family pyrin domain containing 3	Homo sapiens	79-84
32699039-7	2020	Both glucose deprivation and treatment with either 2-deoxyglucose or GLUT1 inhibitor suppressed crystal-induced NLRP3 activation and IL-1beta production, and microcrystal inflammation in vivo.	Deoxyglucose	51-65	NLR family pyrin domain containing 3	Homo sapiens	112-117
33281541-2	2020	Oridonin (Ori), the major active ingredient of Chinese herbal medicine Rabdosia rubescens, has been proved to be a covalent NLRP3 inhibitor with strong anti-inflammation activity.	oridonin	0-8	NLR family pyrin domain containing 3	Homo sapiens	124-129
33281541-2	2020	Oridonin (Ori), the major active ingredient of Chinese herbal medicine Rabdosia rubescens, has been proved to be a covalent NLRP3 inhibitor with strong anti-inflammation activity.	oridonin	0-3	NLR family pyrin domain containing 3	Homo sapiens	124-129
33198300-9	2020	Treatment of PAMs with cell culture supernatants from macrophages subjected to NLRP3 inflammasome activation (via polyinosinic-polycytidylic acid (poly I:C) transfection), prior to PRRSV infection resulted in significantly reduced viral RNA levels compared to PAMs treated with cell culture supernatants from macrophages subjected to NLRP3 inflammasome inhibition (MCC950 treatment/poly I:C transfection).	Poly I	147-153	NLR family pyrin domain containing 3	Homo sapiens	79-84
32805340-0	2020	Acrylamide induces NLRP3 inflammasome activation via oxidative stress- and endoplasmic reticulum stress-mediated MAPK pathway in HepG2 cells.	Acrylamide	0-10	NLR family pyrin domain containing 3	Homo sapiens	19-24
32805340-5	2020	When HepG2 cells were pretreated with ROS (NAC) and ERS (4-PBA) inhibitors separately, the activation of NLRP3 inflammasome was inhibited.	ros	38-41	NLR family pyrin domain containing 3	Homo sapiens	105-110
32892075-0	2020	Dihydroartemisinin prevents dextran sodium sulphate-induced colitisthrough inhibition of the activation of NLRP3 inflammasome and p38 MAPK signaling.	artenimol	0-18	NLR family pyrin domain containing 3	Homo sapiens	107-112
32892075-0	2020	Dihydroartemisinin prevents dextran sodium sulphate-induced colitisthrough inhibition of the activation of NLRP3 inflammasome and p38 MAPK signaling.	dextran sodium sulphate	28-51	NLR family pyrin domain containing 3	Homo sapiens	107-112
32892075-7	2020	Additionally, DHA in vivo improved the clinical symptoms, reduced the production of pro-inflammatory factors IL-1beta, IL-6 and TNF-alpha, and suppressed the formation of NLRP3 inflammasome.	artenimol	14-17	NLR family pyrin domain containing 3	Homo sapiens	171-176
32892075-9	2020	Additionally, we found that DHA suppressed p38 activator-induced pro-inflammatory response, and p38 inhibitor attenuated the clinical symptoms and reduced the expression levels of pro-inflammatory mediators and NLRP3 while up-regulated the expression levels of PPARgamma and Ki-67.	artenimol	28-31	NLR family pyrin domain containing 3	Homo sapiens	211-216
32892075-11	2020	In conclusion, DHA could protect DSS-induced colitis via suppressing the activation of NLRP3 inflammasome and p38 MAPK signaling.	artenimol	15-18	NLR family pyrin domain containing 3	Homo sapiens	87-92
32892075-11	2020	In conclusion, DHA could protect DSS-induced colitis via suppressing the activation of NLRP3 inflammasome and p38 MAPK signaling.	dss	33-36	NLR family pyrin domain containing 3	Homo sapiens	87-92
32945118-4	2020	Intriguingly, DSC specifically down-regulated DSS-induced colonic NADPH oxidase 4 (Nox4) expression, accompanied by a balanced redox status, suppressed nuclear factor-kappaB (NF-kappaB) and NLRP3 inflammasome activation and up-regulated nuclear factor (erythroid-derived 2)-like 2 and haeme oxygenase-1 expression.	dss	46-49	NLR family pyrin domain containing 3	Homo sapiens	190-195
33182075-4	2020	The current study identified that LPS plus nigericin stimulation induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, which was detected by IL-1beta expression.	Nigericin	43-52	NLR family pyrin domain containing 3	Homo sapiens	73-109
33182075-4	2020	The current study identified that LPS plus nigericin stimulation induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, which was detected by IL-1beta expression.	Nigericin	43-52	NLR family pyrin domain containing 3	Homo sapiens	111-116
33182063-3	2020	In the present study, we aimed to explore the underlying detailed upstream mechanism and the cellular status of putative downstream molecules of cigarette smoke condensate (CSC)-activated NLRP3 inflammasome in atherosclerotic disease.	smoke condensate	155-171	NLR family pyrin domain containing 3	Homo sapiens	188-193
33182063-16	2020	Notably, 15 atherosclerotic molecules associated with endothelial dysfunction, scavenger receptors, cholesterol esterification and matrix-metalloproteins were found downstream to CSC-activated NLRP3 inflammasome.	Cholesterol	100-111	NLR family pyrin domain containing 3	Homo sapiens	193-198
33022900-4	2020	It remained unclear whether pre-treated hosts with n-butylidenephthalide can rejuvenate the ageing heart and improve hADSC engraftment by regulating the ROS/NLRP3 inflammasome-mediated cardiac fibrosis after myocardial infarction.	butylidenephthalide	51-72	NLR family pyrin domain containing 3	Homo sapiens	157-162
32827663-0	2020	Resveratrol inhibits tumor progression by down-regulation of NLRP3 in renal cell carcinoma.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	61-66
32827663-6	2020	RSV significantly down-regulated expressions of NLRP3 and its down-stream genes.	Resveratrol	0-3	NLR family pyrin domain containing 3	Homo sapiens	48-53
32827663-7	2020	Inhibition of NLRP3 by NLRP3 small interfering RNA (siRNA) mimicked the effects of RSV on RCC cells.	Resveratrol	83-86	NLR family pyrin domain containing 3	Homo sapiens	14-19
32827663-7	2020	Inhibition of NLRP3 by NLRP3 small interfering RNA (siRNA) mimicked the effects of RSV on RCC cells.	Resveratrol	83-86	NLR family pyrin domain containing 3	Homo sapiens	23-28
32667050-0	2020	Quinones as preventive agents in Alzheimer"s diseases: focus on NLRP3 inflammasomes.	Quinones	0-8	NLR family pyrin domain containing 3	Homo sapiens	64-69
32827663-8	2020	These results suggested that RSV could exert anti-tumor effect by depressing activity of NLRP3, and NLRP3 would be a promising clinical therapeutic strategy for RCC.	Resveratrol	29-32	NLR family pyrin domain containing 3	Homo sapiens	89-94
32667050-3	2020	NLRP3 (Nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3) inflammasome is closely related to the occurrence of neuroinflammation.	Leucine	33-40	NLR family pyrin domain containing 3	Homo sapiens	0-5
33152658-3	2020	Pyroptosis can be triggered by bacterial lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in non-placental macrophages through activation of the NLRP3 inflammasome.	Adenosine Triphosphate	94-97	NLR family pyrin domain containing 3	Homo sapiens	154-159
32667050-9	2020	Docking results showed that the combination of anthraquinones and NLRP3 were the best, and the top two chemical compounds were Purpurin and Rhein, which are the most promising NLRP3 inhibitors.	Anthraquinones	47-61	NLR family pyrin domain containing 3	Homo sapiens	176-181
33152658-9	2020	Together, our data indicate that LPS and ATP treatment stimulated NLRP3 inflammasome activation and pyroptosis in HBCs leading to the rapid release of IL-1beta.	Adenosine Triphosphate	41-44	NLR family pyrin domain containing 3	Homo sapiens	66-71
33011017-5	2020	We underline how the unique dimeric phospholipid structure confers peculiar properties on CL in the regulation of cell death and immune system proteins, such as the Nucleotide-binding domain and leucine-rich repeat-containing pyrin protein 3 (NLRP3), caspases (Casp), and Toll-like receptor 4 (TLR4).	Phospholipids	36-48	NLR family pyrin domain containing 3	Homo sapiens	243-248
32934737-9	2020	Additionally, UA exposure significantly decreased MMP-2 production and induced the activation of NLRP3 inflammasome, which was reversed by MCC950 treatment, indicating that NLRP3 activation may be involved in UA inhibition of A498 cell invasiveness.	ursolic acid	14-16	NLR family pyrin domain containing 3	Homo sapiens	97-102
32934737-9	2020	Additionally, UA exposure significantly decreased MMP-2 production and induced the activation of NLRP3 inflammasome, which was reversed by MCC950 treatment, indicating that NLRP3 activation may be involved in UA inhibition of A498 cell invasiveness.	ursolic acid	14-16	NLR family pyrin domain containing 3	Homo sapiens	173-178
32934737-9	2020	Additionally, UA exposure significantly decreased MMP-2 production and induced the activation of NLRP3 inflammasome, which was reversed by MCC950 treatment, indicating that NLRP3 activation may be involved in UA inhibition of A498 cell invasiveness.	ursolic acid	209-211	NLR family pyrin domain containing 3	Homo sapiens	97-102
32934737-9	2020	Additionally, UA exposure significantly decreased MMP-2 production and induced the activation of NLRP3 inflammasome, which was reversed by MCC950 treatment, indicating that NLRP3 activation may be involved in UA inhibition of A498 cell invasiveness.	ursolic acid	209-211	NLR family pyrin domain containing 3	Homo sapiens	173-178
32518369-4	2020	Consequently, extracellular ADP activated the NLRP3 inflammasome through P2Y1 receptor-mediated calcium signaling, which led to the maturation and secretion of IL-1beta and further aggravation of experimental colitis.	Adenosine Diphosphate	28-31	NLR family pyrin domain containing 3	Homo sapiens	46-51
32518369-4	2020	Consequently, extracellular ADP activated the NLRP3 inflammasome through P2Y1 receptor-mediated calcium signaling, which led to the maturation and secretion of IL-1beta and further aggravation of experimental colitis.	Calcium	96-103	NLR family pyrin domain containing 3	Homo sapiens	46-51
32518369-6	2020	Moreover, ERK5-mediated tyrosine phosphorylation of ASC was essential for activation of the NLRP3 inflammasome.	Tyrosine	24-32	NLR family pyrin domain containing 3	Homo sapiens	92-97
32934737-0	2020	Ursolic acid inhibits the invasiveness of A498 cells via NLRP3 inflammasome activation.	ursolic acid	0-12	NLR family pyrin domain containing 3	Homo sapiens	57-62
32791262-0	2020	MitoQ attenuates brain damage by polarizing microglia towards the M2 phenotype through inhibition of the NLRP3 inflammasome after ICH.	mitoquinone	0-5	NLR family pyrin domain containing 3	Homo sapiens	105-110
32791262-6	2020	Mechanistically, MitoQ blocked overproduction of mitochondrial ROS and activation of the NLRP3 inflammasome in FeCl2-treated microglia.	mitoquinone	17-22	NLR family pyrin domain containing 3	Homo sapiens	89-94
32791262-6	2020	Mechanistically, MitoQ blocked overproduction of mitochondrial ROS and activation of the NLRP3 inflammasome in FeCl2-treated microglia.	ferrous chloride	111-116	NLR family pyrin domain containing 3	Homo sapiens	89-94
32791262-7	2020	Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway.	ferrous chloride	30-35	NLR family pyrin domain containing 3	Homo sapiens	10-15
32791262-7	2020	Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway.	ferrous chloride	30-35	NLR family pyrin domain containing 3	Homo sapiens	172-178
32791262-7	2020	Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway.	mitoquinone	98-103	NLR family pyrin domain containing 3	Homo sapiens	10-15
32791262-7	2020	Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway.	mitoquinone	98-103	NLR family pyrin domain containing 3	Homo sapiens	172-178
32791262-7	2020	Moreover, NLRP3 siRNA shifted FeCl2-treated microglia from the M1 to the M2 cells, revealing that MitoQ-induce polarization states may be mediated by the mitochondrial ROS/NLRP-3 pathway.	ros	168-171	NLR family pyrin domain containing 3	Homo sapiens	10-15
32861708-8	2020	Taken together, these results show that the inhibition of NLRP3 inflammasome assembly in macrophages due to FAO downregulation contributes to the preventative effect of arctigenin against CAC.	arctigenin	169-179	NLR family pyrin domain containing 3	Homo sapiens	58-63
33463499-0	2020	[Activation of NOD like receptor protein 3 signaling pathway in vascular endothelial cells induced by heat stress can be inhibited by ethyl pyruvate].	ethyl pyruvate	134-148	NLR family pyrin domain containing 3	Homo sapiens	15-42
33463499-1	2020	OBJECTIVE: To investigate whether the activation of NOD like receptor protein 3 (NLRP3) signaling pathway in vascular endothelial cells induced by heat stress (HS) could be inhibited by ethyl pyruvate (EP).	ethyl pyruvate	186-200	NLR family pyrin domain containing 3	Homo sapiens	52-79
33463499-1	2020	OBJECTIVE: To investigate whether the activation of NOD like receptor protein 3 (NLRP3) signaling pathway in vascular endothelial cells induced by heat stress (HS) could be inhibited by ethyl pyruvate (EP).	ethyl pyruvate	186-200	NLR family pyrin domain containing 3	Homo sapiens	81-86
33097689-0	2020	Correction: ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.	Desoxycorticosterone Acetate	31-58	NLR family pyrin domain containing 3	Homo sapiens	137-142
33126764-13	2020	Autophagy induction by rapamycin treatment in keloid fibroblasts effectively suppressed expression levels of Notch1 and NLRP3 inflammasome proteins.	Sirolimus	23-32	NLR family pyrin domain containing 3	Homo sapiens	120-125
33098298-7	2021	CONCLUSION: Addition of 60% acetonitrile in the plasma provides a stable storage method for clinical AI, AII and aldosterone.	acetonitrile	28-40	NLR family pyrin domain containing 3	Homo sapiens	105-108
33097689-0	2020	Correction: ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.	Salts	59-63	NLR family pyrin domain containing 3	Homo sapiens	137-142
33497945-7	2020	Taken together, Cd exposure induces duck renal tubular epithelial cell pyroptosis through ROS/NLRP3/Caspase-1 signaling pathway, and inhibiting Caspase-1 dependent pyroptosis attenuates Cd-induced apoptosis.	Cadmium	16-18	NLR family pyrin domain containing 3	Homo sapiens	94-99
33110739-7	2020	Anecdotal experiences have been reported with the use of the anti-IL-1 agent anakinra and the NLRP3 inflammasome inhibitor colchicine in this population.	Colchicine	123-133	NLR family pyrin domain containing 3	Homo sapiens	94-99
33497945-0	2020	Inhibition of ROS/NLRP3/Caspase-1 mediated pyroptosis attenuates cadmium-induced apoptosis in duck renal tubular epithelial cells.	Cadmium	65-72	NLR family pyrin domain containing 3	Homo sapiens	18-23
33144845-5	2020	To address a potential heterogeneity in inflammasome functionality, ATP, chitosan, or silica oxide (SiO2) were used to induce NLRP3 inflammasome activation in THP-1 cells and the subsequent outcomes were quantified.	Adenosine Triphosphate	68-71	NLR family pyrin domain containing 3	Homo sapiens	126-131
33497945-4	2020	Simultaneously, Cd also markedly upregulated NLRP3, Caspase-1, ASC, NEK7, IL-1beta and IL-18 mRNA levels and NLRP3, Caspase-1 p20, GSDMD and ASC protein levels.	Cadmium	16-18	NLR family pyrin domain containing 3	Homo sapiens	45-50
33497945-4	2020	Simultaneously, Cd also markedly upregulated NLRP3, Caspase-1, ASC, NEK7, IL-1beta and IL-18 mRNA levels and NLRP3, Caspase-1 p20, GSDMD and ASC protein levels.	Cadmium	16-18	NLR family pyrin domain containing 3	Homo sapiens	109-114
33144845-5	2020	To address a potential heterogeneity in inflammasome functionality, ATP, chitosan, or silica oxide (SiO2) were used to induce NLRP3 inflammasome activation in THP-1 cells and the subsequent outcomes were quantified.	silica oxide	86-98	NLR family pyrin domain containing 3	Homo sapiens	126-131
33144845-5	2020	To address a potential heterogeneity in inflammasome functionality, ATP, chitosan, or silica oxide (SiO2) were used to induce NLRP3 inflammasome activation in THP-1 cells and the subsequent outcomes were quantified.	Silicon Dioxide	100-104	NLR family pyrin domain containing 3	Homo sapiens	126-131
32980213-0	2020	Corrigendum to "Involvement of NLRP3 inflammasome in methamphetamine-induced microglial activation through miR-143/PUMA axis" [Toxicol.	Methamphetamine	53-68	NLR family pyrin domain containing 3	Homo sapiens	31-36
33111746-0	2020	Baicalin suppresses Propionibacterium acnes-induced skin inflammation by downregulating the NF-kappaB/MAPK signaling pathway and inhibiting activation of NLRP3 inflammasome.	baicalin	0-8	NLR family pyrin domain containing 3	Homo sapiens	154-159
33111746-11	2020	Furthermore, BA inhibited the activation of NLRP3 inflammasome, at both the gene and protein levels.	baicalin	13-15	NLR family pyrin domain containing 3	Homo sapiens	44-49
33111746-12	2020	Taken together, the results demonstrated that BA might exert its anti-inflammatory activity by inhibiting NF-kappaB/MAPK signaling pathways and consequently suppressing the activation of the NLRP3 inflammasome both in vivo and in vitro.	baicalin	46-48	NLR family pyrin domain containing 3	Homo sapiens	191-196
33092247-8	2020	The findings showed that LPS/nigericin-treated cells expressing Rab5-WT indicated increased NALP3 expression and secretion of the IL-1beta as compared to Rab5-DN cells.	Nigericin	29-38	NLR family pyrin domain containing 3	Homo sapiens	92-97
32929041-0	2020	AKT Regulates NLRP3 Inflammasome Activation by Phosphorylating NLRP3 Serine 5.	Serine	69-75	NLR family pyrin domain containing 3	Homo sapiens	14-19
32929041-0	2020	AKT Regulates NLRP3 Inflammasome Activation by Phosphorylating NLRP3 Serine 5.	Serine	69-75	NLR family pyrin domain containing 3	Homo sapiens	63-68
32929041-6	2020	This phosphorylation event also stabilizes NLRP3 by reducing its ubiquitination on lysine 496, which inhibits its proteasome-mediated degradation by the E3 ligase Trim31.	Lysine	83-89	NLR family pyrin domain containing 3	Homo sapiens	43-48
33117011-3	2020	The role of nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome in inducing activation of inflammatory signaling in IOSSD is not clear.	Leucine	42-49	NLR family pyrin domain containing 3	Homo sapiens	73-78
33036374-5	2020	Indeed, newly deposited NLR structures for NLRC4 and NLRP3 have provided unique perspectives on the ATP-dependency of inflammasome activation.	Adenosine Triphosphate	100-103	NLR family pyrin domain containing 3	Homo sapiens	53-58
33100904-9	2020	Guttiferone K could also suppress the NLRP3 inflammasome activity and induce autophagy by inhibiting the protein kinase B (p-Akt) and mammalian target of rapamycin (mTOR) phosphorylation at Ser473 and Ser2448 in both cell lines.	guttiferone K	0-13	NLR family pyrin domain containing 3	Homo sapiens	38-43
32763970-4	2020	Deleting NLRP3 inflammasome components or the downstream cell death executioner gasdermin D (GSDMD) led to an initial reduction in cell death followed by a robust increase in the incidence of caspase-8- and receptor-interacting serine/threonine-protein kinase 3 (RIPK3)-mediated inflammatory cell deathafter coronavirus infection.	Serine	228-234	NLR family pyrin domain containing 3	Homo sapiens	9-14
33117348-3	2020	Cholesterol crystal mediated NLRP3 inflammasome activation is central to cardiovascular disease and the pathway has been implicated in placental inflammation in preeclampsia.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	29-34
33117348-15	2020	Our findings suggest that decidual accumulation of cholesterol crystals may activate the NLRP3 inflammasome and contribute to decidual inflammation and that this pathway is strengthened in areas with close maternal-fetal interaction in preeclampsia without FGR.	Cholesterol	51-62	NLR family pyrin domain containing 3	Homo sapiens	89-94
33163006-7	2020	Autophagic removal of NLRP3 inflammasome activators, such as intracellular DAMPs, NLRP3 inflammasome components, and cytokines can reduce inflammasome activation and inflammatory response.	dinitrophenyl-aminopropyl-methylamine	75-80	NLR family pyrin domain containing 3	Homo sapiens	22-27
33036374-6	2020	Novel molecular dynamic simulations of NLRP3 examined the active site of ADP- and ATP-bound models.	Adenosine Diphosphate	73-76	NLR family pyrin domain containing 3	Homo sapiens	39-44
33036374-6	2020	Novel molecular dynamic simulations of NLRP3 examined the active site of ADP- and ATP-bound models.	Adenosine Triphosphate	82-85	NLR family pyrin domain containing 3	Homo sapiens	39-44
33014529-5	2020	This review summarizes the molecular mechanisms of pyroptosis and shows the critical role of NLRP3 (NLR family, pyrin domain containing 3; NLR refers to "nucleotide-binding domain, leucine-rich repeat") inflammasomes.	Leucine	181-188	NLR family pyrin domain containing 3	Homo sapiens	93-98
33123153-3	2020	Sphingosine is identified as a danger-associated molecular pattern (DAMP), which activates the NLRP3 inflammasome assembly and induces the pyroptosis.	Sphingosine	0-11	NLR family pyrin domain containing 3	Homo sapiens	95-100
33014529-5	2020	This review summarizes the molecular mechanisms of pyroptosis and shows the critical role of NLRP3 (NLR family, pyrin domain containing 3; NLR refers to "nucleotide-binding domain, leucine-rich repeat") inflammasomes.	Leucine	181-188	NLR family pyrin domain containing 3	Homo sapiens	100-137
32893050-0	2020	Corrigendum to "Saikosaponin A inhibits the activation of pancreatic stellate cells by suppressing autophagy and the NLRP3 inflammasome via the AMPK/mTOR pathway" [Biomed.	saikosaponin D	16-30	NLR family pyrin domain containing 3	Homo sapiens	117-122
32945585-6	2020	RESULTS: We verified that crystal-induced extracellular adenosine triphosphate (ATP) upregulation via the membrane purinergic 2X7 receptor (P2X7 R) promotes ROS generation and thereby activates NLRP3 inflammasome-mediated interleukin-1beta/18 maturation and gasdermin D cleavage.	Adenosine	56-65	NLR family pyrin domain containing 3	Homo sapiens	194-199
33004801-5	2020	Mechanistically, BAFF activated NLRP3 inflammasomes by promoting the association of cIAP-TRAF2 with components of NLRP3 inflammasomes, and by inducing Src activity-dependent ROS production and potassium ion efflux.	ros	174-177	NLR family pyrin domain containing 3	Homo sapiens	32-37
33004801-5	2020	Mechanistically, BAFF activated NLRP3 inflammasomes by promoting the association of cIAP-TRAF2 with components of NLRP3 inflammasomes, and by inducing Src activity-dependent ROS production and potassium ion efflux.	Potassium	193-202	NLR family pyrin domain containing 3	Homo sapiens	32-37
32823055-4	2020	Especially, four water molecules can saturate hydrate site AI and while more water molecules will be required to saturate hydrate sites AIII and AII.	Water	17-22	NLR family pyrin domain containing 3	Homo sapiens	136-139
32823055-4	2020	Especially, four water molecules can saturate hydrate site AI and while more water molecules will be required to saturate hydrate sites AIII and AII.	Water	77-82	NLR family pyrin domain containing 3	Homo sapiens	136-139
32945585-6	2020	RESULTS: We verified that crystal-induced extracellular adenosine triphosphate (ATP) upregulation via the membrane purinergic 2X7 receptor (P2X7 R) promotes ROS generation and thereby activates NLRP3 inflammasome-mediated interleukin-1beta/18 maturation and gasdermin D cleavage.	Adenosine Triphosphate	80-83	NLR family pyrin domain containing 3	Homo sapiens	194-199
32611559-3	2020	Colchicine has a unique anti-inflammatory mechanism: it is not only able to concentrate in leucocytes, especially neutrophils, and block tubulin polymerisation, affecting the microtubules assembly, but also inhibits (NOD)-like receptor protein 3 (NLRP3) inflammasome.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	247-252
32420661-8	2020	In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS-induced NSCLC cells and reduced the secretion of IL-1beta.	mangiferin	13-23	NLR family pyrin domain containing 3	Homo sapiens	69-74
32927275-0	2020	Cholesterol crystals use complement to increase NLRP3 signaling pathways in coronary and carotid atherosclerosis.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	48-53
32927275-1	2020	BACKGROUND: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome.	Cholesterol	34-45	NLR family pyrin domain containing 3	Homo sapiens	162-209
32927275-1	2020	BACKGROUND: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome.	Cholesterol	34-45	NLR family pyrin domain containing 3	Homo sapiens	211-216
32927275-1	2020	BACKGROUND: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome.	Cholesterol	64-75	NLR family pyrin domain containing 3	Homo sapiens	162-209
32927275-1	2020	BACKGROUND: During atherogenesis, cholesterol precipitates into cholesterol crystals (CC) in the vessel wall, which trigger plaque inflammation by activating the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome.	Cholesterol	64-75	NLR family pyrin domain containing 3	Homo sapiens	211-216
32736194-0	2020	Acetylase inhibitor SI-2 is a potent anti-inflammatory agent by inhibiting NLRP3 inflammasome activation.	SI-2	20-24	NLR family pyrin domain containing 3	Homo sapiens	75-80
32736194-3	2020	We and others recently demonstrated that acetylation of NLRP3 promotes the inflammasome activity and also suggested lysine acetyltransferases inhibitors could be a kind of promising agents for treating NLRP3 associated disorders.	Lysine	116-122	NLR family pyrin domain containing 3	Homo sapiens	56-61
32736194-3	2020	We and others recently demonstrated that acetylation of NLRP3 promotes the inflammasome activity and also suggested lysine acetyltransferases inhibitors could be a kind of promising agents for treating NLRP3 associated disorders.	Lysine	116-122	NLR family pyrin domain containing 3	Homo sapiens	202-207
32687258-0	2020	Local anesthetic articaine ameliorates LPS-induced acute kidney injury via inhibition of NF-kB activation and the NLRP3 inflammasome pathway.	Carticaine	17-26	NLR family pyrin domain containing 3	Homo sapiens	114-119
32945430-11	2020	In addition, HG activated inflammatory factors, such as TNF-alpha, IL-1beta and IL-6; however, their levels were suppressed when cells were treated with FPS-ZM1 or the TXNIP/NLRP3 pathway inhibitor, resveratrol (Res).	Resveratrol	199-210	NLR family pyrin domain containing 3	Homo sapiens	174-179
33000581-10	2020	The mechanism could be that it reduced ROS produce and inhibited NLRP3 inflammasome activation so that mainly lower the downstream inflammatory cytokines IL-1beta and IL-18.	Reactive Oxygen Species	39-42	NLR family pyrin domain containing 3	Homo sapiens	65-70
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	48-53
32945495-10	2020	To conclude, NAC had anti-inflammatory effects on LPS-stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	116-121
32504923-8	2020	NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1beta and IL18) in vitro, and decrease plasma TNF-alpha in human clinical trials.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	39-44
32505910-5	2020	IL-1beta is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1beta.	Leucine	87-94	NLR family pyrin domain containing 3	Homo sapiens	70-75
32505910-5	2020	IL-1beta is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1beta.	Leucine	87-94	NLR family pyrin domain containing 3	Homo sapiens	179-184
32945495-0	2020	N-acetyl cysteine inhibits the lipopolysaccharide-induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	0-17	NLR family pyrin domain containing 3	Homo sapiens	143-148
33117724-0	2020	The Shigella Type III Secretion Effector IpaH4.5 Targets NLRP3 to Activate Inflammasome Signaling.	ipah4	41-46	NLR family pyrin domain containing 3	Homo sapiens	57-62
32651843-0	2020	Phoenixin-20 Ameliorates Lipopolysaccharide-Induced Activation of Microglial NLRP3 Inflammasome.	phoenixin-20	0-12	NLR family pyrin domain containing 3	Homo sapiens	77-82
32651843-4	2020	This study investigated whether PNX-20 possesses a protective effect against lipopolysaccharide (LPS)-induced activation of the NLRP3 inflammasome in microglia.	pnx-20	32-38	NLR family pyrin domain containing 3	Homo sapiens	128-133
32651843-6	2020	Secondly, PNX-20 mitigated LPS-induced upregulation of TxNIP, an upstream regulator of NLRP3 inflammasome activation.	pnx-20	10-16	NLR family pyrin domain containing 3	Homo sapiens	87-92
32651843-7	2020	Thirdly, further evaluation of the major components of the NLRP3 inflammasome revealed that PNX-20 inhibited LPS-mediated upregulation of NLRP3, ASC, and cleaved caspase-1 (P10).	pnx-20	92-98	NLR family pyrin domain containing 3	Homo sapiens	59-64
32651843-7	2020	Thirdly, further evaluation of the major components of the NLRP3 inflammasome revealed that PNX-20 inhibited LPS-mediated upregulation of NLRP3, ASC, and cleaved caspase-1 (P10).	pnx-20	92-98	NLR family pyrin domain containing 3	Homo sapiens	138-143
32301055-0	2020	Alpinumisoflavone suppresses hepatocellular carcinoma cell growth and metastasis via NLRP3 inflammasome-mediated pyroptosis.	alpinumisoflavone	0-17	NLR family pyrin domain containing 3	Homo sapiens	85-90
32661868-4	2020	At the molecular level, functional deficiency of the Nlrp3 inflammasome in HSPCs leads to their defective migration in response to the major BM homing chemoattractant stromal-derived factor 1 (SDF-1) and to other supportive chemoattractants, including sphingosine-1-phosphate (S1P) and extracellular adenosine triphosphate (eATP).	sphingosine 1-phosphate	252-275	NLR family pyrin domain containing 3	Homo sapiens	53-58
32661868-4	2020	At the molecular level, functional deficiency of the Nlrp3 inflammasome in HSPCs leads to their defective migration in response to the major BM homing chemoattractant stromal-derived factor 1 (SDF-1) and to other supportive chemoattractants, including sphingosine-1-phosphate (S1P) and extracellular adenosine triphosphate (eATP).	sphingosine 1-phosphate	277-280	NLR family pyrin domain containing 3	Homo sapiens	53-58
32661868-4	2020	At the molecular level, functional deficiency of the Nlrp3 inflammasome in HSPCs leads to their defective migration in response to the major BM homing chemoattractant stromal-derived factor 1 (SDF-1) and to other supportive chemoattractants, including sphingosine-1-phosphate (S1P) and extracellular adenosine triphosphate (eATP).	Adenosine	300-309	NLR family pyrin domain containing 3	Homo sapiens	53-58
32661868-4	2020	At the molecular level, functional deficiency of the Nlrp3 inflammasome in HSPCs leads to their defective migration in response to the major BM homing chemoattractant stromal-derived factor 1 (SDF-1) and to other supportive chemoattractants, including sphingosine-1-phosphate (S1P) and extracellular adenosine triphosphate (eATP).	eatp	324-328	NLR family pyrin domain containing 3	Homo sapiens	53-58
32859544-2	2020	Extracellular calcium is capable to increase NLRP3 inflammasome activity of the innate immune system and deletion of this proinflammatory pathway mitigated pancreatitis severity in vivo.	Calcium	14-21	NLR family pyrin domain containing 3	Homo sapiens	45-50
33117724-3	2020	Here, we demonstrate that IpaH4.5, a Shigella T3SS effector, triggers inflammasome activation by regulating NLRP3 expression through the E3 ubiquitin ligase activity of IpaH4.5.	ipah4	26-31	NLR family pyrin domain containing 3	Homo sapiens	108-113
33117724-3	2020	Here, we demonstrate that IpaH4.5, a Shigella T3SS effector, triggers inflammasome activation by regulating NLRP3 expression through the E3 ubiquitin ligase activity of IpaH4.5.	ipah4	169-174	NLR family pyrin domain containing 3	Homo sapiens	108-113
33101286-6	2020	NLRP3 activator nigericin caused the processing and release of constitutively expressed IL-18 in an unprimed setting.	Nigericin	16-25	NLR family pyrin domain containing 3	Homo sapiens	0-5
33117724-4	2020	First, we found that IpaH4.5 interacted with NLRP3.	ipah4	21-26	NLR family pyrin domain containing 3	Homo sapiens	45-50
33117724-5	2020	As a result, IpaH4.5 modulated NLRP3 protein stability and inflammasome activation.	ipah4	13-18	NLR family pyrin domain containing 3	Homo sapiens	31-36
32942936-10	2020	More importantly, downregulation of ROCK2 inhibited the activation of NF-kappaB signaling pathway and NLRP3 inflammasome.Conclusion: Therefore, ROCK2 could be a potential target to treat alcohol-induced astrocytic injury and the downregulation of ROCK2 might be a promising approach to protect against alcohol-induced astrocytic injury.	Alcohols	302-309	NLR family pyrin domain containing 3	Homo sapiens	102-107
32992548-9	2020	In conclusion, MG inhibited hepatic steatosis-induced NLRP3 inflammasome activation through the restoration of autophagy to promote HO-1 signaling capable of ameliorating oxidative stress and inflammatory responses.	magnolol	15-17	NLR family pyrin domain containing 3	Homo sapiens	54-59
32992548-0	2020	Involvement of HO-1 and Autophagy in the Protective Effect of Magnolol in Hepatic Steatosis-Induced NLRP3 Inflammasome Activation In Vivo and In Vitro.	magnolol	62-70	NLR family pyrin domain containing 3	Homo sapiens	100-105
32942936-6	2020	Proteins involved in nuclear factor kappa B (NF-kappaB) signaling pathway and NOD-like receptor protein 3 (NLRP3) inflammasome were analyzed by Western blotting.Results: Alcohol exposure dramatically upregulated ROCK2 expression and lactate dehydrogenase (LDH) activity in astrocytes.	Alcohols	170-177	NLR family pyrin domain containing 3	Homo sapiens	78-105
32942936-6	2020	Proteins involved in nuclear factor kappa B (NF-kappaB) signaling pathway and NOD-like receptor protein 3 (NLRP3) inflammasome were analyzed by Western blotting.Results: Alcohol exposure dramatically upregulated ROCK2 expression and lactate dehydrogenase (LDH) activity in astrocytes.	Alcohols	170-177	NLR family pyrin domain containing 3	Homo sapiens	107-112
32942936-10	2020	More importantly, downregulation of ROCK2 inhibited the activation of NF-kappaB signaling pathway and NLRP3 inflammasome.Conclusion: Therefore, ROCK2 could be a potential target to treat alcohol-induced astrocytic injury and the downregulation of ROCK2 might be a promising approach to protect against alcohol-induced astrocytic injury.	Alcohols	187-194	NLR family pyrin domain containing 3	Homo sapiens	102-107
32961826-10	2020	In cancer cells, TAT-FADD suppresses the canonical NLRP3 inflammasome priming and restricts the processing and secretion of proinflammatory IL-1beta.	tat-fadd	17-25	NLR family pyrin domain containing 3	Homo sapiens	51-56
33072119-0	2020	The Human-Specific STING Agonist G10 Activates Type I Interferon and the NLRP3 Inflammasome in Porcine Cells.	STING agonist-1	33-36	NLR family pyrin domain containing 3	Homo sapiens	73-78
32966239-4	2020	Here, in an in vitro model for AS, we showed that NLRP3-depleted human aortic endothelial cells (HAECs) became resistant to apoptotic cell death, maintained proliferative potential and reduced reactive oxygen species (ROS) production upon treatment with oxidized low-density lipoprotein (ox-LDL).	Reactive Oxygen Species	193-216	NLR family pyrin domain containing 3	Homo sapiens	50-55
32966239-4	2020	Here, in an in vitro model for AS, we showed that NLRP3-depleted human aortic endothelial cells (HAECs) became resistant to apoptotic cell death, maintained proliferative potential and reduced reactive oxygen species (ROS) production upon treatment with oxidized low-density lipoprotein (ox-LDL).	Reactive Oxygen Species	218-221	NLR family pyrin domain containing 3	Homo sapiens	50-55
32977573-9	2020	This study further revealed that sauchinone ameliorated AngII-induced mesangial inflammation through disturbing activation of inflammatory factors, and NLRP3 inflammasome, which is composed of the NLRP3 protein, procaspase-1, and apoptosis-associated speck-like protein containing a CARD (ASC).	sauchinone	33-43	NLR family pyrin domain containing 3	Homo sapiens	197-202
32967076-0	2020	Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Treated with Metformin.	Metformin	159-168	NLR family pyrin domain containing 3	Homo sapiens	67-72
32967076-7	2020	This downregulation of both the NLRP3 inflammasome and autophagy in VAT may be associated with the improved inflammatory profile and leukocyte homeostasis seen in obese T2D patients treated with metformin with respect to MHO subjects and endorses the cardiometabolic protective effect of this drug.	Metformin	195-204	NLR family pyrin domain containing 3	Homo sapiens	32-37
33101293-0	2020	Immunomodulatory Effects of Diterpenes and Their Derivatives Through NLRP3 Inflammasome Pathway: A Review.	Diterpenes	28-38	NLR family pyrin domain containing 3	Homo sapiens	69-74
33101293-4	2020	This review sketches a current scenario of diterpenes or their derivatives acting through NLRPs, especially NLRP3-associated pathways with anti-inflammatory effects.	Diterpenes	43-53	NLR family pyrin domain containing 3	Homo sapiens	108-113
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	andrographolide	0-15	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	triptolide	17-27	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	kaurenoic acid	29-43	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	salvin	45-58	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	oridonin	60-68	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	teuvincenone f	70-84	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	tanshinone	110-124	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-7	2020	Andrographolide, triptolide, kaurenoic acid, carnosic acid, oridonin, teuvincenone F, and some derivatives of tanshinone IIA and phorbol have been found to act through NLRP3 inflammasome pathways.	phorbol	129-136	NLR family pyrin domain containing 3	Homo sapiens	168-173
33101293-8	2020	In conclusion, diterpenes and their derivatives could be one of the promising compounds for the treatment of NLRP3-mediated inflammatory diseases and disorders.	Diterpenes	15-25	NLR family pyrin domain containing 3	Homo sapiens	109-114
32968928-9	2021	Further, lncRNA HOTAIR positively regulated ELAVL1 expression by targeting miR-326, and downregulation of HOTAIR or ELAVL1 notably suppressed promotive effects of miR-326 inhibitor on MPP+ induced pyroptosis via activation of NLRP3 inflammasome.	mangion-purified polysaccharide (Candida albicans)	184-188	NLR family pyrin domain containing 3	Homo sapiens	226-231
32958021-4	2020	One of the ketone bodies produced as a result of ketogenesis, beta-hydroxybutyrate (BHB), is known to inhibit NLRP3 inflammasome activation.	Ketones	11-17	NLR family pyrin domain containing 3	Homo sapiens	110-115
32958021-4	2020	One of the ketone bodies produced as a result of ketogenesis, beta-hydroxybutyrate (BHB), is known to inhibit NLRP3 inflammasome activation.	3-Hydroxybutyric Acid	62-82	NLR family pyrin domain containing 3	Homo sapiens	110-115
32958021-4	2020	One of the ketone bodies produced as a result of ketogenesis, beta-hydroxybutyrate (BHB), is known to inhibit NLRP3 inflammasome activation.	3-Hydroxybutyric Acid	84-87	NLR family pyrin domain containing 3	Homo sapiens	110-115
32948742-6	2020	The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	84-107	NLR family pyrin domain containing 3	Homo sapiens	34-39
32948742-6	2020	The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	84-107	NLR family pyrin domain containing 3	Homo sapiens	164-169
32948742-6	2020	The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	109-112	NLR family pyrin domain containing 3	Homo sapiens	34-39
32948742-6	2020	The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	109-112	NLR family pyrin domain containing 3	Homo sapiens	164-169
32659366-14	2020	SIGNIFICANCE: FL118 restrains the growth and metastasis of colorectal cancer by inducing NLRP3-ASC-Caspase-1 mediated pyroptosis, which provides important evidence in the study on the role of pyroptosis and different tumors.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	14-19	NLR family pyrin domain containing 3	Homo sapiens	89-94
32926257-7	2022	Morphine and fentanyl activated NLRP3 inflammasome in astrocytes and serotonergic (TPH-2-positive) neurons, but fentanyl effects were more pronounced.	Morphine	0-8	NLR family pyrin domain containing 3	Homo sapiens	32-37
32926257-7	2022	Morphine and fentanyl activated NLRP3 inflammasome in astrocytes and serotonergic (TPH-2-positive) neurons, but fentanyl effects were more pronounced.	Fentanyl	13-21	NLR family pyrin domain containing 3	Homo sapiens	32-37
32926257-9	2022	The opioid receptor antagonist (-)-naloxone, but not the TLR4 receptor antagonist (+)-naloxone, prevented microglia activation and NLRP3 oligomerization.	Naloxone	35-43	NLR family pyrin domain containing 3	Homo sapiens	131-136
32917982-0	2021	Synthetic vitamin K analogs inhibit inflammation by targeting the NLRP3 inflammasome.	Vitamin K	10-19	NLR family pyrin domain containing 3	Homo sapiens	66-71
32926257-11	2022	The anti-inflammatory agent minocycline and the NLRP3 inhibitor MCC950 delayed tolerance to morphine and fentanyl antinociception and prevented fentanyl-induced hyperalgesia.	Morphine	92-100	NLR family pyrin domain containing 3	Homo sapiens	48-53
32926257-11	2022	The anti-inflammatory agent minocycline and the NLRP3 inhibitor MCC950 delayed tolerance to morphine and fentanyl antinociception and prevented fentanyl-induced hyperalgesia.	Fentanyl	105-113	NLR family pyrin domain containing 3	Homo sapiens	48-53
32926257-11	2022	The anti-inflammatory agent minocycline and the NLRP3 inhibitor MCC950 delayed tolerance to morphine and fentanyl antinociception and prevented fentanyl-induced hyperalgesia.	Fentanyl	144-152	NLR family pyrin domain containing 3	Homo sapiens	48-53
32926257-13	2022	In conclusion, morphine and fentanyl differentially induce cell-specific activation of NLRP3 inflammasome and pyroptosis in the DRN through TLR4 receptors in astrocytes and through opioid receptors in neurons, indicating that neuroinflammation is involved in opioid-induced analgesia and fentanyl-induced hyperalgesia after repeated administrations.	Morphine	15-23	NLR family pyrin domain containing 3	Homo sapiens	87-92
32926257-13	2022	In conclusion, morphine and fentanyl differentially induce cell-specific activation of NLRP3 inflammasome and pyroptosis in the DRN through TLR4 receptors in astrocytes and through opioid receptors in neurons, indicating that neuroinflammation is involved in opioid-induced analgesia and fentanyl-induced hyperalgesia after repeated administrations.	Fentanyl	28-36	NLR family pyrin domain containing 3	Homo sapiens	87-92
32926257-13	2022	In conclusion, morphine and fentanyl differentially induce cell-specific activation of NLRP3 inflammasome and pyroptosis in the DRN through TLR4 receptors in astrocytes and through opioid receptors in neurons, indicating that neuroinflammation is involved in opioid-induced analgesia and fentanyl-induced hyperalgesia after repeated administrations.	Fentanyl	288-296	NLR family pyrin domain containing 3	Homo sapiens	87-92
32983576-8	2020	Nod-like receptors pyrins-3 (NLRP3), caspase-1, Pro-IL-1beta, and IL-1beta levels were pronouncedly elevated in cells exposed to H2O2.	Hydrogen Peroxide	129-133	NLR family pyrin domain containing 3	Homo sapiens	0-27
32983576-8	2020	Nod-like receptors pyrins-3 (NLRP3), caspase-1, Pro-IL-1beta, and IL-1beta levels were pronouncedly elevated in cells exposed to H2O2.	Hydrogen Peroxide	129-133	NLR family pyrin domain containing 3	Homo sapiens	29-34
32982435-0	2020	Ursolic Acid Protects Against Proliferation and Inflammatory Response in LPS-Treated Gastric Tumour Model and Cells by Inhibiting NLRP3 Inflammasome Activation.	ursolic acid	0-12	NLR family pyrin domain containing 3	Homo sapiens	130-135
32982435-5	2020	This study also aimed to confirm whether ursolic acid can protect against proliferation and the inflammatory response induced by LPS, by inhibiting the activation of the NLRP3 inflammasome via the NF-kappaB pathway.	ursolic acid	41-53	NLR family pyrin domain containing 3	Homo sapiens	170-175
32982435-6	2020	Results: The present study demonstrated that ursolic acid significantly attenuated LPS-treated proliferation in a gastric tumour mouse model and the human gastric carcinoma BGC-823 cell line, reduced the expression of the NLRP3 inflammasome and suppressed the release of pro-inflammatory cytokines.	ursolic acid	45-57	NLR family pyrin domain containing 3	Homo sapiens	222-227
32982435-9	2020	Conclusion: In conclusion, these results demonstrated that ursolic acid could suppress proliferation and the inflammatory response in an LPS-induced mouse gastric tumour model and human BGC-823 cells by inhibiting the activation of the NLRP3 inflammasome via the NF-kappaB pathway.	ursolic acid	59-71	NLR family pyrin domain containing 3	Homo sapiens	236-241
32963812-9	2020	Furthermore, NET and mCRAMP (component of NETs, the murine equivalent of cathelicidin LL-37 in human)-mediated activation of NLRP3 inflammasome and production of IL-1beta/IL-18 were significantly elevated in Mfge8 -/- macrophages compared with WT macrophages, which were also significantly dampened by the administration of rmMFG-E8.	rmmfg	324-329	NLR family pyrin domain containing 3	Homo sapiens	125-130
32963812-10	2020	Therefore, our study demonstrated that as inhibitor of the "NLRP3 inflammasome-NETs" inflammatory loop, exogenous rMFG-E8 improves angiogenesis and accelerates wound healing, highlighting possible therapeutic potential for DFUs.	rmfg-e8	114-121	NLR family pyrin domain containing 3	Homo sapiens	60-65
32445196-5	2020	Nigericin-induced NLRP3 inflammasome activation was dynamically visualised in microglia through ASC speck formation.	Nigericin	0-9	NLR family pyrin domain containing 3	Homo sapiens	18-23
32791101-0	2020	The Immunomodulatory Metabolite Itaconate Modifies NLRP3 and Inhibits Inflammasome Activation.	itaconic acid	32-41	NLR family pyrin domain containing 3	Homo sapiens	51-56
32791101-3	2020	Here we provide evidence that itaconate modifies NLRP3 and inhibits inflammasome activation.	itaconic acid	30-39	NLR family pyrin domain containing 3	Homo sapiens	49-54
32791101-4	2020	Itaconate and its derivative, 4-octyl itaconate (4-OI), inhibited NLRP3 inflammasome activation, but not AIM2 or NLRC4.	itaconic acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	66-71
32791101-4	2020	Itaconate and its derivative, 4-octyl itaconate (4-OI), inhibited NLRP3 inflammasome activation, but not AIM2 or NLRC4.	4-Octyl Itaconate	30-47	NLR family pyrin domain containing 3	Homo sapiens	66-71
32791101-4	2020	Itaconate and its derivative, 4-octyl itaconate (4-OI), inhibited NLRP3 inflammasome activation, but not AIM2 or NLRC4.	4-oi	49-53	NLR family pyrin domain containing 3	Homo sapiens	66-71
32791101-5	2020	Conversely, NLRP3 activation was increased in itaconate-depleted Irg1-/- macrophages.	itaconic acid	46-55	NLR family pyrin domain containing 3	Homo sapiens	12-17
32791101-8	2020	Our results identify itaconate as an endogenous metabolic regulator of the NLRP3 inflammasome and describe a process that may be exploited therapeutically to alleviate inflammation in NLRP3-driven disorders.	itaconic acid	21-30	NLR family pyrin domain containing 3	Homo sapiens	75-80
32791101-8	2020	Our results identify itaconate as an endogenous metabolic regulator of the NLRP3 inflammasome and describe a process that may be exploited therapeutically to alleviate inflammation in NLRP3-driven disorders.	itaconic acid	21-30	NLR family pyrin domain containing 3	Homo sapiens	184-189
32615411-2	2020	During the formation of inflammatory conditions, the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome activation plays an important regulator.	Leucine	83-90	NLR family pyrin domain containing 3	Homo sapiens	114-119
32765715-5	2020	Nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome has been studied predominantly and several hypotheses have been issued.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	61-66
32529290-5	2020	However, the identification of MS patients harboring rare homozygote variants in NLRP1 (p.Ile601Phe and p.Ser1387Ile), a variant in NLRP3 (p.Leu832Ile) resulting in the substitution of a critical amino acid for the formation of its leucine-rich repeat domain, and several MS patients with NLRC4 variants (p.Arg310Ter and p.Glu600Ter) causing protein truncations suggest that rare protein-altering variants in inflammasome-activating NLR receptors may contribute to MS risk.	leu832ile	141-150	NLR family pyrin domain containing 3	Homo sapiens	132-137
32529290-5	2020	However, the identification of MS patients harboring rare homozygote variants in NLRP1 (p.Ile601Phe and p.Ser1387Ile), a variant in NLRP3 (p.Leu832Ile) resulting in the substitution of a critical amino acid for the formation of its leucine-rich repeat domain, and several MS patients with NLRC4 variants (p.Arg310Ter and p.Glu600Ter) causing protein truncations suggest that rare protein-altering variants in inflammasome-activating NLR receptors may contribute to MS risk.	Leucine	232-239	NLR family pyrin domain containing 3	Homo sapiens	132-137
32529290-5	2020	However, the identification of MS patients harboring rare homozygote variants in NLRP1 (p.Ile601Phe and p.Ser1387Ile), a variant in NLRP3 (p.Leu832Ile) resulting in the substitution of a critical amino acid for the formation of its leucine-rich repeat domain, and several MS patients with NLRC4 variants (p.Arg310Ter and p.Glu600Ter) causing protein truncations suggest that rare protein-altering variants in inflammasome-activating NLR receptors may contribute to MS risk.	arg310ter	307-316	NLR family pyrin domain containing 3	Homo sapiens	132-137
32529290-5	2020	However, the identification of MS patients harboring rare homozygote variants in NLRP1 (p.Ile601Phe and p.Ser1387Ile), a variant in NLRP3 (p.Leu832Ile) resulting in the substitution of a critical amino acid for the formation of its leucine-rich repeat domain, and several MS patients with NLRC4 variants (p.Arg310Ter and p.Glu600Ter) causing protein truncations suggest that rare protein-altering variants in inflammasome-activating NLR receptors may contribute to MS risk.	glu600ter	323-332	NLR family pyrin domain containing 3	Homo sapiens	132-137
32954194-0	2020	Ropivacaine Prevents the Activation of the NLRP3 Inflammasome Caused by High Glucose in HUVECs.	Ropivacaine	0-11	NLR family pyrin domain containing 3	Homo sapiens	43-48
32954194-6	2020	Importantly, sirtuin-1 (SIRT1) knockdown experiments show that the inhibitory effects of ropivacaine against NLRP3 inflammasome activation are dependent on SIRT1.	Ropivacaine	89-100	NLR family pyrin domain containing 3	Homo sapiens	109-114
32750036-8	2020	Targeting aberrant glucose metabolism with shikonin, a pyruvate kinase M2 inhibitor, dampened NLRP3-mediated inflammation (caspase-1 (p<0.05), IL1beta (p<0.01)) and improved healing in vivo.	shikonin	43-51	NLR family pyrin domain containing 3	Homo sapiens	94-99
32757967-5	2020	EXPERT OPINION: NLRP3 inflammasome activity lies at the nexus between inflammation and cholesterol metabolism; it offers unique opportunities for understanding atherosclerotic pathophysiology and identifying novel modes of treatment.	Cholesterol	87-98	NLR family pyrin domain containing 3	Homo sapiens	16-21
32507974-7	2020	RESULTS: LPS-induced inflammation in the presence of ATP activates NLRP3 that subsequently increases pancreatic cancer cell proliferation by increasing caspase-1 activity leading to overall production of IL-1beta.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	67-72
32716363-5	2020	beta-Glucan acted upstream of the NLRP3 inflammasome by preventing potassium (K+) efflux, mitochondrial ROS (mtROS) generation, and, ultimately, apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and speck formation.	beta-Glucans	0-11	NLR family pyrin domain containing 3	Homo sapiens	34-39
32703754-4	2020	The activation of NLRP3 inflammasome is thought to be tightly associated with a regulator never in mitosis A (NIMA)-related kinase 7 (NEK7), apart from other signaling events such as K+ efflux and reactive oxygen species (ROS).	Reactive Oxygen Species	197-220	NLR family pyrin domain containing 3	Homo sapiens	18-23
32703754-4	2020	The activation of NLRP3 inflammasome is thought to be tightly associated with a regulator never in mitosis A (NIMA)-related kinase 7 (NEK7), apart from other signaling events such as K+ efflux and reactive oxygen species (ROS).	Reactive Oxygen Species	222-225	NLR family pyrin domain containing 3	Homo sapiens	18-23
32716363-0	2020	beta-Glucan-induced reprogramming of human macrophages inhibits NLRP3 inflammasome activation in cryopyrinopathies.	beta-Glucans	0-11	NLR family pyrin domain containing 3	Homo sapiens	64-69
32716363-4	2020	We found that NLRP3 inflammasome-mediated caspase-1 activation and subsequent IL-1beta production were reduced in beta-glucan-reprogrammed macrophages.	beta-Glucans	114-125	NLR family pyrin domain containing 3	Homo sapiens	14-19
32716363-5	2020	beta-Glucan acted upstream of the NLRP3 inflammasome by preventing potassium (K+) efflux, mitochondrial ROS (mtROS) generation, and, ultimately, apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and speck formation.	Potassium	67-76	NLR family pyrin domain containing 3	Homo sapiens	34-39
32716363-5	2020	beta-Glucan acted upstream of the NLRP3 inflammasome by preventing potassium (K+) efflux, mitochondrial ROS (mtROS) generation, and, ultimately, apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and speck formation.	ros	104-107	NLR family pyrin domain containing 3	Homo sapiens	34-39
32716363-6	2020	Importantly, beta-glucan-induced memory in macrophages resulted in a remarkable attenuation of IL-1beta secretion and caspase-1 activation in patients with an NLRP3-associated autoinflammatory disease, cryopyrin-associated periodic syndromes (CAPS).	beta-Glucans	13-24	NLR family pyrin domain containing 3	Homo sapiens	159-164
32716363-7	2020	Our findings demonstrate that beta-glucan-induced innate immune memory represses IL-1beta-mediated inflammation and support its potential clinical use in NLRP3-driven diseases.	beta-Glucans	30-41	NLR family pyrin domain containing 3	Homo sapiens	154-159
32854254-7	2020	Our studies revealed that RSV induces lytic cell death in macrophages via both of these mechanisms, specifically through the ASC (Apoptosis-associated speck like protein containing a caspase recruitment domain)-NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome activation of both caspase-1 dependent pyroptosis and receptor-interacting serine/threonine-protein kinase 3 (RIPK3), as well as a mixed lineage kinase domain like pseudokinase (MLKL)-dependent necroptosis.	Leucine	245-252	NLR family pyrin domain containing 3	Homo sapiens	211-216
32531864-5	2020	hiPSC-dM cell death after LukAB exposure, however, was only temporarily dependent of NLRP3, although NLRP3 triggered marked cell death after PVL treatment.	lukab	26-31	NLR family pyrin domain containing 3	Homo sapiens	85-90
32390276-3	2020	Compelling evidence has indicated the activation of the nucleotide-binding and oligomerization domain-like receptor, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome, a cytoplasmic complex containing multiple proteins, in a variety of lipid-related diseases including obesity, atherosclerosis, liver diseases, and type 2 diabetes.	Leucine	117-124	NLR family pyrin domain containing 3	Homo sapiens	168-173
33110394-0	2020	Hydrogen Sulfide Plays an Important Role by Influencing NLRP3 inflammasome.	Hydrogen Sulfide	0-16	NLR family pyrin domain containing 3	Homo sapiens	56-61
33110394-5	2020	Recent studies indicated that H2S played anti-inflammatory and pro-inflammatory roles in many diseases through influencing NLRP3 inflammasome, but its mechanism was not fully understood.	Deuterium	30-33	NLR family pyrin domain containing 3	Homo sapiens	123-128
33110394-6	2020	This article reviewed the progress about the effects of H2S on NLRP3 inflammasome and its mechanisms involved in recent years to provide theoretical basis for in-depth study.	Deuterium	56-59	NLR family pyrin domain containing 3	Homo sapiens	63-68
32391974-0	2020	LncRNA MALAT1 promoted high glucose-induced pyroptosis of renal tubular epithelial cell by sponging miR-30c targeting for NLRP3.	Glucose	28-35	NLR family pyrin domain containing 3	Homo sapiens	122-127
32982973-0	2020	Commentary: Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto"s Thyroiditis Through the ROS-NF-kappaB-NLRP3 Pathway.	Iodine	22-28	NLR family pyrin domain containing 3	Homo sapiens	141-146
32923762-0	2020	Humanin Ameliorates Free Fatty Acid-Induced Endothelial Inflammation by Suppressing the NLRP3 Inflammasome.	Fatty Acids, Nonesterified	20-35	NLR family pyrin domain containing 3	Homo sapiens	88-93
32974137-4	2020	3,4-Methylenedioxy-beta-nitrostyrene (MNS) was selected as a specific NLRP3 inflammasome inhibitor.	3,4-methylenedioxy-beta-nitrostyrene	0-36	NLR family pyrin domain containing 3	Homo sapiens	70-75
32829380-0	2020	ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.	Salts	47-51	NLR family pyrin domain containing 3	Homo sapiens	125-130
32829380-6	2020	The inhibitory effects of ELA on Aldosterone-stimulated NADPH oxidase/ROS/NLRP3 inflammasome pathway were confirmed in the human renal tubular cells.	Aldosterone	33-44	NLR family pyrin domain containing 3	Homo sapiens	74-79
32974137-4	2020	3,4-Methylenedioxy-beta-nitrostyrene (MNS) was selected as a specific NLRP3 inflammasome inhibitor.	3,4-methylenedioxy-beta-nitrostyrene	38-41	NLR family pyrin domain containing 3	Homo sapiens	70-75
32824985-9	2020	Of the three tested antibiotics, DDS was effective in the molecular regulation of NLRP3 inflammasome activators that are important in mild cognitive impairment (MCI), Parkinson"s disease (PD), and AD.	Dapsone	33-36	NLR family pyrin domain containing 3	Homo sapiens	82-87
32929357-0	2020	Statins ameliorate cholesterol-induced inflammation and improve AQP2 expression by inhibiting NLRP3 activation in the kidney.	Cholesterol	19-30	NLR family pyrin domain containing 3	Homo sapiens	94-99
32817626-0	2020	Quercetin negatively regulates IL-1beta production in Pseudomonas aeruginosa-infected human macrophages through the inhibition of MAPK/NLRP3 inflammasome pathways.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	135-140
32817626-9	2020	Moreover, quercetin reduced the NLRP3 expression and inhibited the P. aeruginosa-mediated cleavage of caspase-1 as well as mature IL-1beta.	Quercetin	10-19	NLR family pyrin domain containing 3	Homo sapiens	32-37
32817626-10	2020	These results thus indicated that quercetin inhibition of P. aeruginosa-induced IL-1beta production is mediated by suppressing the initial priming step and by inhibiting the NLRP3 inflammasome activation.	Quercetin	34-43	NLR family pyrin domain containing 3	Homo sapiens	174-179
32824985-10	2020	The specific targeting of NLRP3 itself or up-/downstream factors of the NLRP3 inflammasome by DDS may be responsible for its observed preventive effects, functioning as a competitor.	Dapsone	94-97	NLR family pyrin domain containing 3	Homo sapiens	26-31
32824985-10	2020	The specific targeting of NLRP3 itself or up-/downstream factors of the NLRP3 inflammasome by DDS may be responsible for its observed preventive effects, functioning as a competitor.	Dapsone	94-97	NLR family pyrin domain containing 3	Homo sapiens	72-77
32507349-6	2020	METHOD: Three phytochemicals; Sulforaphane, Curcumin, and Resveratrol were selected, and studies were reviewed to clarify their intracellular signaling mechanism in NLRP3 inflammasome activity.	Resveratrol	58-69	NLR family pyrin domain containing 3	Homo sapiens	165-170
32574674-9	2020	More, CYP2J2 reduced LPS-induced reactive oxygen species (ROS) production and mitochondrial depolarization in heart cells, thereby inhibiting NLRP3 inflammasome activation.	Reactive Oxygen Species	33-56	NLR family pyrin domain containing 3	Homo sapiens	142-147
32574674-9	2020	More, CYP2J2 reduced LPS-induced reactive oxygen species (ROS) production and mitochondrial depolarization in heart cells, thereby inhibiting NLRP3 inflammasome activation.	Reactive Oxygen Species	58-61	NLR family pyrin domain containing 3	Homo sapiens	142-147
32507349-6	2020	METHOD: Three phytochemicals; Sulforaphane, Curcumin, and Resveratrol were selected, and studies were reviewed to clarify their intracellular signaling mechanism in NLRP3 inflammasome activity.	sulforaphane	30-42	NLR family pyrin domain containing 3	Homo sapiens	165-170
32787872-2	2020	Ethanol-induced calcium overload causes NOD-like receptor protein 3 (NLRP3) inflammasome formation and an imbalance in mitochondrial dynamics, closely associated with the pathogenesis of neurodegeneration.	Calcium	16-23	NLR family pyrin domain containing 3	Homo sapiens	40-67
32507349-6	2020	METHOD: Three phytochemicals; Sulforaphane, Curcumin, and Resveratrol were selected, and studies were reviewed to clarify their intracellular signaling mechanism in NLRP3 inflammasome activity.	Curcumin	44-52	NLR family pyrin domain containing 3	Homo sapiens	165-170
32787872-2	2020	Ethanol-induced calcium overload causes NOD-like receptor protein 3 (NLRP3) inflammasome formation and an imbalance in mitochondrial dynamics, closely associated with the pathogenesis of neurodegeneration.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	40-67
32787872-2	2020	Ethanol-induced calcium overload causes NOD-like receptor protein 3 (NLRP3) inflammasome formation and an imbalance in mitochondrial dynamics, closely associated with the pathogenesis of neurodegeneration.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	69-74
32787872-2	2020	Ethanol-induced calcium overload causes NOD-like receptor protein 3 (NLRP3) inflammasome formation and an imbalance in mitochondrial dynamics, closely associated with the pathogenesis of neurodegeneration.	Calcium	16-23	NLR family pyrin domain containing 3	Homo sapiens	69-74
32787872-4	2020	Therefore, the present study investigated the detailed mechanism of calcium-regulated mitochondrial dynamics and NLRP3 inflammasome formation in neuronal cells by ethanol.	Ethanol	163-170	NLR family pyrin domain containing 3	Homo sapiens	113-118
32787872-13	2020	Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	51-56
32787872-13	2020	Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death.	Reactive Oxygen Species	146-149	NLR family pyrin domain containing 3	Homo sapiens	51-56
32787872-15	2020	CONCLUSIONS: Our results demonstrated that ethanol upregulated NMDAR-dependent CaMKII phosphorylation which is essential for Drp1-mediated excessive mitochondrial fission and the JNK1-induced NLRP3 inflammasome activation resulting in neuronal apoptosis.	Ethanol	43-50	NLR family pyrin domain containing 3	Homo sapiens	192-197
32782316-9	2020	Screening identified KN3014, a piperidine-containing compound targeting the interaction between NLRP3 and ASC through the PYD.	kn3014	21-27	NLR family pyrin domain containing 3	Homo sapiens	96-101
32782316-9	2020	Screening identified KN3014, a piperidine-containing compound targeting the interaction between NLRP3 and ASC through the PYD.	piperidine	31-41	NLR family pyrin domain containing 3	Homo sapiens	96-101
32968631-14	2020	Cur attenuated DOX-induced cardiomyocyte pyroptosis as evidenced by NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and interleukin-18 levels.	Doxorubicin	15-18	NLR family pyrin domain containing 3	Homo sapiens	68-104
33505579-0	2020	Fucoidan Inhibits NLRP3 Inflammasome Activation by Enhancing p62/SQSTM1-Dependent Selective Autophagy to Alleviate Atherosclerosis.	fucoidan	0-8	NLR family pyrin domain containing 3	Homo sapiens	18-23
33505579-3	2020	Fucoidan significantly ameliorated lipid accumulation, attenuated progression of carotid atherosclerotic plaques, deregulated the expression of NLRP3 inflammasome, autophagy receptor p62, and upregulated microtubule-associated protein light chain 3 (LC3)-II/I levels.	fucoidan	0-8	NLR family pyrin domain containing 3	Homo sapiens	144-149
33505579-5	2020	Mechanistically, fucoidan remarkably inhibited NLRP3 inflammasome activation, which was mostly dependent on autophagy.	fucoidan	17-25	NLR family pyrin domain containing 3	Homo sapiens	47-52
33505579-6	2020	The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA).	fucoidan	26-34	NLR family pyrin domain containing 3	Homo sapiens	38-43
33505579-6	2020	The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA).	Sirolimus	94-103	NLR family pyrin domain containing 3	Homo sapiens	38-43
33505579-6	2020	The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA).	Sirolimus	105-109	NLR family pyrin domain containing 3	Homo sapiens	38-43
33505579-6	2020	The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA).	3-methyladenine	149-164	NLR family pyrin domain containing 3	Homo sapiens	38-43
33505579-6	2020	The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA).	3-methyladenine	166-170	NLR family pyrin domain containing 3	Homo sapiens	38-43
33505579-7	2020	Fucoidan promoted the colocalization of NLRP3 and p62.	fucoidan	0-8	NLR family pyrin domain containing 3	Homo sapiens	40-45
33505579-8	2020	Knockdown of p62 and ATG5 by small interfering RNA significantly reduced the inhibitory effects of fucoidan treatment on NLRP3 inflammasome.	fucoidan	99-107	NLR family pyrin domain containing 3	Homo sapiens	121-126
33505579-9	2020	The data suggest that fucoidan can inhibit NLRP3 inflammasome activation by enhancing p62/SQSTM1-dependent selective autophagy to alleviate atherosclerosis.	fucoidan	22-30	NLR family pyrin domain containing 3	Homo sapiens	43-48
32524615-7	2020	RESULTS: Alcohol-induced in vivo pyroptosis occurs because of an increase in the levels of pyroptotic proteins such as nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3), caspase-1, gasdermin-D (GSDMD), and amplified inflammatory response.	Alcohols	9-16	NLR family pyrin domain containing 3	Homo sapiens	176-181
32968631-14	2020	Cur attenuated DOX-induced cardiomyocyte pyroptosis as evidenced by NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and interleukin-18 levels.	Doxorubicin	15-18	NLR family pyrin domain containing 3	Homo sapiens	106-111
32196713-0	2020	Atractylenolide III reduces NLRP3 inflammasome activation and Th1/Th2 imbalances in both in vitro and in vivo models of asthma.	(+)-Atractylenolide	0-15	NLR family pyrin domain containing 3	Homo sapiens	28-33
31970602-0	2020	Correction to: novel biphenyl diester derivative AB-38b inhibits NLRP3 inflammasome through Nrf2 activation in diabetic nephropathy.	diphenyl	21-29	NLR family pyrin domain containing 3	Homo sapiens	65-70
32196713-8	2020	These results indicate that atractylenolide III reduced NLRP3 inflammasome activation and regulated the Th1/Th2 balance in IL-4 induced 16HBE cells and ovalbumin-induced asthmatic mice, suggesting it has a protective effect that may be useful in the treatment of pediatric asthma.	(+)-Atractylenolide	28-43	NLR family pyrin domain containing 3	Homo sapiens	56-61
32128601-6	2020	Also, apelin protects against ALI/ARDS by reducing mitochondrial ROS-triggered oxidative damage, mitochondria apoptosis, and inflammatory responses induced by the activation of NF-kappaB and NLRP3 inflammasome.	ros	65-68	NLR family pyrin domain containing 3	Homo sapiens	191-196
32305666-8	2020	Further, we investigated the effect of CSC exposure on the status of NLRP3 inflammasome markers, i.e. NLRP3, pro-caspase-1, caspase-1, pro-IL-18, pro-IL-1beta, IL-1beta and IL-18 in a stage-specific manner.	8-(3-Chlorostyryl)caffeine	39-42	NLR family pyrin domain containing 3	Homo sapiens	69-74
32305666-9	2020	For this, THP-1 monocytes, PMA-differentiated macrophages and oxidized-low density lipoprotein (ox-LDL)-induced macrophage foam cells were exposed to 10 mug/ml of CSC for 6 h. CSC exposure significantly upregulated the expression of NLRP3 inflammasome in CSC-treated cells at both transcriptional and translational levels.	8-(3-Chlorostyryl)caffeine	163-166	NLR family pyrin domain containing 3	Homo sapiens	233-238
32196713-5	2020	In 16HBE cells, administration of atractylenolide III also significantly suppressed the IL-4-induced increases in the expression of cleaved caspase-1; apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC); and nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3).	(+)-Atractylenolide	34-49	NLR family pyrin domain containing 3	Homo sapiens	303-308
32239395-6	2020	In this study, we investigated the effects of nicardipine and verapamil, both L-type calcium channel antagonists, on the NLRP3 inflammasome using differentiated THP-1 cells.	Nicardipine	46-57	NLR family pyrin domain containing 3	Homo sapiens	121-126
32592441-6	2020	ER stress inhibition with tauroursodeoxycholic acid or 4-phenylbutyric acid and iNOS inhibition with 1400 W dramatically suppressed activation of the NF-kappaB/IkappaB pathway and the NLRP3 inflammasome, and decreased the production of pro-inflammatory cytokines.	ursodoxicoltaurine	26-51	NLR family pyrin domain containing 3	Homo sapiens	184-189
32592441-6	2020	ER stress inhibition with tauroursodeoxycholic acid or 4-phenylbutyric acid and iNOS inhibition with 1400 W dramatically suppressed activation of the NF-kappaB/IkappaB pathway and the NLRP3 inflammasome, and decreased the production of pro-inflammatory cytokines.	4-phenylbutyric acid	55-75	NLR family pyrin domain containing 3	Homo sapiens	184-189
32103437-0	2020	Titanium Ions Play a Synergistic Role in the Activation of NLRP3 Inflammasome in Jurkat T Cells.	Titanium	0-8	NLR family pyrin domain containing 3	Homo sapiens	59-64
32103437-6	2020	Moreover, measurement by confocal microscopy and flow cytometry assay indicates that Ti ions can promote the production of ROS, while NLRP3 expression and IL-1beta secretion are reduced after treatment of Jurkat cells with NAC (ROS scavenger).	ros	228-231	NLR family pyrin domain containing 3	Homo sapiens	134-139
32103437-7	2020	Taken together, we presently show that Ti ions can activate NLRP3 inflammasome and then promote IL-beta secretion in vitro, where ROS may play a mechanistic role in this activation process.	ros	130-133	NLR family pyrin domain containing 3	Homo sapiens	60-65
32239395-0	2020	Nicardipine Inhibits Priming of the NLRP3 Inflammasome via Suppressing LPS-Induced TLR4 Expression.	Nicardipine	0-11	NLR family pyrin domain containing 3	Homo sapiens	36-41
32239395-6	2020	In this study, we investigated the effects of nicardipine and verapamil, both L-type calcium channel antagonists, on the NLRP3 inflammasome using differentiated THP-1 cells.	Verapamil	62-71	NLR family pyrin domain containing 3	Homo sapiens	121-126
32239395-12	2020	Nicardipine also mitigated caspase-1 activation, inhibited ASC oligomerization, and reduced NLRP3 expression.	Nicardipine	0-11	NLR family pyrin domain containing 3	Homo sapiens	92-97
32239395-14	2020	In conclusion, nicardipine exerted anti-inflammatory effects through inhibiting NLRP3 inflammasome pathway.	Nicardipine	15-26	NLR family pyrin domain containing 3	Homo sapiens	80-85
32239395-15	2020	Nicardipine may mitigate NLRP3 priming via inhibiting NF-kappaB activation, mediated by suppressing LPS-induced TLR4 expression.	Nicardipine	0-11	NLR family pyrin domain containing 3	Homo sapiens	25-30
32360740-0	2020	Insulin-like growth factor-I activates NFkappaB and NLRP3 inflammatory signalling via ROS in cancer cells.	Reactive Oxygen Species	86-89	NLR family pyrin domain containing 3	Homo sapiens	52-57
32500758-0	2020	Retraction: Laquinimod inhibits MMP-induced NLRP3 inflammasome activation in human neuronal cells.	laquinimod	12-22	NLR family pyrin domain containing 3	Homo sapiens	44-49
32360740-7	2020	Taken together, this is the first report on the mechanism by which IGF-1 activates NFkappaB and NLRP3 inflammatory signalling via ROS.	Reactive Oxygen Species	130-133	NLR family pyrin domain containing 3	Homo sapiens	96-101
32473843-3	2020	Of note, the nucleotide-binding oligomerization domain leucine rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome acts as a key player in both coordinating the host physiology and shaping the peripheral and central immune/inflammatory responses in CNS diseases.	Leucine	55-62	NLR family pyrin domain containing 3	Homo sapiens	114-119
32124392-14	2020	CONCLUSION: Our finding confirmed that ChIV provides a neuroprotective effect against sevoflurane-induced neuroinflammation and cognitive impairment by blocking the NLRP3/caspase-1 pathway, which may be an effective strategy for the clinical treatment of elderly patients with POCD induced by anesthesia.	Sevoflurane	86-97	NLR family pyrin domain containing 3	Homo sapiens	165-170
32578856-0	2020	NLRP3 augmented resistance to gemcitabine in triple-negative breast cancer  cells(TNBCC) via EMT/IL-1beta/Wnt/beta-catenin signaling pathway.	gemcitabine	30-41	NLR family pyrin domain containing 3	Homo sapiens	0-5
33064063-2	2020	In the present study, we used real-time polymerase chain reactions, Western blot analysis, and a lactate production assay to investigate whether an increase in the NLRP3 inflammasome induced by Ni-refining fumes was associated with the Warburg effect in BEAS-2B cells, a nonmalignant pulmonary epithelial line.	Lactic Acid	97-104	NLR family pyrin domain containing 3	Homo sapiens	164-169
33064063-6	2020	Furthermore, inhibition of the Warburg effect by 2-Deoxy-d-glucose reversed the increased expression of NLRP3 induced by Ni-refining fumes.	Glucose	59-66	NLR family pyrin domain containing 3	Homo sapiens	104-109
32578856-5	2020	We investigated the sensitivity to gemcitabine responsive to regulation of NLRP3 expression in TNBCC in different gemcitabine concentrations.	gemcitabine	35-46	NLR family pyrin domain containing 3	Homo sapiens	75-80
32578856-5	2020	We investigated the sensitivity to gemcitabine responsive to regulation of NLRP3 expression in TNBCC in different gemcitabine concentrations.	gemcitabine	114-125	NLR family pyrin domain containing 3	Homo sapiens	75-80
32578856-7	2020	Gemcitabine resistance was studied in GRC exposed to 0,1,3,5nm gemcitabine after GRC were treated with NLRP3 agonist NSS or antagonist CY-09.	gemcitabine	0-11	NLR family pyrin domain containing 3	Homo sapiens	103-108
32578856-10	2020	RESULTS:  NLRP3 upregulation improved cell survival and reduced sensitivity to gemcitabine (P<0.05).	gemcitabine	79-90	NLR family pyrin domain containing 3	Homo sapiens	10-15
32578856-13	2020	NLRP3 upregulation added to resistance to gemcitabine in GRC(P<0.05).	gemcitabine	42-53	NLR family pyrin domain containing 3	Homo sapiens	0-5
32849554-2	2020	The NOD-, LRR- and pyrin domain containing protein 3 (NLRP3) is an innate immune signaling complex whose assembly and activation can be triggered by various signals ranging from microbial molecules to ATP or the abnormal accumulation of crystals, thus leading to IL-1beta and IL-18 maturation and secretion.	Adenosine Triphosphate	201-204	NLR family pyrin domain containing 3	Homo sapiens	54-59
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	gemcitabine	46-57	NLR family pyrin domain containing 3	Homo sapiens	12-17
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	gemcitabine	46-57	NLR family pyrin domain containing 3	Homo sapiens	124-129
32751912-4	2020	In the subsequent years, it was reported that activation of the inflammasome receptor molecule, NLRP3, is modulated via tyrosine phosphorylation as well, and that NLRP3 de-phosphorylation at specific tyrosine residues was required for inflammasome assembly and sustained IL-1beta/IL-18 release.	Tyrosine	120-128	NLR family pyrin domain containing 3	Homo sapiens	96-101
32751912-4	2020	In the subsequent years, it was reported that activation of the inflammasome receptor molecule, NLRP3, is modulated via tyrosine phosphorylation as well, and that NLRP3 de-phosphorylation at specific tyrosine residues was required for inflammasome assembly and sustained IL-1beta/IL-18 release.	Tyrosine	200-208	NLR family pyrin domain containing 3	Homo sapiens	96-101
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	CY5.5 cyanine dye	141-146	NLR family pyrin domain containing 3	Homo sapiens	12-17
32751912-4	2020	In the subsequent years, it was reported that activation of the inflammasome receptor molecule, NLRP3, is modulated via tyrosine phosphorylation as well, and that NLRP3 de-phosphorylation at specific tyrosine residues was required for inflammasome assembly and sustained IL-1beta/IL-18 release.	Tyrosine	200-208	NLR family pyrin domain containing 3	Homo sapiens	163-168
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	CY5.5 cyanine dye	141-146	NLR family pyrin domain containing 3	Homo sapiens	124-129
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	gemcitabine	174-185	NLR family pyrin domain containing 3	Homo sapiens	12-17
32578856-15	2020	CONCLUSION: NLRP3 could enhance resistance to gemcitabine via IL-1beta/EMT/Wnt/beta-catenin signaling, which suggested that NLRP3 antagonist CY-09 might be incorporated into gemcitabine treatment for TNBC.	gemcitabine	174-185	NLR family pyrin domain containing 3	Homo sapiens	124-129
32849646-0	2020	Retraction: The Increase in IL-1beta in the Early Stage of Heatstroke Might Be Caused by Splenic Lymphocyte Pyroptosis Induced by mtROS-Mediated Activation of the NLRP3 Inflammasome.	mtros	130-135	NLR family pyrin domain containing 3	Homo sapiens	163-168
32751530-2	2020	As a critical component of the innate immune system, the nucleotide-binding and oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) inflammasome can be activated by various endogenous and exogenous danger signals.	Leucine	104-111	NLR family pyrin domain containing 3	Homo sapiens	156-161
32584575-4	2020	In the present study, a series of dehydrohispanolone derivatives (1-19) was synthesized, and their anti-inflammatory activities toward NLRP3 inflammasome activation were evaluated.	Dehydrohispanolone	34-52	NLR family pyrin domain containing 3	Homo sapiens	135-140
32584575-7	2020	Analysis of IL-1beta and caspase-1 expression revealed that the new diterpenoids 15 and 18 are selective inhibitors of the NLRP3 inflammasome, reinforcing the previously demonstrated anti-inflammatory properties of hispanolone derivatives.	Diterpenes	68-80	NLR family pyrin domain containing 3	Homo sapiens	123-128
32584575-7	2020	Analysis of IL-1beta and caspase-1 expression revealed that the new diterpenoids 15 and 18 are selective inhibitors of the NLRP3 inflammasome, reinforcing the previously demonstrated anti-inflammatory properties of hispanolone derivatives.	hispanolone	215-226	NLR family pyrin domain containing 3	Homo sapiens	123-128
32592999-1	2020	Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production.	Reactive Oxygen Species	219-242	NLR family pyrin domain containing 3	Homo sapiens	127-132
32792920-4	2020	The nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome, which is one of the most intensively investigated inflammasomes, has been reported to play a key role in neurodegenerative diseases.	Leucine	46-53	NLR family pyrin domain containing 3	Homo sapiens	105-110
32664349-4	2020	NLRP3 inflammasomes have a specific activation pathway that involves numerous stimuli, including a wide range of PAMPs and DAMPs.	dinitrophenyl-aminopropyl-methylamine	123-128	NLR family pyrin domain containing 3	Homo sapiens	0-5
32801633-0	2020	Loratadine Alleviates Advanced Glycation End Product-Induced Activation of NLRP3 Inflammasome in Human Chondrocytes.	Loratadine	0-10	NLR family pyrin domain containing 3	Homo sapiens	75-80
32801633-5	2020	Materials and Methods: The inhibitory effects of loratadine on NLRP3 inflammasome and the NADPH oxidase subunit NOX4 were assessed in advanced glycation end products (AGEs)-treated SW1353 chondrocytes by real-time PCR, ELISA, and Western blot experiments.	Loratadine	49-59	NLR family pyrin domain containing 3	Homo sapiens	63-68
32801633-10	2020	Loratadine treatment inhibited the expression of TxNIP and several components of the NLRP3 inflammasome complex, including NLRP3, ASC, and cleaved caspase 1 (P10).	Loratadine	0-10	NLR family pyrin domain containing 3	Homo sapiens	85-90
32801633-10	2020	Loratadine treatment inhibited the expression of TxNIP and several components of the NLRP3 inflammasome complex, including NLRP3, ASC, and cleaved caspase 1 (P10).	Loratadine	0-10	NLR family pyrin domain containing 3	Homo sapiens	123-128
32801633-11	2020	Moreover, loratadine suppressed the expression of NRF2, and the silencing of NRF2 abolished the suppressive effect of loratadine on NLRP3 inflammasome activation.	Loratadine	118-128	NLR family pyrin domain containing 3	Homo sapiens	132-137
32801633-12	2020	Conclusion: Our study demonstrates that loratadine protects chondrocytes from AGEs-induced TxNIP/NLRP3 inflammasome activation by modulating the expression of the transcriptional factor NRF2.	Loratadine	40-50	NLR family pyrin domain containing 3	Homo sapiens	97-102
32334032-10	2020	Activation of the NLRP3 inflammasome was mediated by ROS, and ROS inhibitor treatment decreased the production of IL-1beta and IL-18 in vitro.	Reactive Oxygen Species	53-56	NLR family pyrin domain containing 3	Homo sapiens	18-23
32334032-10	2020	Activation of the NLRP3 inflammasome was mediated by ROS, and ROS inhibitor treatment decreased the production of IL-1beta and IL-18 in vitro.	Reactive Oxygen Species	62-65	NLR family pyrin domain containing 3	Homo sapiens	18-23
32733639-9	2020	Therefore, we conclude that colchicine plays a crucial role in alleviating the intracellular inflammatory response and NLRP3 inflammation activation, attenuating the levels of cellular oxidative stress and pyroptosis in endothelial cells via regulating AMPK/SIRT1 signaling, which may be a concrete mechanism for the secondary prevention of cardiovascular diseases.	Colchicine	28-38	NLR family pyrin domain containing 3	Homo sapiens	119-124
32592999-1	2020	Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production.	Reactive Oxygen Species	244-247	NLR family pyrin domain containing 3	Homo sapiens	127-132
32765942-3	2020	Recent studies suggest a role for the nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3) inflammasome activation in lung inflammation and fibrosis in SARS-CoV and SARS-CoV-2 infections.	Leucine	68-75	NLR family pyrin domain containing 3	Homo sapiens	134-139
32808940-4	2020	Studies show that colchicine, among other actions, inhibits the assembly of NLRP3 complex that is responsible for generating the active form of Caspase-1 that will convert Pro-IL-1beta and Pro-IL-18 into their active forms.	Colchicine	18-28	NLR family pyrin domain containing 3	Homo sapiens	76-81
32707731-3	2020	Here, we showed that Cbl dampened NLRP3 inflammasome activation by inhibiting glycolysis, as demonstrated with Cbl knockout cells and treatment with the Cbl inhibitor hydrocotarnine.	hydrocotarnine	167-181	NLR family pyrin domain containing 3	Homo sapiens	34-39
32707731-6	2020	Upon NLRP3 inflammasome activation, inhibiting Cbl increased glycolysis-dependent activation of mitochondrial respiration and increased the production of reactive oxygen species, which contributes to NLRP3 inflammasome activation and IL-1beta secretion.	Oxygen	163-169	NLR family pyrin domain containing 3	Homo sapiens	200-205
32707731-7	2020	Mechanistically, inhibiting Cbl increased surface expression of glucose transporter 1 (GLUT1) protein through post-transcriptional regulation, which increased cellular glucose uptake and consequently raised glycolytic capacity, and in turn enhanced NLRP3 inflammasome activation.	Glucose	64-71	NLR family pyrin domain containing 3	Homo sapiens	249-254
32707731-9	2020	We also show that a novel Cbl inhibitor, hydrocortanine, increased NLRP3 inflammasome activity via its effect on glycolysis.	hydrocortanine	41-55	NLR family pyrin domain containing 3	Homo sapiens	67-72
32356198-7	2020	Conclusively, our study demonstrated that IL-22 exerted ameliorative effects on APAP-induced kidney injury by alleviating mitochondrial dysfunction and NLRP3 inflammasome activation, suggesting that IL-22 represents a potential therapeutic approach to treat APAP-induced kidney injury.	Acetaminophen	80-84	NLR family pyrin domain containing 3	Homo sapiens	152-157
32650532-4	2020	Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D.	Cholesterol	101-112	NLR family pyrin domain containing 3	Homo sapiens	143-148
32650532-4	2020	Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D.	Uric Acid	114-119	NLR family pyrin domain containing 3	Homo sapiens	143-148
32650532-4	2020	Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D.	Glucose	125-132	NLR family pyrin domain containing 3	Homo sapiens	143-148
32733235-0	2020	Caffeic Acid Phenethyl Ester Ameliorates Calcification by Inhibiting Activation of the AKT/NF-kappaB/NLRP3 Inflammasome Pathway in Human Aortic Valve Interstitial Cells.	caffeic acid phenethyl ester	0-28	NLR family pyrin domain containing 3	Homo sapiens	101-106
32733235-6	2020	The regulatory effects of CAPE on activation of the AKT/NF-kappaB and NLRP3 inflammasome were evaluated by Western blot analysis and immunofluorescent staining.	caffeic acid phenethyl ester	26-30	NLR family pyrin domain containing 3	Homo sapiens	70-75
32733235-10	2020	Furthermore, CAPE inhibited phosphorylation of AKT, ERK1/2, and NF-kappaB, and suppressed NLRP3 inflammasome activation in AVICs cultured in OM.	caffeic acid phenethyl ester	13-17	NLR family pyrin domain containing 3	Homo sapiens	90-95
32733235-11	2020	Thus, CAPE is implicated as a potent natural product for the prevention of CAVD by inhibiting activation of the AKT/NF-kappaB pathway and NLRP3 inflammasome.	caffeic acid phenethyl ester	6-10	NLR family pyrin domain containing 3	Homo sapiens	138-143
32447438-9	2020	ERS can activate the NLRP3 inflammasome to induce inflammatory responses via oxidative stress, calcium homeostasis, and NF-kappaB activation.	Calcium	95-102	NLR family pyrin domain containing 3	Homo sapiens	21-26
32630207-8	2020	We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis.	Tretinoin	13-17	NLR family pyrin domain containing 3	Homo sapiens	102-107
32134203-12	2020	CONCLUSION: Our results present beta-carotene as a selective and direct inhibitor of NLRP3 and the binding to NLRP3 PYD as a novel pharmacological strategy to combat NLRP3 inflammasome-driven diseases, including gouty arthritis.	beta Carotene	32-45	NLR family pyrin domain containing 3	Homo sapiens	85-90
32630207-0	2020	All-Trans Retinoic Acid Enhances both the Signaling for Priming and the Glycolysis for Activation of NLRP3 Inflammasome in Human Macrophage.	Tretinoin	10-23	NLR family pyrin domain containing 3	Homo sapiens	101-106
32630207-6	2020	We describe for the first time that ATRA modulates both priming and activation signals required for NLRP3 inflammasome function.	Tretinoin	36-40	NLR family pyrin domain containing 3	Homo sapiens	100-105
32630207-9	2020	We also provide evidence that ATRA enhances hexokinase 2 expression, and shifts the metabolism of LPS-activated macrophages toward glycolysis, leading to the activation of NLRP3 inflammasome.	Tretinoin	30-34	NLR family pyrin domain containing 3	Homo sapiens	172-177
32630207-7	2020	ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK.	Tretinoin	0-4	NLR family pyrin domain containing 3	Homo sapiens	19-24
32630207-7	2020	ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK.	Tretinoin	0-4	NLR family pyrin domain containing 3	Homo sapiens	76-81
32446726-0	2020	Dopamine D1 receptor agonist A68930 attenuates acute kidney injury by inhibiting NLRP3 inflammasome activation.	A 68930	29-35	NLR family pyrin domain containing 3	Homo sapiens	81-86
32452918-3	2020	Despite the controversy over the inflammatory role of uric acid in its soluble form, crystals of uric acid are able to activate the NLRP3 inflammasome in different tissues.	Uric Acid	54-63	NLR family pyrin domain containing 3	Homo sapiens	132-137
32452918-3	2020	Despite the controversy over the inflammatory role of uric acid in its soluble form, crystals of uric acid are able to activate the NLRP3 inflammasome in different tissues.	Uric Acid	97-106	NLR family pyrin domain containing 3	Homo sapiens	132-137
32452918-8	2020	Despite these conflicting views, several studies support the idea that hyperuricemia is indeed a cause of progression of kidney disease, with a putative role for soluble uric acid in activating renal NLRP3 inflammasome, in reprograming renal and immune cell metabolism and, therefore, in promoting kidney inflammation/injury.	Uric Acid	170-179	NLR family pyrin domain containing 3	Homo sapiens	200-205
32452918-9	2020	SUMMARY: Therapies aiming to decrease uric acid levels prevent renal NLRP3 inflammasome activation and exert renoprotective effects in experimental kidney diseases.	Uric Acid	38-47	NLR family pyrin domain containing 3	Homo sapiens	69-74
32202959-3	2020	Recently, glyburide, a hypoglycemic sulfonylurea, has been reported to reduce IL-1beta activation by suppressing activation of the NLRP3 inflammasome.	Glyburide	10-19	NLR family pyrin domain containing 3	Homo sapiens	131-136
32315958-8	2020	RESULTS: Following butyrate supplementation, the relative expression levels of TLR2/4, NF-kappaB1, Caspase-1, NLRP3, IL-1beta & IL-18 were significantly downregulated (p < 0.05).	Butyrates	19-27	NLR family pyrin domain containing 3	Homo sapiens	110-115
32536991-1	2020	Crystalized deposits of monosodium urate activate the Nod-like receptor protein 3 (NLRP3) inflammasome, resulting in kidney damage.	Uric Acid	24-40	NLR family pyrin domain containing 3	Homo sapiens	54-81
32536991-1	2020	Crystalized deposits of monosodium urate activate the Nod-like receptor protein 3 (NLRP3) inflammasome, resulting in kidney damage.	Uric Acid	24-40	NLR family pyrin domain containing 3	Homo sapiens	83-88
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	12-29	NLR family pyrin domain containing 3	Homo sapiens	263-268
32347316-6	2020	RESULTS: In hydrogen peroxide (H2O2)-stimulated HL7702 cells, HBx triggered the release of pro-inflammatory mediators apoptosis-associated speck-like protein containing a CARD (ASC), interleukin (IL)-1beta, IL-18, and high-mobility group box 1 (HMGB1); activated NLRP3; and initiated pro-inflammatory cell death (pyroptosis).	Hydrogen Peroxide	31-35	NLR family pyrin domain containing 3	Homo sapiens	263-268
32347316-8	2020	Treatment of HL7702 cells with a mitoROS scavenger attenuated HBx-induced NLRP3 activation and pyroptosis.	mitoros	33-40	NLR family pyrin domain containing 3	Homo sapiens	74-79
32347316-10	2020	CONCLUSIONS: The NLRP3 inflammasome was activated by elevated mitoROS levels and mediated HBx-induced liver inflammation and hepatocellular pyroptosis under H2O2-stress conditions.	mitoros	62-69	NLR family pyrin domain containing 3	Homo sapiens	17-22
32347316-10	2020	CONCLUSIONS: The NLRP3 inflammasome was activated by elevated mitoROS levels and mediated HBx-induced liver inflammation and hepatocellular pyroptosis under H2O2-stress conditions.	Hydrogen Peroxide	157-161	NLR family pyrin domain containing 3	Homo sapiens	17-22
32202959-3	2020	Recently, glyburide, a hypoglycemic sulfonylurea, has been reported to reduce IL-1beta activation by suppressing activation of the NLRP3 inflammasome.	Sulfonylurea Compounds	36-48	NLR family pyrin domain containing 3	Homo sapiens	131-136
32202959-4	2020	Therefore, we evaluated the possibility of targeting the NLRP3 inflammasome pathway by glyburide to suppress periodontal pathogen-induced inflammation.	Glyburide	87-96	NLR family pyrin domain containing 3	Homo sapiens	57-62
32272506-0	2020	Berberine suppresses influenza virus-triggered NLRP3 inflammasome activation in macrophages by inducing mitophagy and decreasing mitochondrial ROS.	Berberine	0-9	NLR family pyrin domain containing 3	Homo sapiens	47-52
32272506-0	2020	Berberine suppresses influenza virus-triggered NLRP3 inflammasome activation in macrophages by inducing mitophagy and decreasing mitochondrial ROS.	ros	143-146	NLR family pyrin domain containing 3	Homo sapiens	47-52
32272506-4	2020	This study focuses on the reactive oxygen species-Nod-like receptor protein 3 (ROS-NLRP3) pathway to investigate whether BBR inhibits NLRP3 inflammasome activation by inducing mitophagy.	Berberine	121-124	NLR family pyrin domain containing 3	Homo sapiens	83-88
32272506-4	2020	This study focuses on the reactive oxygen species-Nod-like receptor protein 3 (ROS-NLRP3) pathway to investigate whether BBR inhibits NLRP3 inflammasome activation by inducing mitophagy.	Berberine	121-124	NLR family pyrin domain containing 3	Homo sapiens	134-139
32272506-5	2020	Our results demonstrate that BBR and mitochondrion-targeted superoxide dismutase mimetic (Mito-TEMPO; a specific mitochondrial ROS scavenger) significantly restricted NLRP3 inflammasome activation, increased mitochondrial membrane potential (MMP), and decreased mitochondrial ROS (mtROS) generation in J774A.1 macrophages infected with PR8 influenza virus.	ros	127-130	NLR family pyrin domain containing 3	Homo sapiens	167-172
32272506-8	2020	However, 3-methyladenine, an autophagy inhibitor, reversed the inhibitory effects of BBR on mitochondrial damage and NLRP3 inflammasome activation in influenza virus-infected macrophages, indicating the involvement of mitophagy in mediating the inhibitory effects of BBR on NLRP3 inflammasome activation.	3-methyladenine	9-24	NLR family pyrin domain containing 3	Homo sapiens	117-122
32272506-8	2020	However, 3-methyladenine, an autophagy inhibitor, reversed the inhibitory effects of BBR on mitochondrial damage and NLRP3 inflammasome activation in influenza virus-infected macrophages, indicating the involvement of mitophagy in mediating the inhibitory effects of BBR on NLRP3 inflammasome activation.	3-methyladenine	9-24	NLR family pyrin domain containing 3	Homo sapiens	274-279
32272506-8	2020	However, 3-methyladenine, an autophagy inhibitor, reversed the inhibitory effects of BBR on mitochondrial damage and NLRP3 inflammasome activation in influenza virus-infected macrophages, indicating the involvement of mitophagy in mediating the inhibitory effects of BBR on NLRP3 inflammasome activation.	Berberine	85-88	NLR family pyrin domain containing 3	Homo sapiens	274-279
32272506-11	2020	Taken together, these findings suggest that restricting NLRP3 inflammasome activation by decreasing ROS generation through mitophagy induction may be crucial for the BBR-mediated alleviation of influenza virus-induced inflammatory lesions.	ros	100-103	NLR family pyrin domain containing 3	Homo sapiens	56-61
32272506-11	2020	Taken together, these findings suggest that restricting NLRP3 inflammasome activation by decreasing ROS generation through mitophagy induction may be crucial for the BBR-mediated alleviation of influenza virus-induced inflammatory lesions.	Berberine	166-169	NLR family pyrin domain containing 3	Homo sapiens	56-61
32054994-12	2020	Enhanced expression of TNF and the activation of NLRP3 and CASP1 followed by the increased generation of IL-1beta and nuclear translocation of the NF-kappabeta transcription factor occurred in response to hemoglobin-derived peptides, and ferryl hemoglobin in endothelium was upregulated in both pathologies.	ferryl iron	238-244	NLR family pyrin domain containing 3	Homo sapiens	49-54
32446726-4	2020	In this study, we investigated the renal protective effects of A68930, a specific agonist for the D-1 dopamine receptor (DRD1), which was recently recognized to downregulate NLRP3 inflammasome via DRD1 signaling.	A 68930	63-69	NLR family pyrin domain containing 3	Homo sapiens	174-179
32446726-4	2020	In this study, we investigated the renal protective effects of A68930, a specific agonist for the D-1 dopamine receptor (DRD1), which was recently recognized to downregulate NLRP3 inflammasome via DRD1 signaling.	Dopamine	102-110	NLR family pyrin domain containing 3	Homo sapiens	174-179
32446726-9	2020	In summary, our results demonstrated that activation of DRD1 by A68930 inhibited renal and systematic inflammation, and improved kidney function in I/R induced AKI model, which was probably related to the inhibition of the NLRP3 inflammasome activation.	A 68930	64-70	NLR family pyrin domain containing 3	Homo sapiens	223-228
32616234-0	2020	Ammonia induce lung tissue injury in broilers by activating NLRP3 inflammasome via Escherichia/Shigella.	Ammonia	0-7	NLR family pyrin domain containing 3	Homo sapiens	60-65
32323100-2	2020	In the progression of AP, the function of nucleotide-binding oligomerization, leucine-rich repeat and pyrin domain domains-containing protein 3 (NLRP3) inflammasome has been revealed.	Leucine	78-85	NLR family pyrin domain containing 3	Homo sapiens	145-150
32323100-8	2020	We found that co-treatment with LPS and ATP increased the secretion of IL-1beta and expression of NLRP3 in HPDLFs, while TRIM31 overexpression could reverse these effects caused by LPS and ATP.	Adenosine Triphosphate	40-43	NLR family pyrin domain containing 3	Homo sapiens	98-103
32616234-6	2020	After 7-D ammonia exposure, the proportion of the phylum Proteobacteria and the genus Escherichia/Shigella in lung tissue was significantly increased, the expression levels of NLRP3 and caspase-1 mRNA were significantly increased, and the content of IL-1beta in lung tissue and serum was higher than that in the control group.	Ammonia	10-17	NLR family pyrin domain containing 3	Homo sapiens	176-181
32616234-7	2020	In conclusion, high ammonia induced lung tissue inflammation via increasing the proportion of Escherichia/Shigella, activating NLRP3 inflammasome, and promoting IL-1beta release.	Ammonia	20-27	NLR family pyrin domain containing 3	Homo sapiens	127-132
32855848-2	2020	Lamivudine (3TC) is a nucleoside analog reverse transcriptase inhibitor known to inhibit the NLRP3 inflammasome.	Lamivudine	0-10	NLR family pyrin domain containing 3	Homo sapiens	93-98
32413745-9	2020	Concordantly, we observed a significantly elevated level of serum IL-1beta, which indicates an increase of NLRP3 inflammasome activity associated with the reduced level of serum melatonin, in heroin-addicted patients relative to healthy individuals.	Heroin	192-198	NLR family pyrin domain containing 3	Homo sapiens	107-112
32321163-0	2020	Topical application of the antimicrobial agent triclosan induces NLRP3 inflammasome activation and mitochondrial dysfunction.	Triclosan	47-56	NLR family pyrin domain containing 3	Homo sapiens	65-70
32321163-3	2020	Mechanistic studies have identified triclosan as a mitochondrial uncoupler; recent studies suggest that mitochondria play an important role in immune cell function and are involved in activation of the NLRP3 inflammasome.	Triclosan	36-45	NLR family pyrin domain containing 3	Homo sapiens	202-207
32855848-2	2020	Lamivudine (3TC) is a nucleoside analog reverse transcriptase inhibitor known to inhibit the NLRP3 inflammasome.	Lamivudine	12-15	NLR family pyrin domain containing 3	Homo sapiens	93-98
32855848-2	2020	Lamivudine (3TC) is a nucleoside analog reverse transcriptase inhibitor known to inhibit the NLRP3 inflammasome.	Nucleosides	22-32	NLR family pyrin domain containing 3	Homo sapiens	93-98
32374168-0	2020	Inhibitory Effect of Cannabidiol on the Activation of NLRP3 Inflammasome Is Associated with Its Modulation of the P2X7 Receptor in Human Monocytes.	Cannabidiol	21-32	NLR family pyrin domain containing 3	Homo sapiens	54-59
32374168-1	2020	Cannabidiol (CBD), a phytocannabinoid, has been reported to have anti-inflammatory effects associated with NLRP3 inflammasome activation, but its mechanism of anti-inflammasome action remains unclear.	Cannabidiol	0-11	NLR family pyrin domain containing 3	Homo sapiens	107-112
32374168-1	2020	Cannabidiol (CBD), a phytocannabinoid, has been reported to have anti-inflammatory effects associated with NLRP3 inflammasome activation, but its mechanism of anti-inflammasome action remains unclear.	Cannabidiol	13-16	NLR family pyrin domain containing 3	Homo sapiens	107-112
32374168-1	2020	Cannabidiol (CBD), a phytocannabinoid, has been reported to have anti-inflammatory effects associated with NLRP3 inflammasome activation, but its mechanism of anti-inflammasome action remains unclear.	phytocannabinoid	21-37	NLR family pyrin domain containing 3	Homo sapiens	107-112
32374168-2	2020	Herein, we report CBD"s effect on NLRP3 inflammasome activation and its modulation of P2X7, an inflammasome activation-related receptor, in human THP-1 monocytes.	Cannabidiol	18-21	NLR family pyrin domain containing 3	Homo sapiens	34-39
32374168-6	2020	Overall, the observed CBD suppressive effect on NLRP3 inflammasome activation in THP-1 monocytes was associated with decreased potassium efflux, as well as in silico prediction of P2X7 receptor binding.	Potassium	127-136	NLR family pyrin domain containing 3	Homo sapiens	48-53
32374168-7	2020	CBD inhibitory effects on the NLRP3 inflammasome may contribute to the overall anti-inflammatory effects reported for this phytocannabinoid.	Cannabidiol	0-3	NLR family pyrin domain containing 3	Homo sapiens	30-35
32374168-7	2020	CBD inhibitory effects on the NLRP3 inflammasome may contribute to the overall anti-inflammatory effects reported for this phytocannabinoid.	phytocannabinoid	123-139	NLR family pyrin domain containing 3	Homo sapiens	30-35
32200003-6	2020	Additionally, pretreatment with MCC950, a specific small-molecule inhibitor of the NLRP3 inflammasome, yielded a protective effect on cellular viability that was comparable to that of hypothermia treatment.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	32-38	NLR family pyrin domain containing 3	Homo sapiens	83-88
32576967-6	2020	OR analysis showed that the TC rs34298354 genotype in NLRP3 was associated with reduced risk of TB.	Technetium	28-30	NLR family pyrin domain containing 3	Homo sapiens	54-59
32101829-3	2020	Previously, we reported that PA stimulated IL-1beta secretion via activation of NLRP3 inflammasome in human placental cells.	Palmitic Acid	29-31	NLR family pyrin domain containing 3	Homo sapiens	80-85
32101829-4	2020	These observations led us to hypothesize that higher levels of PA induce NLRP3 inflammasome activation and placental inflammation, resulting in pregnancy complications.	Palmitic Acid	63-65	NLR family pyrin domain containing 3	Homo sapiens	73-78
32647690-0	2020	Polydatin relieves paraquat-induced human MRC-5 fibroblast injury through inhibiting the activation of the NLRP3 inflammasome.	polydatin	0-9	NLR family pyrin domain containing 3	Homo sapiens	107-112
32647690-0	2020	Polydatin relieves paraquat-induced human MRC-5 fibroblast injury through inhibiting the activation of the NLRP3 inflammasome.	Paraquat	19-27	NLR family pyrin domain containing 3	Homo sapiens	107-112
32647690-11	2020	Conclusions: PD can relieve PQ-induced human MRC-5 fibroblasts injury by reducing the inflammatory response, improving the antioxidant stress capacity, and inhibiting the activation of the NLRP3 inflammasome.	Paraquat	28-30	NLR family pyrin domain containing 3	Homo sapiens	189-194
32432601-0	2020	Pelargonidin ameliorates CCl4-induced liver fibrosis by suppressing the ROS-NLRP3-IL-1beta axis via activating the Nrf2 pathway.	ros	72-75	NLR family pyrin domain containing 3	Homo sapiens	76-81
32516127-0	2020	LncRNA ADAMTS9-AS2 inhibits gastric cancer (GC) development and sensitizes chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis.	Cisplatin	102-111	NLR family pyrin domain containing 3	Homo sapiens	137-142
32516127-7	2020	Furthermore, LncRNA ADAMTS9-AS2 increased NLRP3 expressions by targeting miR-223-3p, and upregulation of LncRNA ADAMTS9-AS2 triggered pyroptotic cell death in cisplatin treated CR-GC cells by activating NLRP3 inflammasome through downregulating miR-223-3p.	Cisplatin	159-168	NLR family pyrin domain containing 3	Homo sapiens	42-47
32516127-7	2020	Furthermore, LncRNA ADAMTS9-AS2 increased NLRP3 expressions by targeting miR-223-3p, and upregulation of LncRNA ADAMTS9-AS2 triggered pyroptotic cell death in cisplatin treated CR-GC cells by activating NLRP3 inflammasome through downregulating miR-223-3p.	Cisplatin	159-168	NLR family pyrin domain containing 3	Homo sapiens	203-208
32516127-9	2020	Collectively, LncRNA ADAMTS9-AS2 acted as a tumor suppressor and enhanced cisplatin sensitivity in GC cells by activating NLRP3 mediated pyroptotic cell death through sponging miR-223-3p.	Cisplatin	74-83	NLR family pyrin domain containing 3	Homo sapiens	122-127
31765230-0	2020	Black Carbon Induces Cytotoxicity and NLRP3 Inflammasome Activation in Human Corneal Epithelial Cells.	Carbon	6-12	NLR family pyrin domain containing 3	Homo sapiens	38-43
32241426-0	2020	The effect of doxycycline-containing chitosan/carboxymethyl chitosan nanoparticles on NLRP3 inflammasome in periodontal disease.	Doxycycline	14-25	NLR family pyrin domain containing 3	Homo sapiens	86-91
32241426-6	2020	Dox:CS/CMCS-NPs effectively down-regulated both gene and protein levels of NLRP3 inflammasome and IL-1beta in HGFs.	Doxycycline	0-3	NLR family pyrin domain containing 3	Homo sapiens	75-80
32289583-0	2020	Elevated expression of AhR and NLRP3 link polycyclic aromatic hydrocarbon exposure to cytokine storm in preschool children.	Polycyclic Aromatic Hydrocarbons	42-73	NLR family pyrin domain containing 3	Homo sapiens	31-36
32289583-11	2020	After adjusting for age, gender, BMI, family income, parental education level, and second-hand smoke exposure, we found that increased PAH exposure was associated with higher AhR and NLRP3 expression and elevated IL-4, IL-10, IL-12p70, IL-18, IL-22, IL-23, TNF-alpha, and IFN-gamma levels.	Polycyclic Aromatic Hydrocarbons	135-138	NLR family pyrin domain containing 3	Homo sapiens	183-188
32289583-12	2020	The associations between PAH exposure and IL-1beta, IL-18, IFN-gamma, and TNF-beta were mediated by NLRP3 expression, and the relationships between PAH exposure and IL-4, IL-10, IL-12p70, IL-22, IL-23, and TNF-alpha were mediated by AhR expression.	Polycyclic Aromatic Hydrocarbons	25-28	NLR family pyrin domain containing 3	Homo sapiens	100-105
32289583-13	2020	CONCLUSIONS: Our findings suggest that the association between PAH exposure and a cytokine storm may be mediated by AhR and NLRP3 expression among preschoolers.	Polycyclic Aromatic Hydrocarbons	63-66	NLR family pyrin domain containing 3	Homo sapiens	124-129
31267381-11	2020	Moreover, we found that miR-135a reversed the effects of DANCR in the promoting of pancreatic cancer cells, which was achieved by regulating the downstream protein of NLRP3.	mir-135a	24-32	NLR family pyrin domain containing 3	Homo sapiens	167-172
31900828-0	2020	Nicotinamide Phosphoribosyl Transferase Controls NLRP3 Inflammasome Activity Through MAPK and NF-kappaB Signaling in Nucleus Pulposus Cells, as Suppressed by Melatonin.	Melatonin	158-167	NLR family pyrin domain containing 3	Homo sapiens	49-54
31900828-8	2020	Herein, real-time PCR, western blot analysis, and immunofluorescence staining experiments revealed that melatonin showed protective effects against TNF-alpha-induced matrix degradation by downregulating NAMPT and reducing NLRP3 inflammasome activity in NP cells.	Melatonin	104-113	NLR family pyrin domain containing 3	Homo sapiens	222-227
31900828-9	2020	The current investigation verified that melatonin could alleviate matrix degradation induced by TNF-alpha by suppressing NAMPT and NLRP3 inflammasome activity.	Melatonin	40-49	NLR family pyrin domain containing 3	Homo sapiens	131-136
32249647-0	2020	Laquinimod inhibits MMP+ induced NLRP3 inflammasome activation in human neuronal cells.	laquinimod	0-10	NLR family pyrin domain containing 3	Homo sapiens	33-38
32249647-3	2020	This study aims to investigate whether laquinimod possessesa protective effect against MPP+-induced NLRP3 activation.Materials and methods: In a variety of tests on human SH-SY5Y neuronal cells, 1-methyl-4-phenyl Pyridine (MPP+) was used to mimic the microenvironment of PD.	laquinimod	39-49	NLR family pyrin domain containing 3	Homo sapiens	100-105
32249647-3	2020	This study aims to investigate whether laquinimod possessesa protective effect against MPP+-induced NLRP3 activation.Materials and methods: In a variety of tests on human SH-SY5Y neuronal cells, 1-methyl-4-phenyl Pyridine (MPP+) was used to mimic the microenvironment of PD.	mangion-purified polysaccharide (Candida albicans)	87-91	NLR family pyrin domain containing 3	Homo sapiens	100-105
32249647-4	2020	Activation of NLRP3 inflammasome was measured by western blot analysis and enzyme linked immunosorbent assay (ELISA).Results: Laquinimod had a significant protective impact against MPP+-induced neurotoxicity.	mangion-purified polysaccharide (Candida albicans)	181-185	NLR family pyrin domain containing 3	Homo sapiens	14-19
32249647-6	2020	Importantly, treatment with laquinimod significantly inhibited the activation of the NLRP3 inflammasome by reducing the levels of its components, including NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved caspase 1 (P10).	laquinimod	28-38	NLR family pyrin domain containing 3	Homo sapiens	85-90
32249647-6	2020	Importantly, treatment with laquinimod significantly inhibited the activation of the NLRP3 inflammasome by reducing the levels of its components, including NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved caspase 1 (P10).	laquinimod	28-38	NLR family pyrin domain containing 3	Homo sapiens	156-161
32249647-10	2020	Inhibition of SIRT1 abolished the protective effects of laquinimod against the activation of the NLRP3 inflammasome, suggesting the involvement of SIRT1 in this process.Conclusion: These findings suggest that laquinimod treatment might be a possible therapeutic strategy for neuroinflammation in PD.	laquinimod	56-66	NLR family pyrin domain containing 3	Homo sapiens	97-102
32249647-10	2020	Inhibition of SIRT1 abolished the protective effects of laquinimod against the activation of the NLRP3 inflammasome, suggesting the involvement of SIRT1 in this process.Conclusion: These findings suggest that laquinimod treatment might be a possible therapeutic strategy for neuroinflammation in PD.	laquinimod	209-219	NLR family pyrin domain containing 3	Homo sapiens	97-102
32695290-0	2020	Soluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells.	Uric Acid	8-17	NLR family pyrin domain containing 3	Homo sapiens	48-53
32695290-12	2020	Results: We found soluble uric acid alone increased the release of ROS, depolarized the mitochondrial membrane potential, up-regulated TSPO, increased the expression of TLR4 and NLRP3, and then activated NLRP3 inflammasome and NF-kappaB signaling, which further resulted in lower expression of tight junction protein and exerted adverse effects on intestinal epithelial cells.	Uric Acid	26-35	NLR family pyrin domain containing 3	Homo sapiens	178-183
32695290-12	2020	Results: We found soluble uric acid alone increased the release of ROS, depolarized the mitochondrial membrane potential, up-regulated TSPO, increased the expression of TLR4 and NLRP3, and then activated NLRP3 inflammasome and NF-kappaB signaling, which further resulted in lower expression of tight junction protein and exerted adverse effects on intestinal epithelial cells.	Uric Acid	26-35	NLR family pyrin domain containing 3	Homo sapiens	204-209
32695290-13	2020	Furthermore, the elevated IL-1beta could be restored by silencing of TLR4, indicating soluble uric acid induces inflammation via the TLR4/NLRP3 pathway.	Uric Acid	94-103	NLR family pyrin domain containing 3	Homo sapiens	138-143
32695290-14	2020	Conclusion: Soluble uric acid exerted detrimental effect on intestinal epithelial cells through the TLR4/NLRP3 pathway.	Uric Acid	20-29	NLR family pyrin domain containing 3	Homo sapiens	105-110
32125791-0	2020	Prefrontal cortex infusion of beta-hydroxybutyrate, an endogenous NLRP3 inflammasome inhibitor, produces antidepressant-like effects in a rodent model of depression.	3-Hydroxybutyric Acid	30-50	NLR family pyrin domain containing 3	Homo sapiens	66-71
32298723-9	2020	In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression.	TEPP-46	49-56	NLR family pyrin domain containing 3	Homo sapiens	177-182
32298723-9	2020	In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression.	Glucose	90-97	NLR family pyrin domain containing 3	Homo sapiens	177-182
32298723-9	2020	In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression.	Glucose	107-114	NLR family pyrin domain containing 3	Homo sapiens	177-182
32469177-2	2020	The aim of this study was to identify the mechanism by which ethanol affects uric acid-induced NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation by regulation of aryl hydrocarbon receptor (AhR) and thioredoxin-interacting protein (TXNIP).	Uric Acid	77-86	NLR family pyrin domain containing 3	Homo sapiens	95-131
31839209-7	2020	Also, allopurinol blocks the stimulating effects of thioredoxin-interacting protein and interacts directly with the redox-active domain of thioredoxin as a negative regulator, decreasing NLRP3 activation.	Allopurinol	6-17	NLR family pyrin domain containing 3	Homo sapiens	187-192
32469177-0	2020	Ethanol Augments Monosodium Urate-Induced NLRP3 Inflammasome Activation via Regulation of AhR and TXNIP in Human Macrophages.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	42-47
32469177-0	2020	Ethanol Augments Monosodium Urate-Induced NLRP3 Inflammasome Activation via Regulation of AhR and TXNIP in Human Macrophages.	Uric Acid	17-33	NLR family pyrin domain containing 3	Homo sapiens	42-47
32469177-2	2020	The aim of this study was to identify the mechanism by which ethanol affects uric acid-induced NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation by regulation of aryl hydrocarbon receptor (AhR) and thioredoxin-interacting protein (TXNIP).	Uric Acid	77-86	NLR family pyrin domain containing 3	Homo sapiens	133-138
32469177-2	2020	The aim of this study was to identify the mechanism by which ethanol affects uric acid-induced NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation by regulation of aryl hydrocarbon receptor (AhR) and thioredoxin-interacting protein (TXNIP).	Ethanol	61-68	NLR family pyrin domain containing 3	Homo sapiens	95-131
32469177-2	2020	The aim of this study was to identify the mechanism by which ethanol affects uric acid-induced NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation by regulation of aryl hydrocarbon receptor (AhR) and thioredoxin-interacting protein (TXNIP).	Ethanol	61-68	NLR family pyrin domain containing 3	Homo sapiens	133-138
32469177-3	2020	MATERIALS AND METHODS: Human myeloid leukemia cells (U937 cells) were used to assess the role of ethanol in NLRP3 inflammasome activation induced by monosodium urate (MSU) crystals.	Ethanol	97-104	NLR family pyrin domain containing 3	Homo sapiens	108-113
32469177-3	2020	MATERIALS AND METHODS: Human myeloid leukemia cells (U937 cells) were used to assess the role of ethanol in NLRP3 inflammasome activation induced by monosodium urate (MSU) crystals.	Uric Acid	149-165	NLR family pyrin domain containing 3	Homo sapiens	108-113
32469177-3	2020	MATERIALS AND METHODS: Human myeloid leukemia cells (U937 cells) were used to assess the role of ethanol in NLRP3 inflammasome activation induced by monosodium urate (MSU) crystals.	Uric Acid	167-170	NLR family pyrin domain containing 3	Homo sapiens	108-113
32469177-5	2020	The effect of ethanol-induced TXNIP on the NLRP3 inflammasome was assessed in human macrophages transfected with TXNIP siRNA.	Ethanol	14-21	NLR family pyrin domain containing 3	Homo sapiens	43-48
32469177-6	2020	RESULTS: U937 cells treated with 100 mM ethanol for 24 h induced NLRP3 and interleukin (IL)-1beta expression.	Ethanol	40-47	NLR family pyrin domain containing 3	Homo sapiens	65-70
32469177-9	2020	Treatment with ethanol increased NLRP3 and IL-1beta mRNA and protein expression in U937 cells exposed to 1.0 mg/mL of MSU crystals for 24 h. TXNIP expression in U937 cells incubated with both 100 mM ethanol and 1.0 mg/mL of MSU crystals was significantly higher than in cells incubated with MSU crystals alone.	Ethanol	15-22	NLR family pyrin domain containing 3	Homo sapiens	33-38
32469177-9	2020	Treatment with ethanol increased NLRP3 and IL-1beta mRNA and protein expression in U937 cells exposed to 1.0 mg/mL of MSU crystals for 24 h. TXNIP expression in U937 cells incubated with both 100 mM ethanol and 1.0 mg/mL of MSU crystals was significantly higher than in cells incubated with MSU crystals alone.	Uric Acid	118-121	NLR family pyrin domain containing 3	Homo sapiens	33-38
32469177-10	2020	Treatment with 100mM ethanol for 24 h downregulated NLRP3 and IL-1beta expression in MSU crystal-activated U937 cells transfected with TXNIP siRNA, compared to those with scramble siRNA.	Ethanol	21-28	NLR family pyrin domain containing 3	Homo sapiens	52-57
32469177-11	2020	CONCLUSION: Ethanol stimulates uric acid-induced NLRP3 inflammasome activation through regression of AhR and upregulation of TXNIP.	Ethanol	12-19	NLR family pyrin domain containing 3	Homo sapiens	49-54
32469177-11	2020	CONCLUSION: Ethanol stimulates uric acid-induced NLRP3 inflammasome activation through regression of AhR and upregulation of TXNIP.	Uric Acid	31-40	NLR family pyrin domain containing 3	Homo sapiens	49-54
32546974-0	2020	Epigallocatechin-3-Gallate Protects H2O2-Induced Nucleus Pulposus Cell Apoptosis and Inflammation by Inhibiting cGAS/Sting/NLRP3 Activation.	epigallocatechin gallate	0-26	NLR family pyrin domain containing 3	Homo sapiens	123-128
32546974-0	2020	Epigallocatechin-3-Gallate Protects H2O2-Induced Nucleus Pulposus Cell Apoptosis and Inflammation by Inhibiting cGAS/Sting/NLRP3 Activation.	Hydrogen Peroxide	36-40	NLR family pyrin domain containing 3	Homo sapiens	123-128
32546974-10	2020	Advanced in-vitro study showed that H2O2 significantly increased the expression of cGAS, Sting and NLRP3 protein levels.	Hydrogen Peroxide	36-40	NLR family pyrin domain containing 3	Homo sapiens	99-104
32546974-11	2020	Advanced experiments showed that EGCG treatment demonstrated significant protective effects in cell viability, apoptosis, cell cycle arrest and inflammatory status through down-regulation of cGAS/Sting/NLRP3 pathway.	epigallocatechin gallate	33-37	NLR family pyrin domain containing 3	Homo sapiens	202-207
32546974-13	2020	Our findings also suggest that EGCG treatment would provide anti-apoptosis, anti-inflammation and promote cell viability in H2O2 treatment-incubated NPCs through inhibiting cGAS/Sting/NLRP3 pathway.	epigallocatechin gallate	31-35	NLR family pyrin domain containing 3	Homo sapiens	184-189
32546974-13	2020	Our findings also suggest that EGCG treatment would provide anti-apoptosis, anti-inflammation and promote cell viability in H2O2 treatment-incubated NPCs through inhibiting cGAS/Sting/NLRP3 pathway.	Hydrogen Peroxide	124-128	NLR family pyrin domain containing 3	Homo sapiens	184-189
32508821-7	2020	NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption.	Adenosine Triphosphate	58-61	NLR family pyrin domain containing 3	Homo sapiens	0-5
32466385-0	2020	Progesterone Attenuates Stress-Induced NLRP3 Inflammasome Activation and Enhances Autophagy following Ischemic Brain Injury.	Progesterone	0-12	NLR family pyrin domain containing 3	Homo sapiens	39-44
32466385-12	2020	Treatment with PROG reduced HMGB1 release and NLRP3 inflammasome activation, and enhanced autophagy in stressed and unstressed ischemic animals.	Progesterone	15-19	NLR family pyrin domain containing 3	Homo sapiens	46-51
32450899-15	2020	Uncoupled hemichannels permit the release of adenosine triphosphate (ATP) in to the extracellular space ( [ATP]e), where ATP binds to the P2X7 purinoreceptor and activates the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome.	Adenosine	45-54	NLR family pyrin domain containing 3	Homo sapiens	254-259
32450899-15	2020	Uncoupled hemichannels permit the release of adenosine triphosphate (ATP) in to the extracellular space ( [ATP]e), where ATP binds to the P2X7 purinoreceptor and activates the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome.	Adenosine Triphosphate	69-72	NLR family pyrin domain containing 3	Homo sapiens	254-259
32450899-15	2020	Uncoupled hemichannels permit the release of adenosine triphosphate (ATP) in to the extracellular space ( [ATP]e), where ATP binds to the P2X7 purinoreceptor and activates the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome.	Adenosine Triphosphate	107-110	NLR family pyrin domain containing 3	Homo sapiens	254-259
32450899-15	2020	Uncoupled hemichannels permit the release of adenosine triphosphate (ATP) in to the extracellular space ( [ATP]e), where ATP binds to the P2X7 purinoreceptor and activates the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome.	Adenosine Triphosphate	107-110	NLR family pyrin domain containing 3	Homo sapiens	254-259
32450899-15	2020	Uncoupled hemichannels permit the release of adenosine triphosphate (ATP) in to the extracellular space ( [ATP]e), where ATP binds to the P2X7 purinoreceptor and activates the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome.	Leucine	206-213	NLR family pyrin domain containing 3	Homo sapiens	254-259
32439949-0	2020	High glucose mediates NLRP3 inflammasome activation via upregulation of ELF3 expression.	Glucose	5-12	NLR family pyrin domain containing 3	Homo sapiens	22-27
32439949-3	2020	We hypothesized that ELF3 modulates MARK4 expression in vascular endothelial cells, thus contributing to high glucose-mediated NLRP3 inflammasome activation.	Glucose	110-117	NLR family pyrin domain containing 3	Homo sapiens	127-132
32439949-5	2020	An in vitro study indicated that high glucose increased IL-1beta and IL-18 expression and activated the NLRP3 inflammasome via upregulation of MARK4 in human umbilical vein endothelial cells (HUVECs).	Glucose	38-45	NLR family pyrin domain containing 3	Homo sapiens	104-109
32449901-12	2020	Besides, roflumilast inhibited the activation of NLRP3 (nucleotide-binding domain (NOD)-like receptor protein 3) and NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells).	Roflumilast	9-20	NLR family pyrin domain containing 3	Homo sapiens	49-54
32151746-0	2020	Disulfiram suppresses NLRP3 inflammasome activation to treat peritoneal and gouty inflammation.	Disulfiram	0-10	NLR family pyrin domain containing 3	Homo sapiens	22-27
32151746-5	2020	In this study, we identified disulfiram (DSF), an old marketed drug as a treatment for alcoholism, could effectively inhibit NLRP3 inflammasome activation and suppress pyroptotic cell death.	Disulfiram	29-39	NLR family pyrin domain containing 3	Homo sapiens	125-130
32151746-5	2020	In this study, we identified disulfiram (DSF), an old marketed drug as a treatment for alcoholism, could effectively inhibit NLRP3 inflammasome activation and suppress pyroptotic cell death.	Disulfiram	41-44	NLR family pyrin domain containing 3	Homo sapiens	125-130
32508821-7	2020	NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption.	Reactive Oxygen Species	63-86	NLR family pyrin domain containing 3	Homo sapiens	0-5
32508821-7	2020	NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption.	Reactive Oxygen Species	88-91	NLR family pyrin domain containing 3	Homo sapiens	0-5
32508821-7	2020	NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption.	Potassium	94-103	NLR family pyrin domain containing 3	Homo sapiens	0-5
32508821-7	2020	NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption.	Calcium	112-119	NLR family pyrin domain containing 3	Homo sapiens	0-5
32423023-1	2020	The NLRP3 (nucleotide-binding domain, leucine-rich-repeat-containing family, pyrin domain-containing 3) inflammasome senses pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), and activates caspase-1, which provokes release of proinflammatory cytokines such as interleukin-1beta (IL-1beta) and IL-18 as well as pyroptosis to engage in innate immune defense.	Leucine	38-45	NLR family pyrin domain containing 3	Homo sapiens	4-9
32423023-6	2020	Lipid perturbation and cholesterol trafficking to the ER activate the NLRP3 inflammasome.	Cholesterol	23-34	NLR family pyrin domain containing 3	Homo sapiens	70-75
32088265-4	2020	Chloroquine and hydroxychloroquine increased IL-1beta-induced CXCL8 secretion in macrophages which was critically dependent on the lysosomotropic character and inhibition of macroautophagy but independent from the NLRP3 inflammasome.	Chloroquine	0-11	NLR family pyrin domain containing 3	Homo sapiens	214-219
32435622-0	2020	Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome.	caffeic acid phenethyl ester	0-28	NLR family pyrin domain containing 3	Homo sapiens	78-83
32435622-6	2020	We found that CAPE decreased NLRP3 inflammasome activation in BMDMs and THP-1 cells and protected mice from colorectal cancer induced by AOM/DSS.	caffeic acid phenethyl ester	14-18	NLR family pyrin domain containing 3	Homo sapiens	29-34
32194260-0	2020	Tumor Necrosis Factor Primes and Metal Particles Activate the NLRP3 Inflammasome in Human Primary Macrophages.	Metals	33-38	NLR family pyrin domain containing 3	Homo sapiens	62-67
32088265-4	2020	Chloroquine and hydroxychloroquine increased IL-1beta-induced CXCL8 secretion in macrophages which was critically dependent on the lysosomotropic character and inhibition of macroautophagy but independent from the NLRP3 inflammasome.	Hydroxychloroquine	16-34	NLR family pyrin domain containing 3	Homo sapiens	214-219
32282893-6	2020	Functional experiments at baseline measuring apoptosis-associated speck-like protein containing a CARD (ASC) speck formation showed that the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome was overactive in monocytes from patients with primary progressive multiple sclerosis, and canonical NLRP3 inflammasome activation with a combination of ATP plus lipopolysaccharide was associated with increased IL1B production in this group of patients.	Leucine	145-152	NLR family pyrin domain containing 3	Homo sapiens	197-202
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	28-35	NLR family pyrin domain containing 3	Homo sapiens	103-108
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	173-180	NLR family pyrin domain containing 3	Homo sapiens	103-108
32317086-9	2020	Also, mRNA levels of tamoxifen-induced pyroptosis-related genes, IL-1beta, NLRP3, and procaspase-1, also decreased in the presence of sulfasalazine in RPE cells.	Tamoxifen	21-30	NLR family pyrin domain containing 3	Homo sapiens	75-80
32317086-9	2020	Also, mRNA levels of tamoxifen-induced pyroptosis-related genes, IL-1beta, NLRP3, and procaspase-1, also decreased in the presence of sulfasalazine in RPE cells.	Sulfasalazine	134-147	NLR family pyrin domain containing 3	Homo sapiens	75-80
32282893-6	2020	Functional experiments at baseline measuring apoptosis-associated speck-like protein containing a CARD (ASC) speck formation showed that the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome was overactive in monocytes from patients with primary progressive multiple sclerosis, and canonical NLRP3 inflammasome activation with a combination of ATP plus lipopolysaccharide was associated with increased IL1B production in this group of patients.	Adenosine Triphosphate	370-373	NLR family pyrin domain containing 3	Homo sapiens	197-202
32014690-7	2020	As expected, TDI-induced inflammatory cell death was significantly blocked by a specific NLRP3 inflammasome inhibitor.	Toluene 2,4-Diisocyanate	13-16	NLR family pyrin domain containing 3	Homo sapiens	89-94
32179281-2	2020	The results indicated that most bispiperazinochalcone derivatives displayed good inhibition of NO (IC50 < 20 muM) and low cytotoxicity (CC50 > 40 muM), and selectively inhibited the production of IL-1beta via inhibiting NLRP3 inflammasome activation, as promising candidate compounds for the treatment of NLRP3 inflammasome-driven diseases.	bispiperazinochalcone	32-53	NLR family pyrin domain containing 3	Homo sapiens	220-225
32179281-2	2020	The results indicated that most bispiperazinochalcone derivatives displayed good inhibition of NO (IC50 < 20 muM) and low cytotoxicity (CC50 > 40 muM), and selectively inhibited the production of IL-1beta via inhibiting NLRP3 inflammasome activation, as promising candidate compounds for the treatment of NLRP3 inflammasome-driven diseases.	bispiperazinochalcone	32-53	NLR family pyrin domain containing 3	Homo sapiens	305-310
32282893-6	2020	Functional experiments at baseline measuring apoptosis-associated speck-like protein containing a CARD (ASC) speck formation showed that the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome was overactive in monocytes from patients with primary progressive multiple sclerosis, and canonical NLRP3 inflammasome activation with a combination of ATP plus lipopolysaccharide was associated with increased IL1B production in this group of patients.	Leucine	145-152	NLR family pyrin domain containing 3	Homo sapiens	318-323
31714001-4	2020	Since glyburide (a specific inhibitor of K+ efflux channels) inhibited the transcription of NLRP3, IL-1beta, and IL-18, the role of K+ efflux in the activation of inflammasomes in APOL1 risk milieu was implicated.	Glyburide	6-15	NLR family pyrin domain containing 3	Homo sapiens	92-97
31943712-0	2020	Resveratrol protects human bronchial epithelial cells against nickel-induced toxicity via suppressing p38 MAPK, NF-kappaB signaling, and NLRP3 inflammasome activation.	resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	137-142
31943712-0	2020	Resveratrol protects human bronchial epithelial cells against nickel-induced toxicity via suppressing p38 MAPK, NF-kappaB signaling, and NLRP3 inflammasome activation.	Nickel	62-68	NLR family pyrin domain containing 3	Homo sapiens	137-142
32358544-0	2020	SGLT2 inhibition modulates NLRP3 inflammasome activity via ketones and insulin in diabetes with cardiovascular disease.	Ketones	59-66	NLR family pyrin domain containing 3	Homo sapiens	27-32
32156572-7	2020	Microbial derivatives, bacterial pore-forming toxins, extracellular ATP and other pathogen-associated molecular patterns trigger activation of NLRP3 inflammasomes.	Adenosine Triphosphate	68-71	NLR family pyrin domain containing 3	Homo sapiens	143-148
32156572-8	2020	Recent studies have reported that viroporin activity is capable of inducing inflammasome activity and production of IL-1beta, where NLRP3 is shown to be regulated by fluxes of K+, H+ and Ca2+ in addition to reactive oxygen species, autophagy and endoplasmic reticulum stress.	Reactive Oxygen Species	207-230	NLR family pyrin domain containing 3	Homo sapiens	132-137
33005902-0	2020	Dapansutrile, an oral selective NLRP3 inflammasome inhibitor, for treatment of gout flares: an open-label, dose-adaptive, proof-of-concept, phase 2a trial.	dapansutrile	0-12	NLR family pyrin domain containing 3	Homo sapiens	32-37
33005902-2	2020	Dapansutrile inhibits the NLRP3 inflammasome and subsequent activation of IL-1beta.	dapansutrile	0-12	NLR family pyrin domain containing 3	Homo sapiens	26-31
33005902-13	2020	Interpretation: Dapansutrile is a specific NLRP3 inflammasome inhibitor with a satisfactory safety profile and efficacy in the reduction of target joint pain in this study.	dapansutrile	16-28	NLR family pyrin domain containing 3	Homo sapiens	43-48
32358544-3	2020	Here we show the effect of SGLT2 inhibitor empagliflozin on NLRP3 inflammasome activity.	empagliflozin	43-56	NLR family pyrin domain containing 3	Homo sapiens	60-65
32320383-7	2020	The results showed that ROS induced the pyroptosis of NPCs and it depended on the expression of NLRP3 and PYCARD.	Reactive Oxygen Species	24-27	NLR family pyrin domain containing 3	Homo sapiens	96-101
32358544-6	2020	Ex vivo experiments with macrophages verify the inhibitory effects of high BHB and low insulin levels on NLRP3 inflammasome activation.	3-Hydroxybutyric Acid	75-78	NLR family pyrin domain containing 3	Homo sapiens	105-110
32410849-0	2020	Pioglitazone Metformin Complex Improves Polycystic Ovary Syndrome Comorbid Psychological Distress via Inhibiting NLRP3 Inflammasome Activation: A Prospective Clinical Study.	Pioglitazone	0-12	NLR family pyrin domain containing 3	Homo sapiens	113-118
32410849-0	2020	Pioglitazone Metformin Complex Improves Polycystic Ovary Syndrome Comorbid Psychological Distress via Inhibiting NLRP3 Inflammasome Activation: A Prospective Clinical Study.	Metformin	13-22	NLR family pyrin domain containing 3	Homo sapiens	113-118
32410849-11	2020	Conclusions: This study is the first to reveal that PM alleviates psychological distress via inhibiting NLRP3 inflammasome and improves several markers, including total testosterone.	Promethium	52-54	NLR family pyrin domain containing 3	Homo sapiens	104-109
32320383-9	2020	In summary, ROS induces the pyroptosis of NPCs through the NLRP3/ PYCARD pathway, and establishes negative regulation by increasing autophagy and NFE2L2.	Reactive Oxygen Species	12-15	NLR family pyrin domain containing 3	Homo sapiens	59-64
32330868-0	2020	Metformin protects against intestinal ischemia-reperfusion injury and cell pyroptosis via TXNIP-NLRP3-GSDMD pathway.	Metformin	0-9	NLR family pyrin domain containing 3	Homo sapiens	96-101
32330868-11	2020	Importantly, Metformin reduced pyroptosis-related proteins, including NLRP3, cleaved caspase-1, and the N-terminus of GSDMD.	Metformin	13-22	NLR family pyrin domain containing 3	Homo sapiens	70-75
32330868-13	2020	We also discovered that Metformin suppressed the expression of TXNIP and the interaction between TXNIP and NLRP3.	Metformin	24-33	NLR family pyrin domain containing 3	Homo sapiens	107-112
32330868-15	2020	In conclusion, we believe that Metformin protects against intestinal I/R injury in a TXNIP-NLRP3-GSDMD-dependent manner.	Metformin	31-40	NLR family pyrin domain containing 3	Homo sapiens	91-96
32420343-6	2020	Our data showed that high glucose induced NLRP3-caspase-1-GSDMD activation and pore formation in a dose- and time-dependent manner (p < 0.05) and resulted in the inflammatory cytokines IL-1beta and IL-18 and lactate dehydrogenase (LDH) release from HRPs (p < 0.05), which are all signs of HRP pyroptosis.	Glucose	26-33	NLR family pyrin domain containing 3	Homo sapiens	42-47
32420343-9	2020	Taken together, our results firstly revealed that high glucose induced the loss of retinal pericytes partly via NLRP3-caspase-1-GSDMD-mediated pyroptosis.	Glucose	55-62	NLR family pyrin domain containing 3	Homo sapiens	112-117
32331389-6	2020	The activation of the NLRP3 inflammasome requires the activation by extracellular adenosine tri-phosphate (ATP) of a specific purinergic receptor named P2X7 located in the target cells, although other pathways have been described.	Adenosine	82-91	NLR family pyrin domain containing 3	Homo sapiens	22-27
32331389-6	2020	The activation of the NLRP3 inflammasome requires the activation by extracellular adenosine tri-phosphate (ATP) of a specific purinergic receptor named P2X7 located in the target cells, although other pathways have been described.	Adenosine Triphosphate	107-110	NLR family pyrin domain containing 3	Homo sapiens	22-27
32252692-0	2020	Ripasudil alleviated the inflammation of RPE cells by targeting the miR-136-5p/ROCK/NLRP3 pathway.	K-115	0-9	NLR family pyrin domain containing 3	Homo sapiens	84-89
32313131-0	2020	Polymorphism of nucleotide binding domain-like receptor protein 3 (NLRP3) increases susceptibility of total urinary arsenic to renal cell carcinoma.	Arsenic	116-123	NLR family pyrin domain containing 3	Homo sapiens	67-72
32313131-13	2020	This study is the first to identify the modified effects of NLRP3 risk alleles involved in the association between arsenic and RCC risk in a population with low arsenic exposure.	Arsenic	115-122	NLR family pyrin domain containing 3	Homo sapiens	60-65
32313131-13	2020	This study is the first to identify the modified effects of NLRP3 risk alleles involved in the association between arsenic and RCC risk in a population with low arsenic exposure.	Arsenic	161-168	NLR family pyrin domain containing 3	Homo sapiens	60-65
32252692-11	2020	The levels of inflammation related proteins NLRP3, ASC, caspase1, IL-1beta and IL-18 was also inhibited after the treatment of ripasudil.	K-115	127-136	NLR family pyrin domain containing 3	Homo sapiens	44-49
32252692-13	2020	CONCLUSION: Ripasudil relieved the inflammatory injury of RPE cells by upregulating miR-136-5p, therefore inhibiting the expression of ROCK1, ROCK2, NLRP3, ASC, caspase1, IL-1beta and IL-18.	K-115	12-21	NLR family pyrin domain containing 3	Homo sapiens	149-154
32057583-0	2020	Discovery and optimization of 4-oxo-2-thioxo-thiazolidinones as NOD-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inhibitors.	Rhodanine	30-60	NLR family pyrin domain containing 3	Homo sapiens	131-136
31999304-5	2020	Cbl-b binds to the K63-ubiquitin chains attached to the NLRP3 leucine-rich repeat domain (LRR) via its ubiquitin-associated region (UBA) and then targets NLRP3 at K496 for K48-linked ubiquitination and proteasome-mediated degradation.	Leucine	62-69	NLR family pyrin domain containing 3	Homo sapiens	56-61
32410829-4	2020	In this study, we investigated the effects of hot water extract derived from the tendrils of C. moschata Duchesne (TCMD) on NLRP3 inflammasome activation in murine macrophages and human trophoblast cells.	Water	50-55	NLR family pyrin domain containing 3	Homo sapiens	124-129
32410829-5	2020	The TCMD treatment of LPS-primed bone marrow-derived macrophages (BMDMs) and human trophoblast cells attenuated NLRP3 inflammasome activation induced by inflammasome activators such as ATP, nigericin, and monosodium urate (MSU).	Adenosine Triphosphate	185-188	NLR family pyrin domain containing 3	Homo sapiens	112-117
32410829-5	2020	The TCMD treatment of LPS-primed bone marrow-derived macrophages (BMDMs) and human trophoblast cells attenuated NLRP3 inflammasome activation induced by inflammasome activators such as ATP, nigericin, and monosodium urate (MSU).	Nigericin	190-199	NLR family pyrin domain containing 3	Homo sapiens	112-117
32057583-0	2020	Discovery and optimization of 4-oxo-2-thioxo-thiazolidinones as NOD-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inhibitors.	MRT67307	96-101	NLR family pyrin domain containing 3	Homo sapiens	131-136
31758699-7	2020	Treating the HepG2 cells with NGN or NLRP3 inhibitor MCC950 reduced lipid accumulation, and NGN inhibited activation of NLRP3/NF-kappaB pathway stimulated by OA together with LPS.	naringenin	92-95	NLR family pyrin domain containing 3	Homo sapiens	120-125
32057583-3	2020	Cellular structure-activity relationship-guided optimization resulted in the identification of 4-oxo-2-thioxo-thiazolidinone derivative 9 as a selective and direct small-molecule inhibitor of NLRP3 with IC50 of 2.4 muM, possessing favorable ex vivo and in vivo pharmacokinetic properties.	Rhodanine	95-124	NLR family pyrin domain containing 3	Homo sapiens	192-197
31758699-7	2020	Treating the HepG2 cells with NGN or NLRP3 inhibitor MCC950 reduced lipid accumulation, and NGN inhibited activation of NLRP3/NF-kappaB pathway stimulated by OA together with LPS.	Oleic Acids	158-160	NLR family pyrin domain containing 3	Homo sapiens	120-125
32076940-9	2020	Our data indicate that SAL inhibit NLRP3-related pyroptosis, which might be the underlying mechanism of SAL anti-inflammatory in atherosclerosis.	rhodioloside	23-26	NLR family pyrin domain containing 3	Homo sapiens	35-40
31917290-9	2020	In addition, DEX suppressed the expression of taurine, TXNIP, NLRP3, ASC and cleaved caspase-1 and activated the expression of p-AMPK and p-GSK3beta.	Dexmedetomidine	13-16	NLR family pyrin domain containing 3	Homo sapiens	62-67
32028242-5	2020	And then through transcriptomes screening, a significant down-regulation of NLR pyrin domain containing 3 (Nlrp3), gasdermin D (Gsdmd), andinterleukin-1 beta (IL-1beta) expression were found after BA treatment.	baicalin	197-199	NLR family pyrin domain containing 3	Homo sapiens	107-112
32028242-6	2020	Further analysis confirmed that BA could decrease the levels of NLRP3 and GSDMD, as well as the release of IL-1beta and IL-18, resulting in the reduction of pyroptosis.	baicalin	32-34	NLR family pyrin domain containing 3	Homo sapiens	64-69
32028242-8	2020	In conclusion, BA can reduce pyroptosis of hepatocyte by blocking NLRP3-GSDMD signaling in vitro.	baicalin	15-17	NLR family pyrin domain containing 3	Homo sapiens	66-71
32076940-9	2020	Our data indicate that SAL inhibit NLRP3-related pyroptosis, which might be the underlying mechanism of SAL anti-inflammatory in atherosclerosis.	rhodioloside	104-107	NLR family pyrin domain containing 3	Homo sapiens	35-40
32132181-8	2020	Thus, AmB induced IL-1beta and IL-18 secretions, which are reduced by specific inhibitors of caspase activation (Q-VD) and NLRP3 activation (MCC950).	Amphotericin B	6-9	NLR family pyrin domain containing 3	Homo sapiens	123-128
31895698-4	2020	In mechanistic studies, we found that BTK binds to NLRP3 during the priming phase of inflammasome activation and in doing so inhibits LPS/nigericin-induced assembly of the NLRP3 inflammasome during the activation phase of inflammasome activation.	Nigericin	138-147	NLR family pyrin domain containing 3	Homo sapiens	51-56
31895698-4	2020	In mechanistic studies, we found that BTK binds to NLRP3 during the priming phase of inflammasome activation and in doing so inhibits LPS/nigericin-induced assembly of the NLRP3 inflammasome during the activation phase of inflammasome activation.	Nigericin	138-147	NLR family pyrin domain containing 3	Homo sapiens	172-177
31895698-5	2020	This inhibitory effect was caused by BTK inhibition of PP2A-mediated dephosphorylation of Ser5 in the pyrin domain of NLRP3.	seryl-seryl-seryl-arginine	90-94	NLR family pyrin domain containing 3	Homo sapiens	118-123
32587943-2	2020	The trimethylamine N-oxide (TMAO) metaorganismal pathway is the most deeply investigated one, which comprises trimethylamine precursors, such as choline, trimethylamine lyase, trimethylamine, host liver FMO3, TMAO, and downstream effectors involving unfolded protein response (UPR), NF-kappaB and NLRP3 inflammasome.	trimethyloxamine	4-26	NLR family pyrin domain containing 3	Homo sapiens	297-302
32587943-2	2020	The trimethylamine N-oxide (TMAO) metaorganismal pathway is the most deeply investigated one, which comprises trimethylamine precursors, such as choline, trimethylamine lyase, trimethylamine, host liver FMO3, TMAO, and downstream effectors involving unfolded protein response (UPR), NF-kappaB and NLRP3 inflammasome.	trimethyloxamine	28-32	NLR family pyrin domain containing 3	Homo sapiens	297-302
32587943-2	2020	The trimethylamine N-oxide (TMAO) metaorganismal pathway is the most deeply investigated one, which comprises trimethylamine precursors, such as choline, trimethylamine lyase, trimethylamine, host liver FMO3, TMAO, and downstream effectors involving unfolded protein response (UPR), NF-kappaB and NLRP3 inflammasome.	trimethylamine	4-18	NLR family pyrin domain containing 3	Homo sapiens	297-302
32587943-2	2020	The trimethylamine N-oxide (TMAO) metaorganismal pathway is the most deeply investigated one, which comprises trimethylamine precursors, such as choline, trimethylamine lyase, trimethylamine, host liver FMO3, TMAO, and downstream effectors involving unfolded protein response (UPR), NF-kappaB and NLRP3 inflammasome.	trimethylamine	110-124	NLR family pyrin domain containing 3	Homo sapiens	297-302
32169738-8	2020	Compared with H-LPS or L-LPS alone, L-LPS sequential H-LPS can significantly inhibit the expression of NLRP3 and its related cytokines.	l-lps	23-28	NLR family pyrin domain containing 3	Homo sapiens	103-108
32169738-8	2020	Compared with H-LPS or L-LPS alone, L-LPS sequential H-LPS can significantly inhibit the expression of NLRP3 and its related cytokines.	l-lps	36-41	NLR family pyrin domain containing 3	Homo sapiens	103-108
32062019-7	2020	Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1beta pathway, which could be reversed by activated Nrf2-HO-1 pathway.	Glucose	31-38	NLR family pyrin domain containing 3	Homo sapiens	276-281
32062019-7	2020	Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1beta pathway, which could be reversed by activated Nrf2-HO-1 pathway.	Palmitic Acid	43-45	NLR family pyrin domain containing 3	Homo sapiens	276-281
32296327-1	2020	Aim: To investigate the role of histone deacetylase 6 (HDAC6) deacetylation activity in nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammatory response and explore the effects of pharmacological inhibition of HDAC6 with tubastatin A (TBA) on dopaminergic injury.	Leucine	134-141	NLR family pyrin domain containing 3	Homo sapiens	170-175
32328491-3	2020	However, pathways triggering NLRP3 activation, such as potassium efflux, ROS production or lysosomal permeabilization, can be required or not, depending on the activators used.	Potassium	55-64	NLR family pyrin domain containing 3	Homo sapiens	29-34
32328491-3	2020	However, pathways triggering NLRP3 activation, such as potassium efflux, ROS production or lysosomal permeabilization, can be required or not, depending on the activators used.	ros	73-76	NLR family pyrin domain containing 3	Homo sapiens	29-34
32222695-11	2020	In vitro experiments indicated that DOP increased the LO2 cell viability; prevented LDH release prominently; reduced the secretion of IL-1beta, IL-6, and TNF-alpha; and reversed the expression of IL-1beta, IL-6, TNF-alpha, caspase 1, NLRP3, p-NF-kappaB, and TLR4.	Diethylhexyl Phthalate	36-39	NLR family pyrin domain containing 3	Homo sapiens	234-239
32057231-3	2020	The ultrasmall-size (<10 nm) Au nanoparticles preferentially activate the NLRP3 inflammasome for Caspase-1 maturation and interleukin-1beta production, while the larger-size Au nanoparticles (>10 nm) trigger the NF-kappaB signaling pathway.	Gold	29-31	NLR family pyrin domain containing 3	Homo sapiens	74-79
32057231-4	2020	Ultrasmall (4.5 nm) Au nanoparticles (Au4.5) activate the NLRP3 inflammasome through directly penetrating into cell cytoplasm to promote robust ROS production and target autophagy protein-LC3 (microtubule-associated protein 1-light chain 3) for proteasomal degradation in an endocytic/phagocytic-independent manner.	Gold	20-22	NLR family pyrin domain containing 3	Homo sapiens	58-63
32057231-4	2020	Ultrasmall (4.5 nm) Au nanoparticles (Au4.5) activate the NLRP3 inflammasome through directly penetrating into cell cytoplasm to promote robust ROS production and target autophagy protein-LC3 (microtubule-associated protein 1-light chain 3) for proteasomal degradation in an endocytic/phagocytic-independent manner.	ros	144-147	NLR family pyrin domain containing 3	Homo sapiens	58-63
32209983-0	2020	The Impact of Acute Ingestion of a Ketone Monoester Drink on LPS-Stimulated NLRP3 Activation in Humans with Obesity.	Ketones	35-41	NLR family pyrin domain containing 3	Homo sapiens	76-81
32209983-2	2020	Mechanistic studies have shown that beta-hydroxybutyrate (OHB) attenuates activation of NLRP3, but human data are limited.	3-Hydroxybutyric Acid	36-56	NLR family pyrin domain containing 3	Homo sapiens	88-93
32209983-2	2020	Mechanistic studies have shown that beta-hydroxybutyrate (OHB) attenuates activation of NLRP3, but human data are limited.	salicylamide	58-61	NLR family pyrin domain containing 3	Homo sapiens	88-93
32209983-3	2020	In a randomized, double-blind, placebo-controlled crossover trial (n = 11) we tested the hypothesis that acutely raising beta-OHB by ingestion of exogenous ketones would attenuate NLRP3 activation in humans with obesity.	beta-ohb	121-129	NLR family pyrin domain containing 3	Homo sapiens	180-185
32209983-3	2020	In a randomized, double-blind, placebo-controlled crossover trial (n = 11) we tested the hypothesis that acutely raising beta-OHB by ingestion of exogenous ketones would attenuate NLRP3 activation in humans with obesity.	Ketones	156-163	NLR family pyrin domain containing 3	Homo sapiens	180-185
32209983-6	2020	NLRP3 activation was quantified by assessing monocyte caspase-1 activation and interleukin (IL)-1beta secretion in ex vivo lipopolysaccharide (LPS)-stimulated whole-blood cultures.	ex vivo lipopolysaccharide	115-141	NLR family pyrin domain containing 3	Homo sapiens	0-5
31941382-0	2020	Trimethylamine-N-Oxide Promotes Vascular Calcification Through Activation of NLRP3 (Nucleotide-Binding Domain, Leucine-Rich-Containing Family, Pyrin Domain-Containing-3) Inflammasome and NF-kappaB (Nuclear Factor kappaB) Signals.	trimethyloxamine	0-22	NLR family pyrin domain containing 3	Homo sapiens	77-82
31941382-0	2020	Trimethylamine-N-Oxide Promotes Vascular Calcification Through Activation of NLRP3 (Nucleotide-Binding Domain, Leucine-Rich-Containing Family, Pyrin Domain-Containing-3) Inflammasome and NF-kappaB (Nuclear Factor kappaB) Signals.	Leucine	111-118	NLR family pyrin domain containing 3	Homo sapiens	77-82
31941382-10	2020	Interestingly, TMAO activated NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome and NF-kappaB (nuclear factor kappaB) signals during vascular calcification.	Leucine	64-71	NLR family pyrin domain containing 3	Homo sapiens	30-35
31941382-11	2020	Inhibition of NLRP3 inflammasome and NF-kappaB signals attenuated TMAO-induced vascular smooth muscle cell calcification.	trimethyloxamine	66-70	NLR family pyrin domain containing 3	Homo sapiens	14-19
32057354-0	2020	Dehydrocostus lactone inhibits NLRP3 inflammasome activation by blocking ASC oligomerization and prevents LPS-mediated inflammation in vivo.	Lactones	14-21	NLR family pyrin domain containing 3	Homo sapiens	31-36
32057354-3	2020	Here, we reported that dehydrocostus lactone (DCL), a main component of Saussurea lappa from the traditional Chinese medicine, inhibited NLRP3 inflammasome-mediated caspase-1 activation and subsequent interleukin (IL)-1beta production in primary mouse macrophages and human peripheral blood mononuclear cells and exerted an inhibitory effect on NLRP3-driven inflammation.	dehydrocostus lactone	23-44	NLR family pyrin domain containing 3	Homo sapiens	345-350
32057354-3	2020	Here, we reported that dehydrocostus lactone (DCL), a main component of Saussurea lappa from the traditional Chinese medicine, inhibited NLRP3 inflammasome-mediated caspase-1 activation and subsequent interleukin (IL)-1beta production in primary mouse macrophages and human peripheral blood mononuclear cells and exerted an inhibitory effect on NLRP3-driven inflammation.	dehydrocostus lactone	46-49	NLR family pyrin domain containing 3	Homo sapiens	345-350
31927297-2	2020	This paper briefly discusses biological bases for thresholds and nonlinearities in exposure-response functions for respirable crystalline silica (RCS) and asbestos, based on modeling a chronic inflammation mode of action (mediated by activation of the NLRP3 inflammasome, for both RCS and asbestos).	Asbestos	155-163	NLR family pyrin domain containing 3	Homo sapiens	252-257
31408370-8	2020	The ketone body ss-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits.	Ketones	4-10	NLR family pyrin domain containing 3	Homo sapiens	62-68
31408370-8	2020	The ketone body ss-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits.	ss-hydroxybutyrate	16-34	NLR family pyrin domain containing 3	Homo sapiens	62-68
32329444-0	2020	HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-kappaB and NLRP3 inflammasome pathway.	CAY10603	16-24	NLR family pyrin domain containing 3	Homo sapiens	165-170
32329444-0	2020	HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-kappaB and NLRP3 inflammasome pathway.	Glucose	39-46	NLR family pyrin domain containing 3	Homo sapiens	165-170
32184085-12	2020	Inhibition of the NLRP3 inflammasome in human enterocytes blocked the activation of AMPs and bacterial killing.	Adenylyl sulfate	84-88	NLR family pyrin domain containing 3	Homo sapiens	18-23
32296327-2	2020	Methods: Using 6-OHDA-induced Parkinson"s disease (PD) models, we examined the effects of TBA on NLRP3 activation and cell injury in SH-SY5Y cells.	tubastatin A	90-93	NLR family pyrin domain containing 3	Homo sapiens	97-102
32230726-7	2020	However, application of exogenous control activators such as Nigericin or ATP to infected cells readily induced NLRP3 inflammasome formation and secretion of high amounts of mature IL-1beta.	Nigericin	61-70	NLR family pyrin domain containing 3	Homo sapiens	112-117
32230726-7	2020	However, application of exogenous control activators such as Nigericin or ATP to infected cells readily induced NLRP3 inflammasome formation and secretion of high amounts of mature IL-1beta.	Adenosine Triphosphate	74-77	NLR family pyrin domain containing 3	Homo sapiens	112-117
32183271-6	2020	Furthermore, glycogen metabolism supports DC maturation, inflammatory cytokine production, and priming of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in response to both TLR- and CLR-mediated activation.	Glycogen	13-21	NLR family pyrin domain containing 3	Homo sapiens	196-201
32194991-3	2020	Although metformin reportedly inhibits mature IL-1beta secretion via NLRP3 inflammasome in macrophages of T2DM patients, it remains unclear whether it affects skin inflammation in psoriasis.	Metformin	9-18	NLR family pyrin domain containing 3	Homo sapiens	69-74
32194991-6	2020	To further reveal the mechanism involved, we examined how metformin treatment affected NLRP3 inflammasome activated by TNF-alpha and IL-17A stimulation.	Metformin	58-67	NLR family pyrin domain containing 3	Homo sapiens	87-92
32194991-8	2020	Furthermore, inhibitors of AMPK and SIRT1 abrogated the downregulation of caspase-1 induced by metformin treatment, indicating that AMPK and SIRT1 are essential for the inhibitory effect on NLRP3 inflammasome in NHEKs.	Metformin	95-104	NLR family pyrin domain containing 3	Homo sapiens	190-195
31941382-12	2020	CONCLUSIONS: This study for the first time demonstrates that TMAO promotes vascular calcification through activation of NLRP3 inflammasome and NF-kappaB signals, suggesting the potential link between gut microbial metabolism and vascular calcification.	trimethyloxamine	61-65	NLR family pyrin domain containing 3	Homo sapiens	120-125
31996020-5	2020	Approach and Results: The secretion of IL-1beta from human peripheral blood mononuclear cells mediated by NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome was promoted by physiological levels in serum uric acid.	Uric Acid	221-230	NLR family pyrin domain containing 3	Homo sapiens	106-111
30911117-10	2020	The accumulated ATP bound to the P2X7 receptor, leading to NLRP3 inflammasome activation.	Adenosine Triphosphate	16-19	NLR family pyrin domain containing 3	Homo sapiens	59-64
31622986-8	2020	Here, we found that exogenous H2S dose-dependently inhibited the expression of pro-inflammatory cytokines, NLRP3 inflammasome and activation of NF-kappaB signaling in PA-induced HepG2 cells.	hydrogen sulfite	30-33	NLR family pyrin domain containing 3	Homo sapiens	107-112
31622986-8	2020	Here, we found that exogenous H2S dose-dependently inhibited the expression of pro-inflammatory cytokines, NLRP3 inflammasome and activation of NF-kappaB signaling in PA-induced HepG2 cells.	Palmitic Acid	167-169	NLR family pyrin domain containing 3	Homo sapiens	107-112
32053033-5	2020	A non-systematic literature search was performed on PubMed and ClinicalTrials.gov.Expert opinion: Targeting fructose metabolism, DNL, ER stress, NLRP3 inflammasome, BMP signaling and platelets are promising therapeutic strategies, warranting further preclinical and clinical investigation.	Fructose	108-116	NLR family pyrin domain containing 3	Homo sapiens	145-150
31975558-2	2020	Metformin besides being an insulin sensitizer also induces autophagy; however, its effect on mitophagy and NLRP3 activation in patients with T2DM still remains elusive.	Metformin	0-9	NLR family pyrin domain containing 3	Homo sapiens	107-112
31975558-6	2020	However, multivariate ANCOVA divulged that mRNA and protein expression of mitophagy markers, NLRP3 and p-AMPKalpha (T172), were significantly increased only with metformin therapy.	Metformin	162-171	NLR family pyrin domain containing 3	Homo sapiens	93-98
32121312-8	2020	We compared the profile of cytokine suppression obtained with the use of NLRP3 inflammasome inhibitor, CRID3 to that obtained with clozapine, to test our hypothesis that clozapine inhibits the NLRP3 inflammasome.	Clozapine	170-179	NLR family pyrin domain containing 3	Homo sapiens	193-198
32121312-0	2020	Clozapine Prevents Poly (I:C) Induced Inflammation by Modulating NLRP3 Pathway in Microglial Cells.	Clozapine	0-9	NLR family pyrin domain containing 3	Homo sapiens	65-70
31998952-4	2020	In vivo and in vitro, IOP treatment caused renal damage and elevated the caspase-1 (+) PI (+) cell count, interleukin (IL)-1b and IL-18 levels, lactate dehydrogenase (LDH) release, and the relative expression of nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and gasdermin D (GSDMD), suggesting that IOP induces AKI via the activation of pyroptosis.	iopromide	22-25	NLR family pyrin domain containing 3	Homo sapiens	281-286
32121312-10	2020	Clozapine reduced the level of poly (I:C)-activated NLRP3 expression by 57%, which was higher than the reduction thay was seen with CRID3 treatment (45%).	Clozapine	0-9	NLR family pyrin domain containing 3	Homo sapiens	52-57
32121312-0	2020	Clozapine Prevents Poly (I:C) Induced Inflammation by Modulating NLRP3 Pathway in Microglial Cells.	Poly I-C	19-29	NLR family pyrin domain containing 3	Homo sapiens	65-70
32121312-10	2020	Clozapine reduced the level of poly (I:C)-activated NLRP3 expression by 57%, which was higher than the reduction thay was seen with CRID3 treatment (45%).	Poly I-C	31-41	NLR family pyrin domain containing 3	Homo sapiens	52-57
32121312-11	2020	These results suggest that clozapine might exhibit anti-inflammatory effects by inhibiting NLRP3 inflammasome and this activity is not typical with the use of other antipsychotic drugs under the conditions of strong microglial activation.	Clozapine	27-36	NLR family pyrin domain containing 3	Homo sapiens	91-96
32120988-0	2020	Proinflammatory Effect of Carbon-Based Nanomaterials: In Vitro Study on Stimulation of Inflammasome NLRP3 via Destabilisation of Lysosomes.	Carbon	26-32	NLR family pyrin domain containing 3	Homo sapiens	100-105
32120988-4	2020	In this work, we compared multi-walled carbon nanotubes (MWCNT) and two different types of pristine GP in their potential to activate inflammasome NLRP3 (The nod-like receptor family pyrin domain containing 3) in vitro.	Carbon	39-45	NLR family pyrin domain containing 3	Homo sapiens	147-152
32120988-8	2020	Direct activation of NLRP3 by both GP was statistically insignificant but could be induced by synergic action with muramyl dipeptide (MDP), as a representative molecule of the family of pathogen-associated molecular patterns (PAMPs).	Acetylmuramyl-Alanyl-Isoglutamine	115-132	NLR family pyrin domain containing 3	Homo sapiens	21-26
32120988-8	2020	Direct activation of NLRP3 by both GP was statistically insignificant but could be induced by synergic action with muramyl dipeptide (MDP), as a representative molecule of the family of pathogen-associated molecular patterns (PAMPs).	Acetylmuramyl-Alanyl-Isoglutamine	134-137	NLR family pyrin domain containing 3	Homo sapiens	21-26
31734269-3	2020	THP-1 macrophages exposed to Cinacalcet (CaSR activator, 2 muM, 4 h) showed elevated proinflammatory marker and NLRP3 inflammasome mRNA, pro-IL-1beta protein and caspase-1 activity, whereas preincubation with CaSR negative modulators prevented these effects.	cina	29-39	NLR family pyrin domain containing 3	Homo sapiens	112-117
32088642-0	2020	Hydroxysafflor yellow A inhibits hypoxia/reoxygenation-induced cardiomyocyte injury via regulating the AMPK/NLRP3 inflammasome pathway.	hydroxysafflor yellow A	0-23	NLR family pyrin domain containing 3	Homo sapiens	108-113
31924495-3	2020	Studies have shown that NOD-like receptor protein 3 (NLRP3) inflammasome as pattern recognition receptors can be activated by uric acid crystallization, triggering immune inflammation and causing acute gouty arthritis symptoms.	Uric Acid	126-135	NLR family pyrin domain containing 3	Homo sapiens	24-51
31924495-3	2020	Studies have shown that NOD-like receptor protein 3 (NLRP3) inflammasome as pattern recognition receptors can be activated by uric acid crystallization, triggering immune inflammation and causing acute gouty arthritis symptoms.	Uric Acid	126-135	NLR family pyrin domain containing 3	Homo sapiens	53-58
31734269-0	2020	Calcium sensing receptor activation in THP-1 macrophages triggers NLRP3 inflammasome and human preadipose cell inflammation.	Calcium	0-7	NLR family pyrin domain containing 3	Homo sapiens	66-71
32158192-11	2020	Conclusion: Our results suggest that cholesterol efflux from endothelial cells is reduced by ox-LDLs, and these reductions in cholesterol efflux are accompanied by increased NLRP3 inflammasome signaling, ASK1 and higher levels of endoplasmic reticulum stress.	Cholesterol	126-137	NLR family pyrin domain containing 3	Homo sapiens	174-179
31948593-0	2020	Statin ameliorates adipose inflammation via NLRP3 suppression.	Simvastatin	0-6	NLR family pyrin domain containing 3	Homo sapiens	44-49
31506572-0	2020	Isosibiricin inhibits microglial activation by targeting the dopamine D1/D2 receptor-dependent NLRP3/caspase-1 inflammasome pathway.	Isosibiricin	0-12	NLR family pyrin domain containing 3	Homo sapiens	95-100
31785945-7	2020	The ROS scavenger (+-)-alpha-tocopherol and the NFkappaB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs.	alpha-Tocopherol	18-39	NLR family pyrin domain containing 3	Homo sapiens	107-112
31786260-7	2020	This work provides an overview of the current knowledge on the therapeutic potential of terpenoids as NLRP3 inflammasome inhibitors.	Terpenes	88-98	NLR family pyrin domain containing 3	Homo sapiens	102-107
31683435-0	2020	Carbon black nanoparticles induce pulmonary fibrosis through NLRP3 inflammasome pathway modulated by miR-96 targeted FOXO3a.	Soot	0-12	NLR family pyrin domain containing 3	Homo sapiens	61-66
31683435-10	2020	Both in vivo and in vitro, CBNPs exposure significantly increased the expression of NLRP3 inflammasome, accompanied by the increased reactive oxygen species (ROS), decreased miR-96 and increased FOXO3a expressions dose -and time-dependently.	Oxygen	142-148	NLR family pyrin domain containing 3	Homo sapiens	84-89
32058297-0	2020	TRPM2, linking oxidative stress and Ca2+ permeation to NLRP3 inflammasome activation.	Calcium	36-40	NLR family pyrin domain containing 3	Homo sapiens	55-60
32058297-4	2020	Generation of reactive oxygen species (ROS) and intracellular calcium mobilization can activate the NLRP3 inflammasome.	Oxygen	23-29	NLR family pyrin domain containing 3	Homo sapiens	100-105
32058297-4	2020	Generation of reactive oxygen species (ROS) and intracellular calcium mobilization can activate the NLRP3 inflammasome.	Calcium	62-69	NLR family pyrin domain containing 3	Homo sapiens	100-105
32058297-5	2020	Recent studies suggest that TRPM2 is a calcium-permeable cation channel mediating ROS-dependent NLRP3 activation.	Calcium	39-46	NLR family pyrin domain containing 3	Homo sapiens	96-101
31785945-7	2020	The ROS scavenger (+-)-alpha-tocopherol and the NFkappaB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs.	alpha-Tocopherol	18-39	NLR family pyrin domain containing 3	Homo sapiens	144-149
31785945-7	2020	The ROS scavenger (+-)-alpha-tocopherol and the NFkappaB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs.	3-(4-methylphenylsulfonyl)-2-propenenitrile	67-77	NLR family pyrin domain containing 3	Homo sapiens	107-112
31785945-7	2020	The ROS scavenger (+-)-alpha-tocopherol and the NFkappaB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs.	3-(4-methylphenylsulfonyl)-2-propenenitrile	67-77	NLR family pyrin domain containing 3	Homo sapiens	144-149
32010303-11	2020	The immunofluorescence analyses indicated significantly reduced protein expression levels of NLRP3 and ASC in the pulegone groups, as well as co-localization of the NLRP3 and ASC proteins.	pulegone	114-122	NLR family pyrin domain containing 3	Homo sapiens	93-98
32010254-9	2020	The expression levels of NLRP3, caspase-1 and IL-1beta were inhibited after the addition of autophagy inhibitor 3-MA.	3-methyladenine	112-116	NLR family pyrin domain containing 3	Homo sapiens	25-30
31549730-3	2020	By acting on the P2X7 purinergic receptor, extracellular ATP is one of the major stimuli that activates the NLRP3 inflammasome.	Adenosine Triphosphate	57-60	NLR family pyrin domain containing 3	Homo sapiens	108-113
31549730-12	2020	These results elucidate a novel inflammatory mechanism by which extracellular ADP acts on the P2Y12 receptor to activate NF-kappaB and the NLRP3 inflammasome to enhance microglial inflammation.	Adenosine Diphosphate	78-81	NLR family pyrin domain containing 3	Homo sapiens	139-144
32010303-14	2020	In conclusion, the present study suggested that pulegone exerts its anti-inflammatory effects on LPS + ATP/nigericin-induced THP-1 cells via inhibition of NLRP3 expression, and its regulatory mechanism is associated with potassium channel and ROS pathways.	pulegone	48-56	NLR family pyrin domain containing 3	Homo sapiens	155-160
32010303-4	2020	In the present study, the modulatory effects of pulegone on the NLRP3 inflammasome were investigated.	pulegone	48-56	NLR family pyrin domain containing 3	Homo sapiens	64-69
32010303-15	2020	It was hypothesized that pulegone first inhibits ROS signaling, to then inhibit NLRP3 expression as a downstream event.	pulegone	25-33	NLR family pyrin domain containing 3	Homo sapiens	80-85
31753545-2	2020	In this forum we summarize the main effects of the NLRP3 inflammasome activation, including control of excessive Th2 response and immunopathology induction.	th2	113-116	NLR family pyrin domain containing 3	Homo sapiens	51-56
31756352-10	2020	Furthermore, oxidative stress promoted NLRP3 inflammasome activation in keratinocytes via transient receptor potential cation channel subfamily M member 2 (TRPM2), a redox-sensitive cation channel, which was dependent on TRPM2-mediated calcium influx.	Calcium	236-243	NLR family pyrin domain containing 3	Homo sapiens	39-44
31997696-0	2020	Anisodamine alleviates lipopolysaccharide-induced pancreatic acinar cell injury through NLRP3 inflammasome and NF-kappaB signaling pathway.	anisodamine	0-11	NLR family pyrin domain containing 3	Homo sapiens	88-93
31997696-6	2020	Moreover, overexpressed NLRP3 aggravated the effects of LPS in pancreatic acinar cells, which could be reversed by pretreatment of 100 mug/mL An.Conclusion: An pretreatment attenuated LPS-induced apoptosis and inflammatory response of pancreatic acinar cells through suppressing NLRP3 and inactivating NF-kappaB signaling pathway, thus, it could be explored as a potential therapy for treating acute pancreatitis.	anisodamine	142-144	NLR family pyrin domain containing 3	Homo sapiens	24-29
31997696-6	2020	Moreover, overexpressed NLRP3 aggravated the effects of LPS in pancreatic acinar cells, which could be reversed by pretreatment of 100 mug/mL An.Conclusion: An pretreatment attenuated LPS-induced apoptosis and inflammatory response of pancreatic acinar cells through suppressing NLRP3 and inactivating NF-kappaB signaling pathway, thus, it could be explored as a potential therapy for treating acute pancreatitis.	anisodamine	142-144	NLR family pyrin domain containing 3	Homo sapiens	279-284
31997696-6	2020	Moreover, overexpressed NLRP3 aggravated the effects of LPS in pancreatic acinar cells, which could be reversed by pretreatment of 100 mug/mL An.Conclusion: An pretreatment attenuated LPS-induced apoptosis and inflammatory response of pancreatic acinar cells through suppressing NLRP3 and inactivating NF-kappaB signaling pathway, thus, it could be explored as a potential therapy for treating acute pancreatitis.	anisodamine	157-159	NLR family pyrin domain containing 3	Homo sapiens	24-29
31997696-6	2020	Moreover, overexpressed NLRP3 aggravated the effects of LPS in pancreatic acinar cells, which could be reversed by pretreatment of 100 mug/mL An.Conclusion: An pretreatment attenuated LPS-induced apoptosis and inflammatory response of pancreatic acinar cells through suppressing NLRP3 and inactivating NF-kappaB signaling pathway, thus, it could be explored as a potential therapy for treating acute pancreatitis.	anisodamine	157-159	NLR family pyrin domain containing 3	Homo sapiens	279-284
31905258-11	2020	CONCLUSIONS: Cigarette smoke-induced pyroptosis of bladder tissue by activating ROS/NLRP3/caspase-1 signaling pathway.	Reactive Oxygen Species	80-83	NLR family pyrin domain containing 3	Homo sapiens	84-89
31669392-7	2020	These results suggest that internalized metal nanoparticles in oral mucosal epithelial cells activate the NLRP3 inflammasome through the induction of lysosomal damage and autophagy dysfunction.	Metals	40-45	NLR family pyrin domain containing 3	Homo sapiens	106-111
31646445-3	2020	Accumulating investigations imply that chloride efflux-dependent ASC speck oligomerization and potassium efflux-dependent activation of caspase-1 are the two relatively independent, but indispensable events for NLRP3 inflammasome activation.	Chlorides	39-47	NLR family pyrin domain containing 3	Homo sapiens	211-216
31646445-3	2020	Accumulating investigations imply that chloride efflux-dependent ASC speck oligomerization and potassium efflux-dependent activation of caspase-1 are the two relatively independent, but indispensable events for NLRP3 inflammasome activation.	Potassium	95-104	NLR family pyrin domain containing 3	Homo sapiens	211-216
31646445-4	2020	Previous studies suggested that influence of MCC950 on potassium efflux and its consequent events such as interaction between NEK7 and NLRP3 are limited.	Potassium	55-64	NLR family pyrin domain containing 3	Homo sapiens	135-140
31675164-3	2020	The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3) inflammasome is a multimolecular complex that can sense danger signals associated with neurological diseases.	leucylleucine	31-38	NLR family pyrin domain containing 3	Homo sapiens	90-95
31675164-3	2020	The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3) inflammasome is a multimolecular complex that can sense danger signals associated with neurological diseases.	MRT67307	63-68	NLR family pyrin domain containing 3	Homo sapiens	90-95
31651575-7	2020	Secondary analyses suggest that the effect of Vitamin D on post-MVC pain outcomes may be influenced by genetic variation in IL-10 and NLRP3.	Vitamin D	46-55	NLR family pyrin domain containing 3	Homo sapiens	134-139
31669392-0	2020	Metal nanoparticles-induced activation of NLRP3 inflammasome in human oral keratinocytes is a possible mechanism of oral lichenoid lesions.	Metals	0-5	NLR family pyrin domain containing 3	Homo sapiens	42-47
32005256-9	2020	Our further findings revealed that treatment with SR9009 inhibited NLRP3 inflammasome activation, inflammatory cytokine (IL-1beta, IL-18, IL-6, and TNF-alpha) production, astrocytosis, microgliosis, and neuronal damage in the hippocampus after SE.	SR9009	50-56	NLR family pyrin domain containing 3	Homo sapiens	67-72
32021639-13	2020	More importantly, we found that instead of cell apoptosis, PA induced significant pyroptosis, evidenced by remarkably increased mRNA and protein expressions of inflammasome marker NLRP3, Caspase-1 and IL-1beta, as well as cell membrane perforation driving protein GSDMD (P &lt; 0.05).	Palmitic Acid	59-61	NLR family pyrin domain containing 3	Homo sapiens	180-185
31639433-6	2020	METHOD: In a cohort of Vietnam War (n-299) veterans who have been previously exposed to trauma, NLRP3 polymorphisms were analysed for association with coronary calcium scores using analyses of variance.	Calcium	160-167	NLR family pyrin domain containing 3	Homo sapiens	96-101
31639433-11	2020	RESULTS: The NLRP3 polymorphism, rs10159239 was significantly associated (p = 0.001) with a higher raised coronary calcium score.	Calcium	115-122	NLR family pyrin domain containing 3	Homo sapiens	13-18
31706245-11	2020	Our study proved that COFs-derived PM2.5 could damage the tubule formation of HUVECs in vitro, which could be effectively rescue by co-incubation with VD3, in which processes the ROS/NLRP3/VEGF signaling pathway played a crucial role.	ros	179-182	NLR family pyrin domain containing 3	Homo sapiens	183-188
31993073-0	2020	13-Methylberberine improves endothelial dysfunction by inhibiting NLRP3 inflammasome activation via autophagy induction in human umbilical vein endothelial cells.	13-methylberberrubine	0-18	NLR family pyrin domain containing 3	Homo sapiens	66-71
31993073-5	2020	In atherosclerotic plaques, excessive generation of reactive oxygen species (ROS) activates the NLRP3 inflammasome.	Oxygen	61-67	NLR family pyrin domain containing 3	Homo sapiens	96-101
31993073-15	2020	13-MB also suppressed NLRP3 inflammasome activation and promoted autophagy induction in HUVECs.	13-methylberberrubine	0-5	NLR family pyrin domain containing 3	Homo sapiens	22-27
31993073-16	2020	Conclusion: 13-MB exerts cytoprotective effects in an H2O2-induced cell injury model by inhibiting NLRP3 inflammasome activation via autophagy induction in HUVECs.	13-methylberberrubine	12-17	NLR family pyrin domain containing 3	Homo sapiens	99-104
31993073-16	2020	Conclusion: 13-MB exerts cytoprotective effects in an H2O2-induced cell injury model by inhibiting NLRP3 inflammasome activation via autophagy induction in HUVECs.	Water	54-58	NLR family pyrin domain containing 3	Homo sapiens	99-104
32009974-12	2019	Conclusion: dmDNA activates endothelial NLRP3 inflammasome by mechanisms that involve Ca2+ influx and mitochondrial ROS generation.	Calcium	86-90	NLR family pyrin domain containing 3	Homo sapiens	40-45
31759058-5	2020	Pretreatment with CLI-095, a specific inhibitor of TLR4 signaling, dramatically diminished the TLMP-induced release of IL-1beta and IL-18 by inhibiting the formation of NLRP3/ASC/pro-caspase-1 inflammasome in a dose-dependent manner.	tlmp	95-99	NLR family pyrin domain containing 3	Homo sapiens	169-174
31703838-7	2020	Activation of NLRP3 inflammasome exacerbated podocyte autophagy and reduced podocyte nephrin expression, while silencing of NLRP3 efficiently restored podocyte autophagy and ameliorated podocyte injury induced by high glucose.	Glucose	218-225	NLR family pyrin domain containing 3	Homo sapiens	124-129
31703838-8	2020	The results showed that NLRP3 was a negative regulator of autophagy and suggested that restoration of podocyte autophagy by inactivation of NLRP3 under high glucose could reduce podocyte injury.	Glucose	157-164	NLR family pyrin domain containing 3	Homo sapiens	24-29
31703838-8	2020	The results showed that NLRP3 was a negative regulator of autophagy and suggested that restoration of podocyte autophagy by inactivation of NLRP3 under high glucose could reduce podocyte injury.	Glucose	157-164	NLR family pyrin domain containing 3	Homo sapiens	140-145
31747547-0	2020	Salidroside ameliorates endothelial inflammation and oxidative stress by regulating the AMPK/NF-kappaB/NLRP3 signaling pathway in AGEs-induced HUVECs.	rhodioloside	0-11	NLR family pyrin domain containing 3	Homo sapiens	103-108
31747547-10	2020	Importantly, salidroside alleviated endothelial inflammation and oxidative stress by activating AMPK phosphorylation and inhibiting NF-kB p65 and NLRP3 inflammasome activation.	rhodioloside	13-24	NLR family pyrin domain containing 3	Homo sapiens	146-151
31747547-13	2020	Our findings suggest that salidroside ameliorates AGEs-induced endothelial inflammation and oxidative stress, partially via the AMPK/NF-kappaB/NLRP3 signaling pathway.	rhodioloside	26-37	NLR family pyrin domain containing 3	Homo sapiens	143-148
31759058-6	2020	The TLMP-induced autophagy inhibition in epithelial cells was dependent on the PI3K/Akt signaling pathway, which significantly increased NLRP3 expression and enhanced TLMP-induced inflammation.	tlmp	4-8	NLR family pyrin domain containing 3	Homo sapiens	137-142
31941010-0	2020	Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-kappaB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer.	polyphyllin H	0-14	NLR family pyrin domain containing 3	Homo sapiens	88-93
32056551-6	2020	RESULTS: We found that palmitate alone induced the activation of the nucleotide-binding oligomerization domain-like receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome in placental macrophages, which was associated with increased interleukin 1 beta release and an increase in apoptotic cell death.	Palmitates	23-32	NLR family pyrin domain containing 3	Homo sapiens	165-170
32056551-6	2020	RESULTS: We found that palmitate alone induced the activation of the nucleotide-binding oligomerization domain-like receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome in placental macrophages, which was associated with increased interleukin 1 beta release and an increase in apoptotic cell death.	MRT67307	138-143	NLR family pyrin domain containing 3	Homo sapiens	165-170
31941010-11	2020	Furthermore, the mechanism study found that PPVI could activate the NF-kappaB signaling pathway via increasing reactive oxygen species (ROS) levels in A549 and H1299 cells, and N-acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-kappaB and the NLRP3 inflammasome in PPVI-treated A549 and H1299 cells.	polyphyllin H	44-48	NLR family pyrin domain containing 3	Homo sapiens	301-306
31941010-12	2020	Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-kappaB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.	polyphyllin H	42-46	NLR family pyrin domain containing 3	Homo sapiens	125-130
32009938-4	2019	Nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) are the major neuroinflammatory pathways that intensify AD pathogenesis.	MRT67307	67-72	NLR family pyrin domain containing 3	Homo sapiens	94-99
31941010-5	2020	By using A549 and H1299 cells, the in vitro effect and action mechanism by which PPVI induces activation of the NLRP3 inflammasome in NSCLC were investigated.	polyphyllin H	81-85	NLR family pyrin domain containing 3	Homo sapiens	112-117
31941010-7	2020	The activation of the NLRP3 inflammasome was detected by using Hoechst33324/PI staining, flow cytometry analysis and real-time live cell imaging methods.	icatibant	63-75	NLR family pyrin domain containing 3	Homo sapiens	22-27
31938471-0	2020	The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells.	shogaol	18-27	NLR family pyrin domain containing 3	Homo sapiens	54-59
31998284-0	2019	Lysophosphatidylcholine Induces NLRP3 Inflammasome-Mediated Foam Cell Formation and Pyroptosis in Human Monocytes and Endothelial Cells.	Lysophosphatidylcholines	0-23	NLR family pyrin domain containing 3	Homo sapiens	32-37
31998284-5	2019	Our results showed that LPC induced foam cell formation in both types of cells by increasing LD biogenesis via a NLRP3 inflammasome-dependent pathway.	Lysophosphatidylcholines	24-27	NLR family pyrin domain containing 3	Homo sapiens	113-118
32549782-1	2020	Background: This study aimed to investigate the association between NLRP3 rs35829419 and CARD8 rs2043211 polymorphisms and the risk of developing pleural plaques, asbestosis, and malignant mesothelioma (MM), and to study the influence of the interactions between polymorphisms and asbestos exposure on the risk of developing these diseases.	Asbestos	163-171	NLR family pyrin domain containing 3	Homo sapiens	68-73
32549782-9	2020	However, when testing interactions with asbestos exposure, a decreased risk of asbestosis was found for NLRP3 CA+AA genotypes (OR = 0.09, 95% CI 0.01-0.60, p = 0.014).	Asbestos	40-48	NLR family pyrin domain containing 3	Homo sapiens	104-109
31938471-0	2020	The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells.	Glucose	36-43	NLR family pyrin domain containing 3	Homo sapiens	54-59
31938471-3	2020	Hence, this study was aimed to investigate whether high concentration of glucose (HG), which mimics the hyperglycemia environment, could initiate vascular calcification through NLRP3/IL-1beta inflammasome and the underlying mechanism.	Glucose	73-80	NLR family pyrin domain containing 3	Homo sapiens	177-182
31938471-10	2020	Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1beta inflammasome and hence attenuated HASMC calcification.	shogaol	10-19	NLR family pyrin domain containing 3	Homo sapiens	60-65
31938471-11	2020	Conclusions: This study elucidates the detailed mechanism of HG-initiated HASMC calcification through NLRP3/caspase 1/IL-1beta inflammasome and indicates a potential therapeutic role of 6-shogaol in vascular calcification complication of diabetes.	shogaol	186-195	NLR family pyrin domain containing 3	Homo sapiens	102-107
31830726-5	2020	Atorvastatin inhibited pyroptosis by decreasing the expression levels of the canonical inflammasome pathway biomarkers NLRP3, caspase-1, GSDMD, IL-1beta, and IL-18 at both the mRNA and protein levels.	atorvastatin	0-12	NLR family pyrin domain containing 3	Homo sapiens	119-124
31490096-0	2020	Plumbagin attenuated oxygen-glucose deprivation/reoxygenation-induced injury in human SH-SY5Y cells by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome.	Oxygen	21-27	NLR family pyrin domain containing 3	Homo sapiens	141-146
31490096-0	2020	Plumbagin attenuated oxygen-glucose deprivation/reoxygenation-induced injury in human SH-SY5Y cells by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome.	Reactive Oxygen Species	127-130	NLR family pyrin domain containing 3	Homo sapiens	141-146
31490096-6	2020	Overall, PLB improved OGDR induced neuroinjury by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome.	Reactive Oxygen Species	74-77	NLR family pyrin domain containing 3	Homo sapiens	88-93
32256196-12	2020	Conclusions: The results indicate that exposure levels of PM in the iron foundry environment can affect the NLRP3 inflammasome and systemic inflammation.	Iron	68-72	NLR family pyrin domain containing 3	Homo sapiens	108-113
32999158-5	2020	However, we found that propofol could inhibit the increased expression of NLRP1 and NLRP3 inflammasome induced by oxygen-glucose deprivation (OGD).	Propofol	23-31	NLR family pyrin domain containing 3	Homo sapiens	84-89
31734578-9	2020	The levels of NLRP3-inflammasome-associated components were significantly elevated after cells were inoculated with IAV, whereas the mRNA and protein levels of these components were significantly decreased after treatment with SFJDC and/or oseltamivir in vitro.	Oseltamivir	240-251	NLR family pyrin domain containing 3	Homo sapiens	14-19
31734578-10	2020	Moreover, in vivo, the combination of SFJDC and oseltamivir improved survival rates, attenuated clinical symptoms, induced weight gain, alleviated lung damage, and significantly reduced IL-1beta and IL-18 levels in serum and BALF, as well as reduced the expression levels of NLRP3-associated components and viral titers in lung homogenates.	Oseltamivir	48-59	NLR family pyrin domain containing 3	Homo sapiens	275-280
31885713-0	2020	Hydrogen sulfide modulates high glucose-induced NLRP3 inflammasome activation in 3T3-L1 adipocytes.	Hydrogen Sulfide	0-16	NLR family pyrin domain containing 3	Homo sapiens	48-53
31885713-9	2020	Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG.	Sodium	13-17	NLR family pyrin domain containing 3	Homo sapiens	46-51
31885713-0	2020	Hydrogen sulfide modulates high glucose-induced NLRP3 inflammasome activation in 3T3-L1 adipocytes.	Glucose	32-39	NLR family pyrin domain containing 3	Homo sapiens	48-53
31885713-10	2020	In conclusion, HG may increase and exogenous H2S may inhibit HG-induced NLRP3 inflammasome activation in adipocytes.	hydrogen sulfite	45-48	NLR family pyrin domain containing 3	Homo sapiens	72-77
31885713-4	2020	The present study aimed to investigate the effect of H2S on high glucose (HG)-induced NLRP3 inflammasome activation in adipocytes.	hydrogen sulfite	53-56	NLR family pyrin domain containing 3	Homo sapiens	86-91
31885713-4	2020	The present study aimed to investigate the effect of H2S on high glucose (HG)-induced NLRP3 inflammasome activation in adipocytes.	Glucose	65-72	NLR family pyrin domain containing 3	Homo sapiens	86-91
31585890-5	2020	This protective effect of simvastatin was largely due to improved lysosome function that attenuated lysosome injury-mediated Nlrp3 inflammasome activation and subsequent release of high mobility group box protein-1 (HMGB1).	Simvastatin	26-37	NLR family pyrin domain containing 3	Homo sapiens	125-130
31914640-4	2020	Here we show that ginsenoside Rg3 blocks IL-1beta secretion and caspase-1 activation through inhibiting LPS priming and the NLRP3 inflammasome activation in human and mouse macrophages.	ginsenoside Rg3	18-33	NLR family pyrin domain containing 3	Homo sapiens	124-129
31585890-7	2020	Collectively, simvastatin treatment improves lysosome function via enhancing lysosome biogenesis and its autophagic turnover, which may be an important mechanism to suppress Nlrp3 inflammasome activation and prevents endothelial hyperpermeability in obesity.	Simvastatin	14-25	NLR family pyrin domain containing 3	Homo sapiens	174-179
32363817-1	2020	BACKGROUND AND OBJECTIVE: Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) plays a pivotal role in initiation of inflammation.	Leucine	53-60	NLR family pyrin domain containing 3	Homo sapiens	112-117
31835087-0	2020	Astragaloside IV attenuates sepsis-induced intestinal barrier dysfunction via suppressing RhoA/NLRP3 inflammasome signaling.	astragaloside	0-13	NLR family pyrin domain containing 3	Homo sapiens	95-100
32392921-0	2020	Baicalin attenuates lipopolysaccharide-induced renal tubular epithelial cell injury by inhibiting the TXNIP/NLRP3 signalling pathway via increasing miR-223-3p expression.	baicalin	0-8	NLR family pyrin domain containing 3	Homo sapiens	108-113
32552358-2	2020	The urate monosodium crystals deposit initiates an inflammatory response; mediated by NLRP3 inflammasome, with the release of interleukin 1beta.	Uric Acid	4-20	NLR family pyrin domain containing 3	Homo sapiens	86-91
31746354-0	2020	Honokiol antagonizes doxorubicin-induced cardiomyocyte senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation.	honokiol	0-8	NLR family pyrin domain containing 3	Homo sapiens	95-100
31746354-0	2020	Honokiol antagonizes doxorubicin-induced cardiomyocyte senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation.	Doxorubicin	21-32	NLR family pyrin domain containing 3	Homo sapiens	95-100
31746354-7	2020	Hnk also inhibited TXNIP expression and NLRP3 inflammasome activation in Dox-stimulated H9c2 cardiomyocytes.	honokiol	0-3	NLR family pyrin domain containing 3	Homo sapiens	40-45
31746354-7	2020	Hnk also inhibited TXNIP expression and NLRP3 inflammasome activation in Dox-stimulated H9c2 cardiomyocytes.	Doxorubicin	73-76	NLR family pyrin domain containing 3	Homo sapiens	40-45
31746354-8	2020	When TXNIP expression was enforced by adenovirus-mediated gene overexpression, the NLRP3 inflammasome was activated, which led to inhibition of the anti-inflammation and anti-senescence effects of Hnk on H9c2 cardiomyocytes under Dox treatment.	honokiol	197-200	NLR family pyrin domain containing 3	Homo sapiens	83-88
31746354-8	2020	When TXNIP expression was enforced by adenovirus-mediated gene overexpression, the NLRP3 inflammasome was activated, which led to inhibition of the anti-inflammation and anti-senescence effects of Hnk on H9c2 cardiomyocytes under Dox treatment.	Doxorubicin	230-233	NLR family pyrin domain containing 3	Homo sapiens	83-88
31603717-8	2020	PCB2 prevented LPS-induced tumor necrosis factor-alpha, interleukin-1beta expression, NF-kappaB activation, and NLRP3 inflammasome activation.	procyanidin B	0-4	NLR family pyrin domain containing 3	Homo sapiens	112-117
31603717-9	2020	PCB2 suppressed LPS-induced inflammation and apoptosis in human AECs and LFs by inhibiting NF-kappaB and NLRP3 inflammasome.	procyanidin B	0-4	NLR family pyrin domain containing 3	Homo sapiens	105-110
33012733-9	2020	Additionally, the administration of rCC16 significantly attenuated the increase of pro-IL-1beta, NLRP3 and caspase-1 levels induced by silica particle exposure.	Silicon Dioxide	135-141	NLR family pyrin domain containing 3	Homo sapiens	97-102
31612353-11	2020	Silibinin decreased reactive oxygen species (ROS) generation, leading to inhibition of the NLRP3 inflammasome activation.	Silybin	0-9	NLR family pyrin domain containing 3	Homo sapiens	91-96
31612353-12	2020	In addition, knockdown of mitofusin 1&2 (MFN 1&2) relieved silibinin-induced inhibition of NLRP3 inflammasome activation.	Silybin	59-68	NLR family pyrin domain containing 3	Homo sapiens	91-96
31612353-13	2020	Repression of ROS contributes to the inhibition of the expression of NLRP3, caspase-1 and IL-beta proteins as well as of cell migration.	Reactive Oxygen Species	14-17	NLR family pyrin domain containing 3	Homo sapiens	69-74
31420721-7	2020	Also, it significantly suppresses the mitochondria-generated reactive oxygen species (ROS) required for NLRP3 inflammasome activation.	Reactive Oxygen Species	61-84	NLR family pyrin domain containing 3	Homo sapiens	104-109
31420721-7	2020	Also, it significantly suppresses the mitochondria-generated reactive oxygen species (ROS) required for NLRP3 inflammasome activation.	Reactive Oxygen Species	86-89	NLR family pyrin domain containing 3	Homo sapiens	104-109
31805556-1	2020	BACKGROUNDS/AIMS: To explore whether NLRP3 is involved in the development of cataract and to study the effect of NLRP3 on hydrogen peroxide (H2O2)-induced injury in human lens epithelial cells.	Hydrogen Peroxide	122-139	NLR family pyrin domain containing 3	Homo sapiens	113-118
31805556-1	2020	BACKGROUNDS/AIMS: To explore whether NLRP3 is involved in the development of cataract and to study the effect of NLRP3 on hydrogen peroxide (H2O2)-induced injury in human lens epithelial cells.	Water	141-145	NLR family pyrin domain containing 3	Homo sapiens	113-118
31805556-5	2020	RESULTS: NLRP3 expression significantly increased in H2O2-induced HLEB3 cells.	Water	53-57	NLR family pyrin domain containing 3	Homo sapiens	9-14
31805556-9	2020	The inhibition of NLRP3 obviously attenuated H2O2-induced oxidative stress injury of human lens epithelial cells via NF-kappaB signaling.	Water	45-49	NLR family pyrin domain containing 3	Homo sapiens	18-23
31469975-6	2020	Upstream and serving as an activator of IL-1ss lies the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome that has been well described in animal models to be activated by cholesterol crystals or hypoxia to promote cleavage and secretion of IL-1ss and IL-18 that lead to atherosclerotic deposition in arteries.	Cholesterol	208-219	NLR family pyrin domain containing 3	Homo sapiens	56-121
31578016-10	2020	Mechanistically, baicalin significantly induced upregulation of miR-223 and downregulation of NLRP3, thus suppressing pyroptosis triggered by NLRP3 inflammasome signaling, yet such beneficial effects were reversed by miR-223 knockdown.	baicalin	17-25	NLR family pyrin domain containing 3	Homo sapiens	94-99
31578016-10	2020	Mechanistically, baicalin significantly induced upregulation of miR-223 and downregulation of NLRP3, thus suppressing pyroptosis triggered by NLRP3 inflammasome signaling, yet such beneficial effects were reversed by miR-223 knockdown.	baicalin	17-25	NLR family pyrin domain containing 3	Homo sapiens	142-147
31578016-11	2020	Additionally, MCC950, a NLRP3 inhibitor, restored anti-pyroptosis activity of baicalin under miR-223 silencing.	baicalin	78-86	NLR family pyrin domain containing 3	Homo sapiens	24-29
31578016-12	2020	CONCLUSION: Baicalin alleviates intracellular pyroptosis and viability damage resulted from Abeta inducement in human retinal pigment epithelium cells via negative crosstalk of miR-223/NLRP3 inflammasome signaling, indicating that baicalin may be considered as a potential candidate for AMD therapy.	baicalin	12-20	NLR family pyrin domain containing 3	Homo sapiens	185-190
31639409-4	2020	It was found that acrolein increased the levels of NLRP3 and cleaved caspase-1, which led to the maturation of interleukin-1beta (IL-1beta).	Acrolein	18-26	NLR family pyrin domain containing 3	Homo sapiens	51-56
31639409-8	2020	Furthermore, we found that acrolein activated p38 MAPK and NF-kappaB p65, while pretreatment with p38 MAPK inhibitor, SB203580 and GI 254023X inhibited NF-kappaB p65 activation and NLRP3 inflammasome.	Acrolein	27-35	NLR family pyrin domain containing 3	Homo sapiens	181-186
31639409-8	2020	Furthermore, we found that acrolein activated p38 MAPK and NF-kappaB p65, while pretreatment with p38 MAPK inhibitor, SB203580 and GI 254023X inhibited NF-kappaB p65 activation and NLRP3 inflammasome.	SB 203580	118-126	NLR family pyrin domain containing 3	Homo sapiens	181-186
31639409-8	2020	Furthermore, we found that acrolein activated p38 MAPK and NF-kappaB p65, while pretreatment with p38 MAPK inhibitor, SB203580 and GI 254023X inhibited NF-kappaB p65 activation and NLRP3 inflammasome.	3-(formylhydroxyamino)-2-(3-phenyl-1-propyl)butanoic acid (2,2-dimethyl-1-methylcarbamoyl-1-propyl)amide	131-141	NLR family pyrin domain containing 3	Homo sapiens	181-186
31639409-11	2020	In conclusion, we demonstrate that acrolein induces astrocytic inflammation through NLRP3 inflammasome, which is regulated by ADAM10 and attributed to p38 MAPK-activated NF-kappaB p65 activity.	Acrolein	35-43	NLR family pyrin domain containing 3	Homo sapiens	84-89
31578016-0	2020	Baicalin Alleviates Age-Related Macular Degeneration via miR-223/NLRP3-Regulated Pyroptosis.	baicalin	0-8	NLR family pyrin domain containing 3	Homo sapiens	65-70
31790902-7	2020	The effect of phloretin on NLRP3 pathway was analyzed in human renal tubular cell lines (HK-2).	Phloretin	14-23	NLR family pyrin domain containing 3	Homo sapiens	27-32
31705795-3	2020	The IL-1beta response to excess glucose was mediated by uric acid-induced activation of the NLRP3 inflammasome.	Glucose	32-39	NLR family pyrin domain containing 3	Homo sapiens	92-97
31705795-3	2020	The IL-1beta response to excess glucose was mediated by uric acid-induced activation of the NLRP3 inflammasome.	Uric Acid	56-65	NLR family pyrin domain containing 3	Homo sapiens	92-97
31469975-6	2020	Upstream and serving as an activator of IL-1ss lies the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome that has been well described in animal models to be activated by cholesterol crystals or hypoxia to promote cleavage and secretion of IL-1ss and IL-18 that lead to atherosclerotic deposition in arteries.	Cholesterol	208-219	NLR family pyrin domain containing 3	Homo sapiens	123-128
31878134-0	2019	Cadmium Induces Acute Liver Injury by Inhibiting Nrf2 and the Role of NF-kappaB, NLRP3, and MAPKs Signaling Pathway.	Cadmium	0-7	NLR family pyrin domain containing 3	Homo sapiens	81-86
31905600-0	2019	Transcriptional Suppression of the NLRP3 Inflammasome and Cytokine Release in Primary Macrophages by Low-Dose Anthracyclines.	Anthracyclines	110-124	NLR family pyrin domain containing 3	Homo sapiens	35-40
31905600-5	2019	We investigated the anti-inflammatory properties of epirubicin on the NLRP3 inflammasome and TLR4-mediated inflammation in PMA-primed THP-1 and in primary human peritoneal macrophages (PM).	Epirubicin	52-62	NLR family pyrin domain containing 3	Homo sapiens	70-75
31905600-6	2019	Low-dose epirubicin at non-cytotoxic doses downregulated NLRP3 inflammasome components and reduced the release of cleaved caspase-1, bioactive IL-1beta, and TNF-alpha following NLRP3 activation in a dose-dependent fashion.	Epirubicin	9-19	NLR family pyrin domain containing 3	Homo sapiens	57-62
31905600-6	2019	Low-dose epirubicin at non-cytotoxic doses downregulated NLRP3 inflammasome components and reduced the release of cleaved caspase-1, bioactive IL-1beta, and TNF-alpha following NLRP3 activation in a dose-dependent fashion.	Epirubicin	9-19	NLR family pyrin domain containing 3	Homo sapiens	177-182
31908436-12	2019	Conclusion: Lymphocytes co-cultured with HCB-SCs exhibit a neuroprotective effect after ischemic stroke by promoting Tregs differentiation and suppressing NLRP3 inflammasome activation and neuron apoptosis, and might be a promising therapeutic strategy for ischemic stroke.	Hexachlorobenzene	41-44	NLR family pyrin domain containing 3	Homo sapiens	155-160
31878134-7	2019	Furthermore, NF-kappaB, NLRP3, and MAPKs signaling pathways were all activated by Cd intoxication.	Cadmium	82-84	NLR family pyrin domain containing 3	Homo sapiens	24-29
31878134-8	2019	In conclusion, the inhibition of Nrf2, HO-1, and the activation of NF-kappaB, NLRP3, and MAPKs all contribute to Cd-induced liver injury.	Cadmium	113-115	NLR family pyrin domain containing 3	Homo sapiens	78-83
31870428-2	2019	Reactive oxygen species (ROS) play an important role in OA development; they may activate the NLRP3 inflammasome, thereby inducing the secretion of proinflammatory IL-1beta and IL-18, leading to the aggravation of the downstream inflammatory response.	Oxygen	9-15	NLR family pyrin domain containing 3	Homo sapiens	94-99
31704095-6	2019	The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome regulates the maturation of pro-inflammatory cytokines.	leucylleucine	31-38	NLR family pyrin domain containing 3	Homo sapiens	90-95
30860577-3	2019	Here, we also found MMP collapse and ROS generation induced by Nlrp3 inflammasome activation as previous studies reported.	Reactive Oxygen Species	37-40	NLR family pyrin domain containing 3	Homo sapiens	63-68
30860577-8	2019	These results demonstrate that Gsdmd oxidation serves as a de novo mechanism by which mitochondrial ROS promote Nlrp3 inflammasome-dependent pyroptotic cell death.	Reactive Oxygen Species	100-103	NLR family pyrin domain containing 3	Homo sapiens	112-117
31704095-6	2019	The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome regulates the maturation of pro-inflammatory cytokines.	MRT67307	63-68	NLR family pyrin domain containing 3	Homo sapiens	90-95
31704095-7	2019	CO can regulate NLRP3 inflammasome activation and associated pro-inflammatory cytokines production and promote the resolution of inflammation by upregulating the synthesis of specialized pro-resolving mediators (SPMs).	Carbon Monoxide	0-2	NLR family pyrin domain containing 3	Homo sapiens	16-21
31892810-3	2019	On the other hand, whereas other inflammasomes are mainly detectors of specific molecular motifs, NLRP3 is acting as a general sensor of cellular perturbations including potassium efflux, lysosomal damage, and ROS production.	Potassium	170-179	NLR family pyrin domain containing 3	Homo sapiens	98-103
31835256-0	2019	Nicotine instigates podocyte injury via NLRP3 inflammasomes activation.	Nicotine	0-8	NLR family pyrin domain containing 3	Homo sapiens	40-45
31835256-3	2019	The present study tested whether nicotine induces NLRP3 inflammasomes activation and thereby contributes to podocyte injury.	Nicotine	33-41	NLR family pyrin domain containing 3	Homo sapiens	50-55
31835256-4	2019	RESULTS: Nicotine treatment significantly increased the colocalization of NLRP3 with Asc, caspase-1 activity, IL-beta production, cell permeability in podocytes compared to control cells.	Nicotine	9-17	NLR family pyrin domain containing 3	Homo sapiens	74-79
31835256-5	2019	Pretreatment with caspase-1 inhibitor, WEHD significantly abolished the nicotine-induced colocalization of NLRP3 with Asc, caspase-1 activity, IL-1beta production and cell permeability in podocytes.	Nicotine	72-80	NLR family pyrin domain containing 3	Homo sapiens	107-112
31835256-11	2019	CONCLUSIONS: Nicotine-induced the NLRP3 inflammasome activation in podocytes and thereby results in podocyte injury.	Nicotine	13-21	NLR family pyrin domain containing 3	Homo sapiens	34-39
30945564-0	2019	Vildagliptin inhibits high free fatty acid (FFA)-induced NLRP3 inflammasome activation in endothelial cells.	Vildagliptin	0-12	NLR family pyrin domain containing 3	Homo sapiens	57-62
31822637-0	2019	Nickel induces inflammatory activation via NF-kappaB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages.	Nickel	0-6	NLR family pyrin domain containing 3	Homo sapiens	70-75
31822637-4	2019	We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1beta.	nickel chloride	19-34	NLR family pyrin domain containing 3	Homo sapiens	53-72
31822637-4	2019	We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1beta.	nickel chloride	19-34	NLR family pyrin domain containing 3	Homo sapiens	74-79
31822637-4	2019	We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1beta.	Nickel	36-41	NLR family pyrin domain containing 3	Homo sapiens	53-72
31822637-4	2019	We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1beta.	Nickel	36-41	NLR family pyrin domain containing 3	Homo sapiens	74-79
31822637-5	2019	NiCl2 induced the accumulation of mitochondrial reactive oxygen species (mtROS) and the release of mitochondrial DNA (mtDNA), thus activating NLRP3 inflammasome pathway.	Nickel	0-5	NLR family pyrin domain containing 3	Homo sapiens	142-147
31866999-7	2019	In the absence of VDR, caspase-1 activation and IL-1beta release are increased in response to LPS-induced inflammation or alum-induced peritoneal inflammation, indicating that VDR is a negative regulator of NLRP3 inflammasome activation in vivo.	aluminum sulfate	122-126	NLR family pyrin domain containing 3	Homo sapiens	207-212
31866999-8	2019	In addition, vitamin D negatively regulates the NLRP3 inflammasome via VDR signaling to effectively inhibit IL-1beta secretion.	Vitamin D	13-22	NLR family pyrin domain containing 3	Homo sapiens	48-53
31577960-5	2019	Then, we will debate the NLRP3 inflammasome putting the focus on its activation through the canonical, non-canonical and alternative pathways and the triggers involved herein namely endoplasmic reticulum stress, mitochondrial dysfunction, reactive oxygen species and amyloid beta peptide.	Oxygen	248-254	NLR family pyrin domain containing 3	Homo sapiens	25-30
31822637-7	2019	Altogether, abovementioned results indicate that NiCl2 induces inflammatory activation in BMDMs via NF-kappaB, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.	Nickel	49-54	NLR family pyrin domain containing 3	Homo sapiens	153-158
32042826-10	2019	Candidate genes were identified after adjustment for age, sex and presence of lymphopenia with significantly negative correlations with partial pressure of O2 in an arterial blood (PaO2) and fraction of inspiration O2 (FiO2) ratio, among which NLRP3, SOS1, ELF1 and STAT3 held an increasing expression in ex vivo validation while the others, PSMA5, CLEC4D, CD300A, PRKD2 and PSMA2 showed the opposite alteration from those in vivo.	Oxygen	156-158	NLR family pyrin domain containing 3	Homo sapiens	244-249
32042826-10	2019	Candidate genes were identified after adjustment for age, sex and presence of lymphopenia with significantly negative correlations with partial pressure of O2 in an arterial blood (PaO2) and fraction of inspiration O2 (FiO2) ratio, among which NLRP3, SOS1, ELF1 and STAT3 held an increasing expression in ex vivo validation while the others, PSMA5, CLEC4D, CD300A, PRKD2 and PSMA2 showed the opposite alteration from those in vivo.	Oxygen	183-185	NLR family pyrin domain containing 3	Homo sapiens	244-249
32042826-10	2019	Candidate genes were identified after adjustment for age, sex and presence of lymphopenia with significantly negative correlations with partial pressure of O2 in an arterial blood (PaO2) and fraction of inspiration O2 (FiO2) ratio, among which NLRP3, SOS1, ELF1 and STAT3 held an increasing expression in ex vivo validation while the others, PSMA5, CLEC4D, CD300A, PRKD2 and PSMA2 showed the opposite alteration from those in vivo.	fio2	219-223	NLR family pyrin domain containing 3	Homo sapiens	244-249
30945564-0	2019	Vildagliptin inhibits high free fatty acid (FFA)-induced NLRP3 inflammasome activation in endothelial cells.	Fatty Acids, Nonesterified	27-42	NLR family pyrin domain containing 3	Homo sapiens	57-62
30945564-0	2019	Vildagliptin inhibits high free fatty acid (FFA)-induced NLRP3 inflammasome activation in endothelial cells.	Fatty Acids, Nonesterified	44-47	NLR family pyrin domain containing 3	Homo sapiens	57-62
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Vildagliptin	30-42	NLR family pyrin domain containing 3	Homo sapiens	96-101
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Vildagliptin	30-42	NLR family pyrin domain containing 3	Homo sapiens	134-139
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Fatty Acids, Nonesterified	54-57	NLR family pyrin domain containing 3	Homo sapiens	96-101
31514535-0	2019	Cilostazol ameliorates high free fatty acid (FFA)-induced activation of NLRP3 inflammasome in human vascular endothelial cells.	Cilostazol	0-10	NLR family pyrin domain containing 3	Homo sapiens	72-77
30945564-8	2019	Mechanistically, we show that vildagliptin suppresses FFA-induced expression of proteins of the NLRP3 inflammasome complex, including NLRP3, ASC, p20 and HMGB-1, and mitigates FFA-induced inactivation of the AMPK pathway.	Fatty Acids, Nonesterified	54-57	NLR family pyrin domain containing 3	Homo sapiens	134-139
31514535-0	2019	Cilostazol ameliorates high free fatty acid (FFA)-induced activation of NLRP3 inflammasome in human vascular endothelial cells.	Fatty Acids, Nonesterified	28-43	NLR family pyrin domain containing 3	Homo sapiens	72-77
30945564-9	2019	Consequently, vildagliptin inhibits production of two cytokines that are favored by NLRP3 inflammasome machinery: IL-1beta and IL-18.	Vildagliptin	14-26	NLR family pyrin domain containing 3	Homo sapiens	84-89
31514535-0	2019	Cilostazol ameliorates high free fatty acid (FFA)-induced activation of NLRP3 inflammasome in human vascular endothelial cells.	Fatty Acids, Nonesterified	45-48	NLR family pyrin domain containing 3	Homo sapiens	72-77
30945564-11	2019	Collectively, we conclude that the protective role of vildagliptin in endothelial cells is mediated via suppression of the AMPK-NLRP3 inflammasome-HMGB-1 axis pathway.	Vildagliptin	54-66	NLR family pyrin domain containing 3	Homo sapiens	128-133
31514535-5	2019	We found that cilostazol significantly reduced NLRP3 inflammasome activation, as well as the activity of other related and harmful factors, including oxidative stress, expression of NADPH oxidase 4 (NOX-4), thioredoxin-interacting protein (TxNIP), high mobility group box 1 (HMGB-1), interleukin 1beta (IL-1beta) and IL-18.	Cilostazol	14-24	NLR family pyrin domain containing 3	Homo sapiens	47-52
31514535-6	2019	Cilostazol also protected the functionality of sirtuin 1 (SIRT1), which serves to restrict NLRP3 inflammasome activity, when exposure to FFAs would have otherwise impaired its function.	Cilostazol	0-10	NLR family pyrin domain containing 3	Homo sapiens	91-96
31593687-2	2019	The nucleotide-binding oligomerization domain, leucine-rich repeat-containing receptor-containing pyrin domain 3 (NLRP3) inflammasome and pyroptosis play crucial roles in the progression of NASH.	Leucine	47-54	NLR family pyrin domain containing 3	Homo sapiens	114-119
31514535-7	2019	Thus, it appears that cilostazol"s mechanism of action in reducing NLRP3 inflammasome activation is an indirect one; it protects SIRT1, which then allows SIRT1 to perform its regulatory job.	Cilostazol	22-32	NLR family pyrin domain containing 3	Homo sapiens	67-72
30877711-0	2019	Gemigliptin Attenuates Renal Fibrosis Through Down-Regulation of the NLRP3 Inflammasome.	LC15-0444	0-11	NLR family pyrin domain containing 3	Homo sapiens	69-74
30877711-5	2019	Using immunohistochemical and Western blot analysis, we quantitated components of the NLRP3 inflammasome in kidneys with and without gemigliptin treatment, and in vitro in human kidney tubular epithelial human renal proximal tubule cells (HK-2) cells, we further analyzed the effect of gemigliptin on transforming growth factor-beta (TGF-beta)-stimulated production of profibrotic proteins.	LC15-0444	133-144	NLR family pyrin domain containing 3	Homo sapiens	86-91
30877711-5	2019	Using immunohistochemical and Western blot analysis, we quantitated components of the NLRP3 inflammasome in kidneys with and without gemigliptin treatment, and in vitro in human kidney tubular epithelial human renal proximal tubule cells (HK-2) cells, we further analyzed the effect of gemigliptin on transforming growth factor-beta (TGF-beta)-stimulated production of profibrotic proteins.	LC15-0444	286-297	NLR family pyrin domain containing 3	Homo sapiens	86-91
31677073-11	2019	Our findings also suggest that CBZ may be avoided in patients with NLRP3 inflammasome activation-related diseases that are triggered by ATP or nigericin, which may be risk factors for IDILI.	Carbamazepine	31-34	NLR family pyrin domain containing 3	Homo sapiens	67-72
31677073-11	2019	Our findings also suggest that CBZ may be avoided in patients with NLRP3 inflammasome activation-related diseases that are triggered by ATP or nigericin, which may be risk factors for IDILI.	Adenosine Triphosphate	136-139	NLR family pyrin domain containing 3	Homo sapiens	67-72
31677073-11	2019	Our findings also suggest that CBZ may be avoided in patients with NLRP3 inflammasome activation-related diseases that are triggered by ATP or nigericin, which may be risk factors for IDILI.	Nigericin	143-152	NLR family pyrin domain containing 3	Homo sapiens	67-72
31638409-3	2019	A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-kappaB, NLRP3, caspase 1, interleukin-1beta, inducible nitric oxide synthase, and tumor necrosis factor alpha, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes.	Glucose	7-14	NLR family pyrin domain containing 3	Homo sapiens	122-127
30877711-7	2019	Gemigliptin-treated kidneys showed a reduction in levels of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1, and interleukin-1beta, which had all been markedly increased by UUO.	LC15-0444	0-11	NLR family pyrin domain containing 3	Homo sapiens	60-65
30877711-8	2019	In line with the in vivo results, TGF-beta markedly increased NLRP3 inflammasome markers, which were attenuated by gemigliptin treatment.	LC15-0444	115-126	NLR family pyrin domain containing 3	Homo sapiens	62-67
30877711-10	2019	CONCLUSION: The present study shows that activation of the NLRP3 inflammasome contributes to UUO-induced renal fibrosis and the renoprotective effect of gemigliptin is associated with attenuation of NLRP3 inflammasome activation.	LC15-0444	153-164	NLR family pyrin domain containing 3	Homo sapiens	59-64
30877711-10	2019	CONCLUSION: The present study shows that activation of the NLRP3 inflammasome contributes to UUO-induced renal fibrosis and the renoprotective effect of gemigliptin is associated with attenuation of NLRP3 inflammasome activation.	LC15-0444	153-164	NLR family pyrin domain containing 3	Homo sapiens	199-204
31573048-5	2019	The results revealed that RS downregulated promoter efficiency of MALAT1 and MALAT1 directly targeted miR-22-3p, and luciferase activity of MALAT1 was inhibited by miR-22-3p, and furthermore miR-22-3p inhibited the expression of NLRP3 by binding to complementary sequences in the 3" untranslated region of NLRP3.	resveratrol	26-28	NLR family pyrin domain containing 3	Homo sapiens	229-234
31573048-5	2019	The results revealed that RS downregulated promoter efficiency of MALAT1 and MALAT1 directly targeted miR-22-3p, and luciferase activity of MALAT1 was inhibited by miR-22-3p, and furthermore miR-22-3p inhibited the expression of NLRP3 by binding to complementary sequences in the 3" untranslated region of NLRP3.	resveratrol	26-28	NLR family pyrin domain containing 3	Homo sapiens	306-311
31573048-7	2019	In conclusion, it was demonstrated that RS has been demonstrated to prevent the development of cardiac injury induced by PE via modulating the expression of MALAT1 and further affect miR-22-3p and NLRP3.	resveratrol	40-42	NLR family pyrin domain containing 3	Homo sapiens	197-202
31509298-3	2019	Here, we show that activation of DCs with fungal-associated beta-glucan ligands induces acute glycolytic reprogramming that supports the production of IL-1beta and its secretion subsequent to NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	beta-Glucans	60-71	NLR family pyrin domain containing 3	Homo sapiens	192-240
31815868-0	2019	Dietary Apigenin Reduces Induction of LOX-1 and NLRP3 Expression, Leukocyte Adhesion, and Acetylated Low-Density Lipoprotein Uptake in Human Endothelial Cells Exposed to Trimethylamine-N-Oxide.	Apigenin	8-16	NLR family pyrin domain containing 3	Homo sapiens	48-53
31815868-7	2019	Apigenin reversed the effects of TMAO on mRNA expression of LOX-1, SREC, SR-PSOX, NLRP3, ASC, TXNIP, VCAM-1, ICAM-1, and MCP-1, as well as protein expression of LOX-1, the adhesion molecule ICAM-1, and the inflammasome protein NLRP3.	Apigenin	0-8	NLR family pyrin domain containing 3	Homo sapiens	82-87
31815868-7	2019	Apigenin reversed the effects of TMAO on mRNA expression of LOX-1, SREC, SR-PSOX, NLRP3, ASC, TXNIP, VCAM-1, ICAM-1, and MCP-1, as well as protein expression of LOX-1, the adhesion molecule ICAM-1, and the inflammasome protein NLRP3.	Apigenin	0-8	NLR family pyrin domain containing 3	Homo sapiens	227-232
31815868-7	2019	Apigenin reversed the effects of TMAO on mRNA expression of LOX-1, SREC, SR-PSOX, NLRP3, ASC, TXNIP, VCAM-1, ICAM-1, and MCP-1, as well as protein expression of LOX-1, the adhesion molecule ICAM-1, and the inflammasome protein NLRP3.	trimethyloxamine	33-37	NLR family pyrin domain containing 3	Homo sapiens	82-87
31815868-7	2019	Apigenin reversed the effects of TMAO on mRNA expression of LOX-1, SREC, SR-PSOX, NLRP3, ASC, TXNIP, VCAM-1, ICAM-1, and MCP-1, as well as protein expression of LOX-1, the adhesion molecule ICAM-1, and the inflammasome protein NLRP3.	trimethyloxamine	33-37	NLR family pyrin domain containing 3	Homo sapiens	227-232
31509298-3	2019	Here, we show that activation of DCs with fungal-associated beta-glucan ligands induces acute glycolytic reprogramming that supports the production of IL-1beta and its secretion subsequent to NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.	beta-Glucans	60-71	NLR family pyrin domain containing 3	Homo sapiens	242-247
31086288-9	2019	CONCLUSIONS: Forskolin inhibits the NLRP3 inflammasome activation and the secretion of mature IL-1beta, in human macrophages.	Colforsin	13-22	NLR family pyrin domain containing 3	Homo sapiens	36-41
31485636-10	2019	It was also observed that curcumin treatment downregulated the expression levels of TXNIP, NLRP3, interleukin (IL)-1beta and IL-18, and downstream caspase-1 compared with PQ treatment alone.	Curcumin	26-34	NLR family pyrin domain containing 3	Homo sapiens	91-96
31485636-12	2019	The present findings suggested that the inhibitory effects of curcumin on TXINP1 may inhibit activation of the NLRP3 inflammasome, subsequently suppressing the upregulation of proinflammatory cytokines and ultimately improving PQ-induced ALI.	Curcumin	62-70	NLR family pyrin domain containing 3	Homo sapiens	111-116
31485636-12	2019	The present findings suggested that the inhibitory effects of curcumin on TXINP1 may inhibit activation of the NLRP3 inflammasome, subsequently suppressing the upregulation of proinflammatory cytokines and ultimately improving PQ-induced ALI.	Paraquat	227-229	NLR family pyrin domain containing 3	Homo sapiens	111-116
31086288-0	2019	Forskolin attenuates the NLRP3 inflammasome activation and IL-1beta secretion in human macrophages.	Colforsin	0-9	NLR family pyrin domain containing 3	Homo sapiens	25-30
31086288-2	2019	Here we studied whether cyclic adenosine monophosphate (cAMP) elevator forskolin could attenuate the nigericin-induced NLRP3-inflammasome activation and interleukin-1beta (IL-1beta) secretion in human macrophages.	Cyclic AMP	24-54	NLR family pyrin domain containing 3	Homo sapiens	119-124
31086288-2	2019	Here we studied whether cyclic adenosine monophosphate (cAMP) elevator forskolin could attenuate the nigericin-induced NLRP3-inflammasome activation and interleukin-1beta (IL-1beta) secretion in human macrophages.	Cyclic AMP	56-60	NLR family pyrin domain containing 3	Homo sapiens	119-124
31434103-0	2019	Insights image for Forskolin attenuates the NLRP3 inflammasome activation and IL-1beta secretion in human macrophages.	Colforsin	19-28	NLR family pyrin domain containing 3	Homo sapiens	44-49
31086288-2	2019	Here we studied whether cyclic adenosine monophosphate (cAMP) elevator forskolin could attenuate the nigericin-induced NLRP3-inflammasome activation and interleukin-1beta (IL-1beta) secretion in human macrophages.	Colforsin	71-80	NLR family pyrin domain containing 3	Homo sapiens	119-124
31754153-1	2019	The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome mediates caspase-1 activation and IL-1beta processing and is implicated in autoinflammatory as well as other chronic inflammatory diseases.	MRT67307	68-73	NLR family pyrin domain containing 3	Homo sapiens	95-100
31086288-2	2019	Here we studied whether cyclic adenosine monophosphate (cAMP) elevator forskolin could attenuate the nigericin-induced NLRP3-inflammasome activation and interleukin-1beta (IL-1beta) secretion in human macrophages.	Nigericin	101-110	NLR family pyrin domain containing 3	Homo sapiens	119-124
31086288-4	2019	RESULTS: Activation of THP-1 macrophages with nigericin increased the mRNA expression of NLRP3, IL-1beta, and caspase-1 (P &lt; 0.01).	Nigericin	46-55	NLR family pyrin domain containing 3	Homo sapiens	89-94
31775905-2	2019	We tested the hypothesis that HCQ affects the NLRP3 inflammasome, which is involved in autoinflammation.	Hydroxychloroquine	30-33	NLR family pyrin domain containing 3	Homo sapiens	46-51
31775905-7	2019	HCQ pretreatment significantly inhibited the SAA-induced IL-1beta production in human neutrophils, but did not affect the SAA-induced NF-kappaB activation, pro-IL-1beta mRNA expression, and NLRP3 protein expression.	Hydroxychloroquine	0-3	NLR family pyrin domain containing 3	Homo sapiens	190-195
31775905-9	2019	CONCLUSIONS: Treatment with HCQ was associated with impaired production of IL-1beta in SAA-stimulated human neutrophils without affecting the priming process of the NLRP3 inflammasome such as pro-IL-1beta or NLRP3 induction.	Hydroxychloroquine	28-31	NLR family pyrin domain containing 3	Homo sapiens	208-213
31775905-10	2019	These findings suggest that HCQ affects the NLRP3 activation process, resulting in the impaired IL-1beta production in human neutrophils, as representative innate immune cells.	Hydroxychloroquine	28-31	NLR family pyrin domain containing 3	Homo sapiens	44-49
31754153-3	2019	In this study, we report that febuxostat, an inhibitor of XOR, suppressed NLRP3 inflammasome-mediated IL-1beta secretion and cell death by two mechanisms: in a mitochondrial ROS (mitoROS)-dependent and mitoROS-independent manner.	febuxostat	30-40	NLR family pyrin domain containing 3	Homo sapiens	74-79
31819864-0	2019	Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And TXNIP.	Calcium Pyrophosphate	0-21	NLR family pyrin domain containing 3	Homo sapiens	56-61
31824415-0	2019	Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto"s Thyroiditis Through the ROS-NF-kappaB-NLRP3 Pathway.	Iodine	10-16	NLR family pyrin domain containing 3	Homo sapiens	129-134
31824415-6	2019	In addition, excessive iodine caused NLRP3 inflammasome activation in TFCs, which promoted TFC pyroptosis.	Iodine	23-29	NLR family pyrin domain containing 3	Homo sapiens	37-42
31819864-0	2019	Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And TXNIP.	Uric Acid	26-42	NLR family pyrin domain containing 3	Homo sapiens	56-61
31819864-0	2019	Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And TXNIP.	Oxygen	114-120	NLR family pyrin domain containing 3	Homo sapiens	56-61
31819864-6	2019	Untreated controls were incubated with ATP (1.25 mM) for 1 hr to maximally stimulate NLRP3 inflammasome activity (measured as caspase-1 cleavage of the fluorogenic substrate Ac-YVAD-AFC).	Adenosine Triphosphate	39-42	NLR family pyrin domain containing 3	Homo sapiens	85-90
31819482-12	2019	Conclusion: In summary, MIR22HG may play a tumor-suppressive role in HCC by coordinating with predicted TFs and co-expressed genes, such as NLRP3, CSF1R, SIGLEC10, and ZEB2, or by being controlled by nitidine chloride.	nitidine	200-217	NLR family pyrin domain containing 3	Homo sapiens	140-145
31814905-0	2019	Isochlorogenic acid A attenuates acute lung injury induced by LPS via Nf-kappaB/NLRP3 signaling pathway.	isochlorogenic acid	0-21	NLR family pyrin domain containing 3	Homo sapiens	80-85
31814905-7	2019	The protein expressions of Nf-kappaB/NLRP3 signaling pathway induced by LPS were inhibited by isochlorogenic acid A.	isochlorogenic acid	94-115	NLR family pyrin domain containing 3	Homo sapiens	37-42
31606392-0	2019	Nickel-refining fumes induce NLRP3 activation dependent on mitochondrial damage and ROS production in Beas-2B cells.	Nickel	0-6	NLR family pyrin domain containing 3	Homo sapiens	29-34
31606392-7	2019	During activation of NLRP3, the mitochondrial membrane potential (MMP) decreased, the opening rate of mitochondrial permeability transition pore (MPTP) increased, and the content of reactive oxygen species (ROS) increased.	Oxygen	191-197	NLR family pyrin domain containing 3	Homo sapiens	21-26
31606392-9	2019	After NAC reduced the level of ROS, activation of the NLRP3 inflammasome was significantly inhibited.	Acetylcysteine	6-9	NLR family pyrin domain containing 3	Homo sapiens	54-59
31819864-11	2019	Conclusion: The stone components CPPD and MSU activate NLRP3 in an ROS and TXNIP-dependent manner in bladder urothelium.	Uric Acid	42-45	NLR family pyrin domain containing 3	Homo sapiens	55-60
31827916-0	2019	Low-Dose Mitomycin C Decreases the Postoperative Recurrence Rate of Pterygium by Perturbing NLRP3 Inflammatory Signalling Pathway and Suppressing the Expression of Inflammatory Factors.	Mitomycin	9-20	NLR family pyrin domain containing 3	Homo sapiens	92-97
31707403-0	2019	Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism.	Uric Acid	9-18	NLR family pyrin domain containing 3	Homo sapiens	120-125
31827916-9	2019	Further results indicated that MMC can inhibit the activation of the NLRP3 inflammatory signalling pathway and thus downregulate the expression of downstream molecules, including IL-18 and IL-1beta.	Mitomycin	31-34	NLR family pyrin domain containing 3	Homo sapiens	69-74
31707403-0	2019	Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism.	Uric Acid	9-18	NLR family pyrin domain containing 3	Homo sapiens	91-118
31707403-2	2019	Uric acid has been reported to activate Nod-like receptor protein 3 (NLRP3)-inflammasome and alter vascular smooth muscle cells (VSMC).	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	40-67
31707403-2	2019	Uric acid has been reported to activate Nod-like receptor protein 3 (NLRP3)-inflammasome and alter vascular smooth muscle cells (VSMC).	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	69-74
31707403-9	2019	We also found that uric acid increases the level of NLRP3 and induces NLRP3-inflammasome activation.	Uric Acid	19-28	NLR family pyrin domain containing 3	Homo sapiens	52-57
31707403-9	2019	We also found that uric acid increases the level of NLRP3 and induces NLRP3-inflammasome activation.	Uric Acid	19-28	NLR family pyrin domain containing 3	Homo sapiens	70-75
31707403-11	2019	CONCLUSIONS Our findings revealed that uric acid induces inflammation through NLRP3-inflammasome-mediated VSMC proliferation.	Uric Acid	39-48	NLR family pyrin domain containing 3	Homo sapiens	78-83
31694192-5	2019	Inflammasome-independent NLRP3 regulates apoptosis in tubular epithelial cells by interacting with mitochondria and mediating mitochondrial reactive oxygen species production and mitophagy.	Reactive Oxygen Species	140-163	NLR family pyrin domain containing 3	Homo sapiens	25-30
31521245-0	2019	Melatonin alleviates cigarette smoke-induced endothelial cell pyroptosis through inhibiting ROS/NLRP3 axis.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	96-101
31521245-0	2019	Melatonin alleviates cigarette smoke-induced endothelial cell pyroptosis through inhibiting ROS/NLRP3 axis.	ros	92-95	NLR family pyrin domain containing 3	Homo sapiens	96-101
31521245-6	2019	A specific NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inhibitor (MCC950) pretreatment dramatically reduced CSE-induced pyroptosis.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	82-88	NLR family pyrin domain containing 3	Homo sapiens	64-69
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	NLR family pyrin domain containing 3	Homo sapiens	177-182
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	NLR family pyrin domain containing 3	Homo sapiens	177-182
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	ros	61-64	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	ros	61-64	NLR family pyrin domain containing 3	Homo sapiens	177-182
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	gsdmd-n	208-215	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-10	2019	In this study, melatonin was observed to inhibit ROS production, NLRP3 inflammasome activation and pyroptosis in CSE-treated ECs.	Melatonin	15-24	NLR family pyrin domain containing 3	Homo sapiens	65-70
31521245-12	2019	In conclusion, our study generated two novel findings, (i) CS activates ROS/NLRP3 axis and induces EC pyroptosis; (ii) melatonin attenuates CS-induced EC pyroptosis by inhibiting ROS/NLRP3 axis.	Cesium	59-61	NLR family pyrin domain containing 3	Homo sapiens	76-81
31521245-12	2019	In conclusion, our study generated two novel findings, (i) CS activates ROS/NLRP3 axis and induces EC pyroptosis; (ii) melatonin attenuates CS-induced EC pyroptosis by inhibiting ROS/NLRP3 axis.	Melatonin	119-128	NLR family pyrin domain containing 3	Homo sapiens	183-188
31521245-12	2019	In conclusion, our study generated two novel findings, (i) CS activates ROS/NLRP3 axis and induces EC pyroptosis; (ii) melatonin attenuates CS-induced EC pyroptosis by inhibiting ROS/NLRP3 axis.	Cesium	140-142	NLR family pyrin domain containing 3	Homo sapiens	183-188
31521245-12	2019	In conclusion, our study generated two novel findings, (i) CS activates ROS/NLRP3 axis and induces EC pyroptosis; (ii) melatonin attenuates CS-induced EC pyroptosis by inhibiting ROS/NLRP3 axis.	ros	179-182	NLR family pyrin domain containing 3	Homo sapiens	183-188
31622861-5	2019	Recently, the role of DA receptor in neuroinflammation has been investigated widely, mainly focusing on nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3) inflammasome, renin-angiotensin system, alphaB-crystallin, as well as invading peripheral immune cells, including T cells, dendritic cells, macrophages and monocytes.	Dopamine	22-24	NLR family pyrin domain containing 3	Homo sapiens	187-192
31332667-6	2019	In addition, increase in caspase-1/NLRP3 inflammasome activation was blocked by BAY11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	80-90	NLR family pyrin domain containing 3	Homo sapiens	35-40
31332667-9	2019	However, production of IL-1beta, NO/iNOS as well as caspase-1/NLRP3 activity was significantly reduced in the presence of CRID3.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	122-127	NLR family pyrin domain containing 3	Homo sapiens	62-67
33693087-7	2019	In macrophages, MSU activates the NLRP3 inflammasome and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1beta and IL-18 secretion.	Uric Acid	16-19	NLR family pyrin domain containing 3	Homo sapiens	34-39
31522718-0	2019	Colchicine inhibits endothelial inflammation via NLRP3/CRP pathway.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	49-54
31646907-5	2019	This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol"s harmful effects or accentuate its beneficial effects.	Ethanol	71-78	NLR family pyrin domain containing 3	Homo sapiens	121-126
31646907-5	2019	This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol"s harmful effects or accentuate its beneficial effects.	Ethanol	212-219	NLR family pyrin domain containing 3	Homo sapiens	121-126
31529565-11	2019	MiR-155 is involved in this process through regulating the NLRP3 inflammasome.	mir-155	0-7	NLR family pyrin domain containing 3	Homo sapiens	59-64
31485604-0	2019	Overexpression of miR-200a-3p promoted inflammation in sepsis-induced brain injury through ROS-induced NLRP3.	ros	91-94	NLR family pyrin domain containing 3	Homo sapiens	103-108
31445005-0	2019	Doxorubicin induces cardiomyocyte pyroptosis via the TINCR-mediated posttranscriptional stabilization of NLR family pyrin domain containing 3.	Doxorubicin	0-11	NLR family pyrin domain containing 3	Homo sapiens	105-141
31445005-5	2019	METHODS AND RESULTS: In vitro and in vivo experiments showed that DOX treatment induced cardiomyocyte pyroptosis as evidenced by increased cell death and upregulated expression levels of NLR family pyrin domain containing 3 (NLRP3), caspase-3, IL-1beta, IL-18 and GMDSD-N.	Doxorubicin	66-69	NLR family pyrin domain containing 3	Homo sapiens	187-223
31445005-5	2019	METHODS AND RESULTS: In vitro and in vivo experiments showed that DOX treatment induced cardiomyocyte pyroptosis as evidenced by increased cell death and upregulated expression levels of NLR family pyrin domain containing 3 (NLRP3), caspase-3, IL-1beta, IL-18 and GMDSD-N.	Doxorubicin	66-69	NLR family pyrin domain containing 3	Homo sapiens	225-230
31445005-6	2019	Inhibition of NLRP3 rescued the DOX-induced pyroptosis.	Doxorubicin	32-35	NLR family pyrin domain containing 3	Homo sapiens	14-19
31432628-2	2019	The nod-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL-1beta inflammation and IR.	Fatty Acids	104-125	NLR family pyrin domain containing 3	Homo sapiens	4-47
31432628-2	2019	The nod-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL-1beta inflammation and IR.	Fatty Acids	104-125	NLR family pyrin domain containing 3	Homo sapiens	49-54
31432628-3	2019	Interactions between SFA intake and NLRP3-related genetic variants may alter T2D risk factors.	Fatty Acids	21-24	NLR family pyrin domain containing 3	Homo sapiens	36-41
31739830-1	2019	Two series of 2-imino-coumarin based hybrids: 3-(benzoxazol-2-yl)-2H-chromen-2-imines 3-9 (series A-I) and 3-(benzothiazol-2-yl)-2H-chromen-2-imines 10-16 (series A-II), as well as their coumarin analogues: 3-(benzoxazol-2-yl)-2H-chromen-2-ones 17-21 (series B-I) and 3-(benzothiazol-2-yl)-2H-chromen-2-ones 22-28 (series B-II) were prepared as potential antitumor agents.	coumarin	14-30	NLR family pyrin domain containing 3	Homo sapiens	163-167
31485604-7	2019	In addition, the expression of miRNA-200a-3p was upregulated by the miRNA-200a-3p plasmid in human brain microvascular endothelial cells treated with lipopolysaccharide, which further induced inflammation via the induction of NLR family pyrin domain containing 3 (NLRP3) and suppression of Kelch like ECH associated protein (Keap)-1/nuclear factor erythroid 2 like 2 (Nrf2)/heme oxygenase (HO)-1.	kelch	290-295	NLR family pyrin domain containing 3	Homo sapiens	226-262
31485604-7	2019	In addition, the expression of miRNA-200a-3p was upregulated by the miRNA-200a-3p plasmid in human brain microvascular endothelial cells treated with lipopolysaccharide, which further induced inflammation via the induction of NLR family pyrin domain containing 3 (NLRP3) and suppression of Kelch like ECH associated protein (Keap)-1/nuclear factor erythroid 2 like 2 (Nrf2)/heme oxygenase (HO)-1.	kelch	290-295	NLR family pyrin domain containing 3	Homo sapiens	264-269
31485604-9	2019	However, the inhibition of NLRP3 attenuated the effects of miRNA-200a-3p on inflammation.	mirna-200a-3p	59-72	NLR family pyrin domain containing 3	Homo sapiens	27-32
31485604-10	2019	In conclusion, to the best of our knowledge, the results of the present study demonstrated for the first time that overexpression of miRNA-200a-3p promoted inflammation in sepsis-induced brain injury through reactive oxygen species-induced NLRP3.	mirna-200a-3p	133-146	NLR family pyrin domain containing 3	Homo sapiens	240-245
31485604-10	2019	In conclusion, to the best of our knowledge, the results of the present study demonstrated for the first time that overexpression of miRNA-200a-3p promoted inflammation in sepsis-induced brain injury through reactive oxygen species-induced NLRP3.	Oxygen	217-223	NLR family pyrin domain containing 3	Homo sapiens	240-245
31374144-4	2019	Subsequently, it has been found that EGCG reduces the microglial expressions of caspase-1 p20, NLRP3, and caspase-11 p26.	epigallocatechin gallate	37-41	NLR family pyrin domain containing 3	Homo sapiens	95-100
31529565-0	2019	MiR-155 promotes macrophage pyroptosis induced by Porphyromonas gingivalis through regulating the NLRP3 inflammasome.	mir-155	0-7	NLR family pyrin domain containing 3	Homo sapiens	98-103
31652453-0	2019	Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix.	Ketamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	107-112
31652453-10	2019	NLRP3 inflammatory body and TXNIP were activated by ketamine, which was supported by the changes in TNF-alpha, IL-6, IL-1 and IL-18 in vivo and in vitro.	Ketamine	52-60	NLR family pyrin domain containing 3	Homo sapiens	0-5
31652453-13	2019	Ketamine promoted cell apoptosis and induced inflammation in vivo and in vitro by regulating NLRP3/TXNIP aix.	Ketamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	93-98
31687078-3	2019	ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation.	Calcium	137-144	NLR family pyrin domain containing 3	Homo sapiens	35-40
31736762-3	2019	Methods: THP-1-derived macrophages were treated with high glucose to induce NLRP3 inflammasome activation.	Glucose	58-65	NLR family pyrin domain containing 3	Homo sapiens	76-81
31736762-6	2019	Results: We found that rapamycin reduced NLRP3 inflammasome activation in macrophages.	Sirolimus	23-32	NLR family pyrin domain containing 3	Homo sapiens	41-46
31736762-7	2019	Rapamycin reduced NLRP3 inflammasome activation by inhibiting mTOR phosphorylation and NF-kappaB activation.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	18-23
31749627-3	2019	This study aimed to investigate whether AdipoRon, a small-molecule adiponectin receptor agonist, alleviated saturated free fatty acids such as palmitic acid (PA)-induced cardiomyocyte injury by suppressing Nlrp3 inflammasome activation.	Palmitic Acid	143-156	NLR family pyrin domain containing 3	Homo sapiens	206-211
31749627-3	2019	This study aimed to investigate whether AdipoRon, a small-molecule adiponectin receptor agonist, alleviated saturated free fatty acids such as palmitic acid (PA)-induced cardiomyocyte injury by suppressing Nlrp3 inflammasome activation.	Palmitic Acid	158-160	NLR family pyrin domain containing 3	Homo sapiens	206-211
31749627-9	2019	Moreover, PA markedly activated the first phase of Nlrp3 inflammasome (NF-kb) signaling.	Palmitic Acid	10-12	NLR family pyrin domain containing 3	Homo sapiens	51-56
31749627-10	2019	Notably, the stimulation of PA enhanced ROS production as regulators of Nlrp3 inflammasome activation.	Palmitic Acid	28-30	NLR family pyrin domain containing 3	Homo sapiens	72-77
31749627-11	2019	In addition, treatment with PA increased the Nlrp3 inflammasome protein expression and complex formation, while AdipoRon abolished it.	Palmitic Acid	28-30	NLR family pyrin domain containing 3	Homo sapiens	45-50
31749627-12	2019	Lastly, the suppressive effect of AdipoRon to PA-induced cell injury and Nlrp3 inflammasome activation was significantly reversed by Nlrp3 siRNA and pan-caspase inhibitor (z-vad-fmk).	Palmitic Acid	46-48	NLR family pyrin domain containing 3	Homo sapiens	133-138
31749627-13	2019	Conclusion: Taken together, these data suggested that AdipoRon suppressed PA-induced myocardial cell injury by suppressing Nlrp3 inflammasome activation.	Palmitic Acid	74-76	NLR family pyrin domain containing 3	Homo sapiens	123-128
31649499-14	2019	Conversely, AF-induced LDH release is significantly reduced by MCC950 and Ac-YVAD-cmk (NLRP3 and Caspase-1 inhibitors, respectively), suggesting a pro-inflammatory cell death by pyroptosis.	Actinium	74-76	NLR family pyrin domain containing 3	Homo sapiens	87-92
31649546-9	2019	Allopurinol, an inhibitor of uric acid production, has been shown to decrease renal inflammation by limiting activation of the NLRP3 inflammasome.	Allopurinol	0-11	NLR family pyrin domain containing 3	Homo sapiens	127-132
31649546-9	2019	Allopurinol, an inhibitor of uric acid production, has been shown to decrease renal inflammation by limiting activation of the NLRP3 inflammasome.	Uric Acid	29-38	NLR family pyrin domain containing 3	Homo sapiens	127-132
31587010-0	2019	Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway.	Reactive Oxygen Species	111-134	NLR family pyrin domain containing 3	Homo sapiens	88-93
31587010-0	2019	Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway.	Reactive Oxygen Species	136-139	NLR family pyrin domain containing 3	Homo sapiens	88-93
31587010-13	2019	AGES-induced apoptosis was blocked by BAY 11-7082, an inhibitor of the NLRP3 inflammasome.	3-(4-methylphenylsulfonyl)-2-propenenitrile	38-49	NLR family pyrin domain containing 3	Homo sapiens	71-76
31736762-9	2019	Conclusion: Rapamycin can ameliorate high glucose-induced NLRP3 inflammasome activation by attenuating the mTOR/NF-kappaB signaling pathway in macrophages.	Sirolimus	12-21	NLR family pyrin domain containing 3	Homo sapiens	58-63
31736762-9	2019	Conclusion: Rapamycin can ameliorate high glucose-induced NLRP3 inflammasome activation by attenuating the mTOR/NF-kappaB signaling pathway in macrophages.	Glucose	42-49	NLR family pyrin domain containing 3	Homo sapiens	58-63
31749805-2	2019	By far, the best studied and most characterized inflammasome is NLRP3 inflammasome, which consists of NLRP3 (nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3), ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), and procaspase-1.	Leucine	135-142	NLR family pyrin domain containing 3	Homo sapiens	64-69
31749805-2	2019	By far, the best studied and most characterized inflammasome is NLRP3 inflammasome, which consists of NLRP3 (nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3), ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), and procaspase-1.	Leucine	135-142	NLR family pyrin domain containing 3	Homo sapiens	102-107
31611559-8	2019	In vitro, exposure of human umbilical vein endothelial cells (HUVECs) to KD sera-treated THP1 cells resulted in the activation of NLRP3 inflammasome and subsequent pyroptosis induction, as evidenced by elevated expression of caspase-1, GSDMD, cleaved p30 form of GSDMD, IL-1beta and IL-18, and increased LDH release and TUNEL and propidium iodide (PI)-positive cells.	Propidium	330-346	NLR family pyrin domain containing 3	Homo sapiens	130-135
31600880-1	2019	NLRP3 (NOD-like receptor family, pyrin domain-containing protein 3) activation has been linked to several chronic pathologies, including atherosclerosis, type-II diabetes, fibrosis, rheumatoid arthritis, and Alzheimer"s disease.	MRT67307	33-38	NLR family pyrin domain containing 3	Homo sapiens	0-5
31687078-3	2019	ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation.	Oxygen	179-185	NLR family pyrin domain containing 3	Homo sapiens	35-40
31302424-3	2019	Nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome as a multi-protein complex that activates caspase-1 can give rise to the proinflammatory cytokines such as interleukin-18 (IL-18) and interleukin-1 beta (IL-1beta) maturation.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	77-82
31381888-7	2019	Pharmacologic inhibition with Ac-YVAD-cmk of caspase 1, a critical component of the NLRP3 inflammasome, prevents DICER1 dysregulation- and dsRNA-induced osteoblast cell death.	ac-yvad	30-37	NLR family pyrin domain containing 3	Homo sapiens	84-89
31405564-7	2019	GW3965 treatment, which have shown to facilitate the efflux of cholesterol, eliminated the intracellular lipid droplets of 7-KC laden cells and decreased the expression of CPT1a, TGF-beta1, alpha- SMA and NLRP3.	GW 3965	0-6	NLR family pyrin domain containing 3	Homo sapiens	205-210
31554417-1	2019	Introduction: Chronic inflammatory diseases, including retinal diseases that are a major cause of vision loss, are associated with activation of the nucleotide-binding domain and leucine-rich repeat containing (NLR) protein-3 (NLRP3) inflammasome pathway.	leucylleucine	179-186	NLR family pyrin domain containing 3	Homo sapiens	227-232
31315072-8	2019	Besides, it"s identified that TXNIP induction and RIP1-RIP3-Drp1 pathway were required for the inhibitory routes of Suhuang from ER stress to NLRP3 inflammasome activation.	suhuang	116-123	NLR family pyrin domain containing 3	Homo sapiens	142-147
31315072-9	2019	Consistent with the in vivo findings, Suhuang also attenuated ER stress/NLRP3 inflammasome activation, and thereby restored pulmonary homeostasis in vitro.	suhuang	38-45	NLR family pyrin domain containing 3	Homo sapiens	72-77
31315072-11	2019	A further in vivo analysis showed that Suhuang-driven pharmacological inactivation of NLRP3 inflammasome and amelioration of pulmonary dysfunction were reversed by an ER stress inducer tunicamycin, well confirming the beneficial effects of Suhuang on pulmonary function by regulation of ER stress.	suhuang	39-46	NLR family pyrin domain containing 3	Homo sapiens	86-91
31315072-11	2019	A further in vivo analysis showed that Suhuang-driven pharmacological inactivation of NLRP3 inflammasome and amelioration of pulmonary dysfunction were reversed by an ER stress inducer tunicamycin, well confirming the beneficial effects of Suhuang on pulmonary function by regulation of ER stress.	Tunicamycin	185-196	NLR family pyrin domain containing 3	Homo sapiens	86-91
31315072-11	2019	A further in vivo analysis showed that Suhuang-driven pharmacological inactivation of NLRP3 inflammasome and amelioration of pulmonary dysfunction were reversed by an ER stress inducer tunicamycin, well confirming the beneficial effects of Suhuang on pulmonary function by regulation of ER stress.	suhuang	240-247	NLR family pyrin domain containing 3	Homo sapiens	86-91
31315072-12	2019	Collectively, these results indicated that Suhuang contributed to impairing NLRP3 inflammasome activation via inhibition of ER stress, which was responsible for the protection of pulmonary homeostasis.	suhuang	43-50	NLR family pyrin domain containing 3	Homo sapiens	76-81
31271646-5	2019	EXPERIMENTAL APPROACH: We tested two existing drugs, probenecid and AZ11645373, to target P2X7 receptor signalling and dampen NLRP3 inflammasome responses during severe IAV infection.	Probenecid	53-63	NLR family pyrin domain containing 3	Homo sapiens	126-131
31271646-5	2019	EXPERIMENTAL APPROACH: We tested two existing drugs, probenecid and AZ11645373, to target P2X7 receptor signalling and dampen NLRP3 inflammasome responses during severe IAV infection.	AZ 11645373	68-78	NLR family pyrin domain containing 3	Homo sapiens	126-131
31429348-0	2019	Mycophenolic acid enhanced lipopolysaccharide-induced interleukin-18 release in THP-1 cells via activation of the NLRP3 inflammasome.	Mycophenolic Acid	0-17	NLR family pyrin domain containing 3	Homo sapiens	114-119
31243816-0	2019	Dexmedetomidine alleviates lipopolysaccharide-induced acute kidney injury by inhibiting the NLRP3 inflammasome activation via regulating the TLR4/NOX4/NF-kappaB pathway.	Dexmedetomidine	0-15	NLR family pyrin domain containing 3	Homo sapiens	92-97
31243816-2	2019	In this study, the protective molecular mechanism of DEX in lipopolysaccharide (LPS)-induced acute kidney injury was investigated and its potential pharmacological targets from the perspective of inhibiting oxidative stress damage and the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation.	Dexmedetomidine	53-56	NLR family pyrin domain containing 3	Homo sapiens	239-288
31243816-2	2019	In this study, the protective molecular mechanism of DEX in lipopolysaccharide (LPS)-induced acute kidney injury was investigated and its potential pharmacological targets from the perspective of inhibiting oxidative stress damage and the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation.	Dexmedetomidine	53-56	NLR family pyrin domain containing 3	Homo sapiens	290-295
31243816-5	2019	In addition, DEX prevented nuclear factor-kappa B (NF-kappaB) activation and I-kappa B (IkappaB) phosphorylation, as well as the expressions of NLRP3 inflammasome-associated protein and downstream IL-18 and IL-1beta.	Dexmedetomidine	13-16	NLR family pyrin domain containing 3	Homo sapiens	144-149
31243816-6	2019	The messengerRNA (mRNA) and protein expressions of toll-like receptor 4 (TLR4), NADPH oxidase-4 (NOX4), NF-kappaB, and NLRP3 were also significantly reduced by DEX.	Dexmedetomidine	160-163	NLR family pyrin domain containing 3	Homo sapiens	119-124
31243816-9	2019	In conclusion, DEX attenuated LPS-induced AKI by inhibiting oxidative stress damage and NLRP3 inflammasome activation via regulating the TLR4/NOX4/NF-kappaB pathway, mainly acting on the alpha2 AR rather than IR.	Dexmedetomidine	15-18	NLR family pyrin domain containing 3	Homo sapiens	88-93
31315072-7	2019	Suhuang also inhibited NLRP3 inflammasome activation, as evidenced by disrupting the assembly of NLRP3 inflammasome and reducing the expression of cleaved caspase-1, and decreased IL-1beta secretion.	suhuang	0-7	NLR family pyrin domain containing 3	Homo sapiens	23-28
31315072-7	2019	Suhuang also inhibited NLRP3 inflammasome activation, as evidenced by disrupting the assembly of NLRP3 inflammasome and reducing the expression of cleaved caspase-1, and decreased IL-1beta secretion.	suhuang	0-7	NLR family pyrin domain containing 3	Homo sapiens	97-102
31632394-0	2019	Nigericin Promotes NLRP3-Independent Bacterial Killing in Macrophages.	Nigericin	0-9	NLR family pyrin domain containing 3	Homo sapiens	19-24
31632394-6	2019	Using the NLRP3 inflammasome-deficient Raw 264.7 and PYCARD-deficient J77 macrophages, which both lack PYCARD, we found that the potassium efflux activator nigericin enhances bacterial killing.	Potassium	129-138	NLR family pyrin domain containing 3	Homo sapiens	10-15
31632394-6	2019	Using the NLRP3 inflammasome-deficient Raw 264.7 and PYCARD-deficient J77 macrophages, which both lack PYCARD, we found that the potassium efflux activator nigericin enhances bacterial killing.	Nigericin	156-165	NLR family pyrin domain containing 3	Homo sapiens	10-15
31872639-11	2019	Compared with IR model group,wogonoside not only inhibited the protein expression of inflammatory nuclear transcriptional factors NLRP3,SOCS3,TLR4,NF-kappaB,but also decreased the expression of downstream inflammatory effect factors IL-1beta,IL-6 and TNF-alpha.	wogonoside	29-39	NLR family pyrin domain containing 3	Homo sapiens	130-135
30978354-4	2019	B19V infection increases the production of tumor necrosis factor-alpha and induces NLRP3-mediated caspase-1 activation in both THP-1 cells differentiated with phorbol 12-myristate 13-acetate and in monocytes from patients with SSc but not from healthy controls.	Tetradecanoylphorbol Acetate	159-190	NLR family pyrin domain containing 3	Homo sapiens	83-88
31524270-0	2019	Emodin attenuates adenosine triphosphate-induced pancreatic ductal cell injury in vitro via the inhibition of the P2X7/NLRP3 signaling pathway.	Adenosine Triphosphate	18-40	NLR family pyrin domain containing 3	Homo sapiens	119-124
31524270-9	2019	Collectively, the findings of this study demonstrate that emodin attenuates ATP-induced pancreatic ductal cell injury in AP mainly through the inhibition of the P2X7/NLRP3 signaling pathway.	Adenosine Triphosphate	76-79	NLR family pyrin domain containing 3	Homo sapiens	166-171
31276767-5	2019	Results indicate, that consistent with previous finding, DNCB more rapidly (3 h) induces NLRP3, ASC protein expression and caspase-1 activation compared to PPD.	Dinitrochlorobenzene	57-61	NLR family pyrin domain containing 3	Homo sapiens	89-94
31872639-0	2019	[Study on regulation of NLRP3/SOCS3-TLR4-NF-kappaB inflammatory pathway by wogonoside to improve hepatic insulin resistance].	wogonoside	75-85	NLR family pyrin domain containing 3	Homo sapiens	24-29
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	Dinitrochlorobenzene	68-72	NLR family pyrin domain containing 3	Homo sapiens	167-172
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	Dinitrochlorobenzene	68-72	NLR family pyrin domain containing 3	Homo sapiens	282-287
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	4-phenylenediamine	77-98	NLR family pyrin domain containing 3	Homo sapiens	167-172
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	4-phenylenediamine	100-103	NLR family pyrin domain containing 3	Homo sapiens	167-172
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	4-phenylenediamine	100-103	NLR family pyrin domain containing 3	Homo sapiens	282-287
31558729-5	2019	Anti-inflammatory agents, such corticosteroids, NSAIDs and colchicine, are widely used for the treatment of gout flare; recognition of the importance of NLRP3 inflammasome activation and bioactive IL-1beta release in initiation of the gout flare has led to the development of anti-IL-1beta biological therapy for gout flares.	Colchicine	59-69	NLR family pyrin domain containing 3	Homo sapiens	153-158
31571967-1	2019	Background: NLRP3 inflammasome can be activated by high glucose and links inflammation and metabolic disease.	Glucose	56-63	NLR family pyrin domain containing 3	Homo sapiens	12-17
31571967-9	2019	Moreover, either high glucose or IL-1beta promoted the expression of adhesion molecules, which were suppressed by NLRP3 knockdown or IL-1beta receptor antagonist.	Glucose	22-29	NLR family pyrin domain containing 3	Homo sapiens	114-119
31571967-8	2019	In vitro, the expression of NLRP3 inflammasome components and the secretion of IL-1beta were augmented by high glucose in HUVECs.	Glucose	111-118	NLR family pyrin domain containing 3	Homo sapiens	28-33
31532390-0	2019	ENaC-mediated sodium influx exacerbates NLRP3-dependent inflammation in Cystic Fibrosis.	Sodium	14-20	NLR family pyrin domain containing 3	Homo sapiens	40-45
31532390-6	2019	These data support a role for sodium in modulating NLRP3-inflammasome activation.	Sodium	30-36	NLR family pyrin domain containing 3	Homo sapiens	51-56
31479495-7	2019	We also determined that MAYV triggers NLRP3 inflammasome activation by inducing reactive oxygen species (ROS) and potassium efflux.	Reactive Oxygen Species	80-103	NLR family pyrin domain containing 3	Homo sapiens	38-43
31358323-10	2019	Artemisinin significantly inhibited interaction between NLRP3 and NEK7 in NLRP3 inflammasome activation.	artemisinin	0-11	NLR family pyrin domain containing 3	Homo sapiens	56-61
31358323-10	2019	Artemisinin significantly inhibited interaction between NLRP3 and NEK7 in NLRP3 inflammasome activation.	artemisinin	0-11	NLR family pyrin domain containing 3	Homo sapiens	74-79
31358323-13	2019	CONCLUSION: This study revealed that artemisinin inhibited activation of NLRP3 inflammasome by suppressing interaction between NEK7 and NLRP3 in uric acid-induced inflammation.	artemisinin	37-48	NLR family pyrin domain containing 3	Homo sapiens	73-78
31358323-13	2019	CONCLUSION: This study revealed that artemisinin inhibited activation of NLRP3 inflammasome by suppressing interaction between NEK7 and NLRP3 in uric acid-induced inflammation.	artemisinin	37-48	NLR family pyrin domain containing 3	Homo sapiens	136-141
31358323-13	2019	CONCLUSION: This study revealed that artemisinin inhibited activation of NLRP3 inflammasome by suppressing interaction between NEK7 and NLRP3 in uric acid-induced inflammation.	Uric Acid	145-154	NLR family pyrin domain containing 3	Homo sapiens	73-78
31358323-13	2019	CONCLUSION: This study revealed that artemisinin inhibited activation of NLRP3 inflammasome by suppressing interaction between NEK7 and NLRP3 in uric acid-induced inflammation.	Uric Acid	145-154	NLR family pyrin domain containing 3	Homo sapiens	136-141
31358323-0	2019	Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation through blocking interaction between NLRP3 and NEK7.	artemisinin	28-39	NLR family pyrin domain containing 3	Homo sapiens	61-66
31358323-0	2019	Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation through blocking interaction between NLRP3 and NEK7.	artemisinin	28-39	NLR family pyrin domain containing 3	Homo sapiens	128-133
31358323-0	2019	Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation through blocking interaction between NLRP3 and NEK7.	Uric Acid	43-52	NLR family pyrin domain containing 3	Homo sapiens	61-66
31358323-0	2019	Anti-inflammatory effect of artemisinin on uric acid-induced NLRP3 inflammasome activation through blocking interaction between NLRP3 and NEK7.	Uric Acid	43-52	NLR family pyrin domain containing 3	Homo sapiens	128-133
31358323-3	2019	The aim of this study was to clarify the anti-inflammatory effect of artemisinin on activation of uric acid-induced NLRP3 inflammasome through regulation of NEK7.	artemisinin	69-80	NLR family pyrin domain containing 3	Homo sapiens	116-121
31358323-3	2019	The aim of this study was to clarify the anti-inflammatory effect of artemisinin on activation of uric acid-induced NLRP3 inflammasome through regulation of NEK7.	Uric Acid	98-107	NLR family pyrin domain containing 3	Homo sapiens	116-121
31358323-9	2019	Enhanced expression of NLRP3, caspase-1, and IL-1beta was noted in macrophages treated with LPS (10 ng/ml) and MSU crystals (0.1 mg/ml), which was markedly suppressed by treatment with artemisinin (1, 10, and 100 muM).	Uric Acid	111-114	NLR family pyrin domain containing 3	Homo sapiens	23-28
31358323-9	2019	Enhanced expression of NLRP3, caspase-1, and IL-1beta was noted in macrophages treated with LPS (10 ng/ml) and MSU crystals (0.1 mg/ml), which was markedly suppressed by treatment with artemisinin (1, 10, and 100 muM).	artemisinin	185-196	NLR family pyrin domain containing 3	Homo sapiens	23-28
31351069-0	2019	The protective effects of orexin a against high glucose-induced activation of NLRP3 inflammasome in human vascular endothelial cells.	Glucose	48-55	NLR family pyrin domain containing 3	Homo sapiens	78-83
31351069-5	2019	In the present study, we explored the role of orexin A, an endogenous peptide produced in the hypothalamus, in high glucose-induced activation of the NLRP3 inflammasome, oxidative stress, and expression of several key cytokines.	Glucose	116-123	NLR family pyrin domain containing 3	Homo sapiens	150-155
31351069-7	2019	We also show that orexin A inhibits high glucose-induced expression of TxNIP, which is crucial to the activation of the NLRP3 inflammasome, as well as that of HMGB1.	Glucose	41-48	NLR family pyrin domain containing 3	Homo sapiens	120-125
31479495-7	2019	We also determined that MAYV triggers NLRP3 inflammasome activation by inducing reactive oxygen species (ROS) and potassium efflux.	Reactive Oxygen Species	105-108	NLR family pyrin domain containing 3	Homo sapiens	38-43
31479495-7	2019	We also determined that MAYV triggers NLRP3 inflammasome activation by inducing reactive oxygen species (ROS) and potassium efflux.	Potassium	114-123	NLR family pyrin domain containing 3	Homo sapiens	38-43
31148259-3	2019	In the present research, we attempt to investigate whether molecules with anti-inflammatory activity, alpha-lipoic acid (ALA), and/or myoinositol affect the endometrial NALP-3 expression and activation.	Thioctic Acid	102-119	NLR family pyrin domain containing 3	Homo sapiens	169-175
31062071-5	2019	As a consequence, saturated CLs induce a pro-inflammatory response in macrophages characterized by TNF-alpha and IP-10 secretion, and activate the alternative NLRP3 inflammasome pathway in human blood-derived monocytes.	Cardiolipins	28-31	NLR family pyrin domain containing 3	Homo sapiens	159-164
31059678-0	2019	NLRP3 inflammasome activation is involved in trimethyltin-induced neuroinflammation.	trimethyltin	45-57	NLR family pyrin domain containing 3	Homo sapiens	0-5
31148259-3	2019	In the present research, we attempt to investigate whether molecules with anti-inflammatory activity, alpha-lipoic acid (ALA), and/or myoinositol affect the endometrial NALP-3 expression and activation.	Thioctic Acid	121-124	NLR family pyrin domain containing 3	Homo sapiens	169-175
31148259-3	2019	In the present research, we attempt to investigate whether molecules with anti-inflammatory activity, alpha-lipoic acid (ALA), and/or myoinositol affect the endometrial NALP-3 expression and activation.	Inositol	134-145	NLR family pyrin domain containing 3	Homo sapiens	169-175
31172209-0	2019	Neferine inhibits LPS-ATP-induced endothelial cell pyroptosis via regulation of ROS/NLRP3/Caspase-1 signaling pathway.	Adenosine Triphosphate	22-25	NLR family pyrin domain containing 3	Homo sapiens	84-89
31172209-6	2019	RESULTS: We found that neferine could inhibit LPS-ATP-induced oxidative stress and the activation of NLRP3 inflammasome signaling, and increased the endothelial cell viability and SOD production.	neferine	23-31	NLR family pyrin domain containing 3	Homo sapiens	101-106
31172209-0	2019	Neferine inhibits LPS-ATP-induced endothelial cell pyroptosis via regulation of ROS/NLRP3/Caspase-1 signaling pathway.	neferine	0-8	NLR family pyrin domain containing 3	Homo sapiens	84-89
31172209-7	2019	siRNA which mediated the knockdown of NLRP3 promoted the neferine-induced inhibition effects of cell pyroptosis.	neferine	57-65	NLR family pyrin domain containing 3	Homo sapiens	38-43
31172209-8	2019	Furthermore, these neferine-induced effects were reversed by the over-expression of NLRP3.	neferine	19-27	NLR family pyrin domain containing 3	Homo sapiens	84-89
31172209-9	2019	CONCLUSIONS: Our findings indicated neferine may reduce ROS by anti-oxidation and inhibit LPS-ATP-induced endothelial cell pyroptosis via blocking ROS/NLRP3/Caspase-1 signaling pathway, which provides the evidence for therapeutic effect in CKD.	neferine	36-44	NLR family pyrin domain containing 3	Homo sapiens	151-156
31176046-0	2019	The neuroprotection of progesterone against Abeta-induced NLRP3-Caspase-1 inflammasome activation via enhancing autophagy in astrocytes.	Progesterone	23-35	NLR family pyrin domain containing 3	Homo sapiens	58-63
31176046-4	2019	However, the exact role of PG in regulating NLRP3-Caspase-1 inflammasome remains to be elucidated.	Progesterone	27-29	NLR family pyrin domain containing 3	Homo sapiens	44-49
31176046-6	2019	However, pharmacological activation of autophagy by Rapamycin (RAPA) efficiently suppressed Abeta-, lipopolysaccharides (LPS)-induced IL-1beta expression via regulating NLRP3-Caspase-1 inflammasome in astrocytes.	Sirolimus	52-61	NLR family pyrin domain containing 3	Homo sapiens	169-174
31176046-6	2019	However, pharmacological activation of autophagy by Rapamycin (RAPA) efficiently suppressed Abeta-, lipopolysaccharides (LPS)-induced IL-1beta expression via regulating NLRP3-Caspase-1 inflammasome in astrocytes.	Sirolimus	63-67	NLR family pyrin domain containing 3	Homo sapiens	169-174
31176046-7	2019	Remarkably, PG significantly inhibited Abeta-induced NLRP3-Caspase-1 inflammasome activation.	Progesterone	12-14	NLR family pyrin domain containing 3	Homo sapiens	53-58
31176046-8	2019	Autophagy inhibitor 3-MA blocked the protective effects of PG in mediating NLRP3 inflammasome and IL-1beta processing.	3-methyladenine	20-24	NLR family pyrin domain containing 3	Homo sapiens	75-80
31176046-8	2019	Autophagy inhibitor 3-MA blocked the protective effects of PG in mediating NLRP3 inflammasome and IL-1beta processing.	Progesterone	59-61	NLR family pyrin domain containing 3	Homo sapiens	75-80
31176046-9	2019	Taken together, our observations suggest that autophagy-lysosome pathway is one specific molecular mechanism in regulating Abeta-induced NLRP3-Caspase-1 inflammasome activation in astrocytes, particularly uncover the potential neuroprotection of PG in regulating upstream signaling leading to the sequence events of neuroinflammation.	Progesterone	246-248	NLR family pyrin domain containing 3	Homo sapiens	137-142
31176046-10	2019	That neuroprotective mechanism of PG in regulating NLRP3-Caspase-1 inflammasome can be a potential therapeutic target for ameliorating the pathological procession of AD.	Progesterone	34-36	NLR family pyrin domain containing 3	Homo sapiens	51-56
30897250-7	2019	This mechanism also promotes IL-1beta release and potassium efflux that connects caspase-11 to NLRP3 activation.	Potassium	50-59	NLR family pyrin domain containing 3	Homo sapiens	95-100
30824640-0	2019	Precipitation of Soluble Uric Acid Is Necessary for In Vitro Activation of the NLRP3 Inflammasome in Primary Human Monocytes.	Uric Acid	25-34	NLR family pyrin domain containing 3	Homo sapiens	79-84
30824640-1	2019	OBJECTIVE: To investigate the effects of soluble uric acid (UA) on expression and activation of the NOD-like receptor (NLR) pyrin domain containing protein 3 (NLRP3) inflammasome in human monocytes to elucidate the role of hyperuricemia in the pathogenesis of gout.	Uric Acid	49-58	NLR family pyrin domain containing 3	Homo sapiens	159-164
30824640-1	2019	OBJECTIVE: To investigate the effects of soluble uric acid (UA) on expression and activation of the NOD-like receptor (NLR) pyrin domain containing protein 3 (NLRP3) inflammasome in human monocytes to elucidate the role of hyperuricemia in the pathogenesis of gout.	Uric Acid	60-62	NLR family pyrin domain containing 3	Homo sapiens	159-164
30824640-2	2019	METHODS: Primary human monocytes and the THP-1 human monocyte cell line were used to determine the effects of short- and longterm exposure to UA on activation of the NLRP3 inflammasome and subsequent interleukin 1beta (IL-1beta) secretion by ELISA and cell-based assays.	Uric Acid	142-144	NLR family pyrin domain containing 3	Homo sapiens	166-171
30824640-4	2019	RESULTS: Precipitation of UA was required for activation of the NLRP3 inflammasome and subsequent release of IL-1beta in human monocytes.	Uric Acid	26-28	NLR family pyrin domain containing 3	Homo sapiens	64-69
30824640-9	2019	CONCLUSION: Despite reports indicating that soluble UA can prime and activate the NLRP3 inflammasome in human peripheral blood mononuclear cells, precipitation of soluble UA into MSU crystals is essential for in vitro NLRP3 signaling in primary human monocytes.	Uric Acid	52-54	NLR family pyrin domain containing 3	Homo sapiens	82-87
30824640-9	2019	CONCLUSION: Despite reports indicating that soluble UA can prime and activate the NLRP3 inflammasome in human peripheral blood mononuclear cells, precipitation of soluble UA into MSU crystals is essential for in vitro NLRP3 signaling in primary human monocytes.	Uric Acid	171-173	NLR family pyrin domain containing 3	Homo sapiens	218-223
31383789-8	2019	Mechanistically, Dex attenuated H2O2-mediated activation of NF-kappaB and NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), both of which play key roles in inflammation and inflammatory damage.	Dexmedetomidine	17-20	NLR family pyrin domain containing 3	Homo sapiens	74-122
31695408-0	2019	NLRP3 inflammasome activation by estrogen promotes the progression of human endometrial cancer.	Estrogens	33-41	NLR family pyrin domain containing 3	Homo sapiens	0-5
31300552-3	2019	We report that digoxin and related compounds activate the NLRP3 inflammasome in macrophages and cardiomyocytes at concentrations achievable during clinical use.	Digoxin	15-22	NLR family pyrin domain containing 3	Homo sapiens	58-63
31300552-7	2019	Cardiac glycoside-induced cellular cytotoxicity and IL-1beta signaling are likewise antagonized by inhibitors of the NLRP3 inflammasome or the IL-1 receptor-targeting biological agent anakinra.	Glycosides	8-17	NLR family pyrin domain containing 3	Homo sapiens	117-122
31383789-8	2019	Mechanistically, Dex attenuated H2O2-mediated activation of NF-kappaB and NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), both of which play key roles in inflammation and inflammatory damage.	Dexmedetomidine	17-20	NLR family pyrin domain containing 3	Homo sapiens	124-129
31383789-8	2019	Mechanistically, Dex attenuated H2O2-mediated activation of NF-kappaB and NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), both of which play key roles in inflammation and inflammatory damage.	Hydrogen Peroxide	32-36	NLR family pyrin domain containing 3	Homo sapiens	74-122
31383789-8	2019	Mechanistically, Dex attenuated H2O2-mediated activation of NF-kappaB and NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), both of which play key roles in inflammation and inflammatory damage.	Hydrogen Peroxide	32-36	NLR family pyrin domain containing 3	Homo sapiens	124-129
31383789-9	2019	Dex inactivated NLRP3 through the suppression of NF-kappaB and JNK signals.	Dexmedetomidine	0-3	NLR family pyrin domain containing 3	Homo sapiens	16-21
31481891-6	2019	Raltegravir ameliorated pulmonary fibrosis by reducing the pathology score, collagen deposition, and expression of alpha-smooth muscle actin, NLRP3, HMGB1, TLR4, inhibitor of kappa B, p-NF-kappaB, HIF-1alpha, collagen I, and collagen III.	Raltegravir Potassium	0-11	NLR family pyrin domain containing 3	Homo sapiens	142-147
31531346-0	2019	AVE 0991 Attenuates Pyroptosis and Liver Damage after Heatstroke by Inhibiting the ROS-NLRP3 Inflammatory Signalling Pathway.	AVE 0991	0-8	NLR family pyrin domain containing 3	Homo sapiens	87-92
31531346-0	2019	AVE 0991 Attenuates Pyroptosis and Liver Damage after Heatstroke by Inhibiting the ROS-NLRP3 Inflammatory Signalling Pathway.	Reactive Oxygen Species	83-86	NLR family pyrin domain containing 3	Homo sapiens	87-92
31531346-1	2019	We previously demonstrated that angiotensin-(1-7) (Ang-(1-7)), an essential endocrine factor, inhibits the NLRP3 inflammasome by regulating reactive oxygen species (ROS) in fibrotic livers.	Reactive Oxygen Species	140-163	NLR family pyrin domain containing 3	Homo sapiens	107-112
31302140-1	2019	Activation of the NLRP3 inflammasome plays an important role in high glucose- induced endothelial dysfunction in patients with type 2 diabetes mellitus (T2DM).	Glucose	69-76	NLR family pyrin domain containing 3	Homo sapiens	18-23
31531346-1	2019	We previously demonstrated that angiotensin-(1-7) (Ang-(1-7)), an essential endocrine factor, inhibits the NLRP3 inflammasome by regulating reactive oxygen species (ROS) in fibrotic livers.	Reactive Oxygen Species	165-168	NLR family pyrin domain containing 3	Homo sapiens	107-112
31531346-4	2019	We aimed to examine the change in angiotensin peptides in the livers affected by heatstroke and the effect on the ROS-NLRP3 inflammatory signalling pathway.	Reactive Oxygen Species	114-117	NLR family pyrin domain containing 3	Homo sapiens	118-123
31531346-8	2019	Hepatic damage associated with increased ROS and protein expression levels of NOX4, NLRP3, caspase-1, and IL-1beta was attenuated by AVE 0991, an analogue of Ang-(1-7).	AVE 0991	133-141	NLR family pyrin domain containing 3	Homo sapiens	84-89
31531346-10	2019	In summary, AVE 0991 attenuates pyroptosis and liver damage induced by heat stress by inhibiting the ROS-NLRP3 inflammatory signalling pathway.	Reactive Oxygen Species	101-104	NLR family pyrin domain containing 3	Homo sapiens	105-110
31302140-3	2019	In the current study, we aimed to investigate whether dulaglutide possesses a protective effect against high glucose- induced activation of the NLRP3 inflammasome.	Glucose	109-116	NLR family pyrin domain containing 3	Homo sapiens	144-149
31302140-6	2019	Dulaglutide suppressed high glucose- induced activation of NLRP3 inflammasome by reducing the expression of NLRP3, ASC, and cleaved caspase 1 (P10).	Glucose	28-35	NLR family pyrin domain containing 3	Homo sapiens	59-64
31302140-6	2019	Dulaglutide suppressed high glucose- induced activation of NLRP3 inflammasome by reducing the expression of NLRP3, ASC, and cleaved caspase 1 (P10).	Glucose	28-35	NLR family pyrin domain containing 3	Homo sapiens	108-113
31485193-0	2019	RIPK2-Mediated Autophagy and Negatively Regulated ROS-NLRP3 Inflammasome Signaling in GMCs Stimulated with High Glucose.	ros	50-53	NLR family pyrin domain containing 3	Homo sapiens	54-59
31108165-12	2019	Taken together, these results suggest that downregulation of hsa_circ_0068087 ameliorates TLR4/NF-kappaB/NLRP3 inflammasome-mediated inflammation and endothelial cell dysfunction in the high glucose condition by sponging miR-197.	Glucose	191-198	NLR family pyrin domain containing 3	Homo sapiens	105-110
31409766-0	2019	Publisher Correction: Acetate attenuates inflammasome activation through GPR43-mediated Ca2+-dependent NLRP3 ubiquitination.	Acetates	22-29	NLR family pyrin domain containing 3	Homo sapiens	103-108
31412804-0	2019	Uric acid regulates NLRP3/IL-1beta signaling pathway and further induces vascular endothelial cells injury in early CKD through ROS activation and K+ efflux.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	20-25
31412804-0	2019	Uric acid regulates NLRP3/IL-1beta signaling pathway and further induces vascular endothelial cells injury in early CKD through ROS activation and K+ efflux.	ros	128-131	NLR family pyrin domain containing 3	Homo sapiens	20-25
31412804-9	2019	RESULTS: The expression of IL-1beta, ICAM-1, NLRP3 complexes, and activation of NLRP3 inflammasome could be induced by UA, but the changes induced by UA were partially reversed by siRNA NLRP3 or caspase 1 inhibitor.	Uric Acid	119-121	NLR family pyrin domain containing 3	Homo sapiens	45-50
31412804-9	2019	RESULTS: The expression of IL-1beta, ICAM-1, NLRP3 complexes, and activation of NLRP3 inflammasome could be induced by UA, but the changes induced by UA were partially reversed by siRNA NLRP3 or caspase 1 inhibitor.	Uric Acid	119-121	NLR family pyrin domain containing 3	Homo sapiens	80-85
31412804-9	2019	RESULTS: The expression of IL-1beta, ICAM-1, NLRP3 complexes, and activation of NLRP3 inflammasome could be induced by UA, but the changes induced by UA were partially reversed by siRNA NLRP3 or caspase 1 inhibitor.	Uric Acid	119-121	NLR family pyrin domain containing 3	Homo sapiens	80-85
31412804-10	2019	Furthermore, we identified that UA regulated the activation of NLRP3 inflammasome by activating ROS and K+ efflux.	ros	96-99	NLR family pyrin domain containing 3	Homo sapiens	63-68
31412804-11	2019	In vivo results showed that UA caused the vascular endothelial injury by activating NLRP3/IL-1beta pathway.	Uric Acid	28-30	NLR family pyrin domain containing 3	Homo sapiens	84-89
31412804-13	2019	CONCLUSIONS: UA could regulate NLRP3/IL-1beta signaling pathway through ROS activation and K+ efflux and further induce vascular endothelial cells injury in early stages of CKD.	ros	72-75	NLR family pyrin domain containing 3	Homo sapiens	31-36
31485193-1	2019	Background: Hyperglycemia plays a vital role in diabetic nephropathy (DN); autophagy and its potential upregulator receptor-interacting protein kinase 2 (RIPK2) are associated with ROS, which play a potential role in regulating NLRP3, and may be involved in inflammation in DN.	ros	181-184	NLR family pyrin domain containing 3	Homo sapiens	228-233
31485193-2	2019	Aim: In this study, we aimed to explore the mechanisms mediated by RIPK2 in autophagy and the relationship with ROS-NLRP3 of DN, by investigating the levels of RIPK2 and autophagy in glomerular mesangial cells (GMCs) stimulated with high glucose.	ros	112-115	NLR family pyrin domain containing 3	Homo sapiens	116-121
31485193-10	2019	RIPK2 regulates ROS-NLRP3 inflammasome signaling through autophagy and may be involved in the pathogenesis of DN.	ros	16-19	NLR family pyrin domain containing 3	Homo sapiens	20-25
31265218-7	2019	XO-produced ROS also increase the synthesis of pro-IL-1beta, while the parasite activates caspase-1, providing the two necessary signals for the activation of the NLRP3 inflammasome.	Reactive Oxygen Species	12-15	NLR family pyrin domain containing 3	Homo sapiens	163-168
31129157-0	2019	KHG21834 attenuates glutamate-induced mitochondrial damage, apoptosis, and NLRP3 inflammasome activation in SH-SY5Y human neuroblastoma cells.	Glutamic Acid	20-29	NLR family pyrin domain containing 3	Homo sapiens	75-80
31129157-6	2019	Furthermore, KHG21834 efficiently reduced glutamate-induced ER stress and NLRP3 inflammasome activation (59% and 65% of glutamate group, respectively).	KHG21834	13-21	NLR family pyrin domain containing 3	Homo sapiens	74-79
31129157-6	2019	Furthermore, KHG21834 efficiently reduced glutamate-induced ER stress and NLRP3 inflammasome activation (59% and 65% of glutamate group, respectively).	Glutamic Acid	42-51	NLR family pyrin domain containing 3	Homo sapiens	74-79
31905042-3	2019	This paper draws on recent scientific progress in inflammation biology, especially elucidation of the activation thresholds for NLRP3 inflammasomes and resulting chronic inflammation, to model dose-response relationships for malignant mesothelioma and lung cancer risks caused by asbestos exposures.	Asbestos	280-288	NLR family pyrin domain containing 3	Homo sapiens	128-133
31129157-0	2019	KHG21834 attenuates glutamate-induced mitochondrial damage, apoptosis, and NLRP3 inflammasome activation in SH-SY5Y human neuroblastoma cells.	KHG21834	0-8	NLR family pyrin domain containing 3	Homo sapiens	75-80
31100709-2	2019	The NLRP3 inflammasome as a molecular platform regulates the activation of ATP signaling, K+ efflux, cathepsin-B activity, lysosomal function and pro-inflammatory cytokines (i.e. IL-1beta and IL-18).	Adenosine Triphosphate	75-78	NLR family pyrin domain containing 3	Homo sapiens	4-9
31132733-0	2019	L-Fucose ameliorates DSS-induced acute colitis via inhibiting macrophage M1 polarization and inhibiting NLRP3 inflammasome and NF-kB activation.	Fucose	0-8	NLR family pyrin domain containing 3	Homo sapiens	104-109
31129418-5	2019	Herein, we demonstrate that Rev-erbalpha reduces IL-1beta production and lung injury following an intraperitoneal injection of LPS, which is dependent on the NF-kappaB/NALP3 pathway.	rev-erbalpha	28-40	NLR family pyrin domain containing 3	Homo sapiens	168-173
31129418-0	2019	Rev-erbalpha can regulate the NF-kappaB/NALP3 pathway to modulate lipopolysaccharide-induced acute lung injury and inflammation.	rev-erbalpha	0-12	NLR family pyrin domain containing 3	Homo sapiens	40-45
31132733-0	2019	L-Fucose ameliorates DSS-induced acute colitis via inhibiting macrophage M1 polarization and inhibiting NLRP3 inflammasome and NF-kB activation.	Dextran Sulfate	21-24	NLR family pyrin domain containing 3	Homo sapiens	104-109
31132733-5	2019	In addition, L-fucose can inhibit macrophage M1 polarization, inactivate the NLRP3 inflammasome and reduce the release of TNFalpha, IL1beta, IL6 pro-inflammatory cytokines.	Fucose	13-21	NLR family pyrin domain containing 3	Homo sapiens	77-82
31132733-6	2019	In vitro studies showed that L-fucose ameliorated cell damage resulting from the administration of LPS with ATP in BMDMs, inhibited NLRP3 inflammasome activation and reduced the release of corresponding pro-inflammatory cytokines.	Fucose	29-37	NLR family pyrin domain containing 3	Homo sapiens	132-137
31132733-8	2019	Overall, our results show that L-fucose can attenuate colitis by inhibiting macrophage M1 polarization, inhibiting NLRP3 inflammasome and NF-kB activation, and down-regulation of pro-inflammatory cytokines.	Fucose	31-39	NLR family pyrin domain containing 3	Homo sapiens	115-120
30872118-9	2019	APOE-dependent NLRP3 inflammasome activation in macrophages was primarily mediated through a potassium efflux-dependent mechanism.	Potassium	93-102	NLR family pyrin domain containing 3	Homo sapiens	15-20
31257469-0	2019	NLRP3 inflammasome expression in peripheral blood monocytes of coronary heart disease patients and its modulation by rosuvastatin.	Rosuvastatin Calcium	117-129	NLR family pyrin domain containing 3	Homo sapiens	0-5
31374828-0	2019	Fucoxanthin and Rosmarinic Acid Combination Has Anti-Inflammatory Effects through Regulation of NLRP3 Inflammasome in UVB-Exposed HaCaT Keratinocytes.	fucoxanthin	0-11	NLR family pyrin domain containing 3	Homo sapiens	96-101
31374828-0	2019	Fucoxanthin and Rosmarinic Acid Combination Has Anti-Inflammatory Effects through Regulation of NLRP3 Inflammasome in UVB-Exposed HaCaT Keratinocytes.	rosmarinic acid	16-31	NLR family pyrin domain containing 3	Homo sapiens	96-101
31257469-9	2019	Interference with rosuvastatin in vitro revealed that the expression of NLRP3 inflammasome and its downstream cytokines were significantly downregulated in both SAP and AMI groups in a time-dependent manner.	Rosuvastatin Calcium	18-30	NLR family pyrin domain containing 3	Homo sapiens	72-77
31257469-10	2019	The activation of NLRP3 inflammasome may be involved in the development of CHD, and rosuvastatin could attenuate the inflammatory process of atherosclerosis by downregulating NLRP3 expression and its downstream mediators.	Rosuvastatin Calcium	84-96	NLR family pyrin domain containing 3	Homo sapiens	175-180
31366948-0	2019	Miltefosine increases macrophage cholesterol release and inhibits NLRP3-inflammasome assembly and IL-1beta release.	miltefosine	0-11	NLR family pyrin domain containing 3	Homo sapiens	66-71
31020518-4	2019	In this review we will present a concept that aberrant purinergic signaling and increases in extracellular level of adenosine triphosphate (ATP) in the brain parenchyma may lead to activation of Nlrp3 inflammasome in microglia cells and as a consequence microglia released danger associated molecular pattern (DAMP) proteins activate complement cascade (ComC) in mannan binding lectin (MBL) - dependent manner.	Adenosine Triphosphate	116-138	NLR family pyrin domain containing 3	Homo sapiens	195-200
31020518-4	2019	In this review we will present a concept that aberrant purinergic signaling and increases in extracellular level of adenosine triphosphate (ATP) in the brain parenchyma may lead to activation of Nlrp3 inflammasome in microglia cells and as a consequence microglia released danger associated molecular pattern (DAMP) proteins activate complement cascade (ComC) in mannan binding lectin (MBL) - dependent manner.	Adenosine Triphosphate	140-143	NLR family pyrin domain containing 3	Homo sapiens	195-200
30704542-3	2019	Our work demonstrated that different fatty acids differentially modulate metabolic-inflammation, initially focusing on Nod-like receptor family, pyrin domain-containing three protein (NLRP3) inflammasome mediated IL-1beta biology and insulin signalling.	Fatty Acids	37-48	NLR family pyrin domain containing 3	Homo sapiens	184-189
31366948-9	2019	Miltefosine treatment induced mitophagy and dampened NLRP3 inflammasome assembly.	miltefosine	0-11	NLR family pyrin domain containing 3	Homo sapiens	53-58
31366948-10	2019	Collectively, our data shows that Miltefosine induced ABCA1 mediated cholesterol release, induced AMPK phosphorylation and mitophagy, while dampening NLRP3 inflammasome assembly and IL-1beta release.	miltefosine	34-45	NLR family pyrin domain containing 3	Homo sapiens	150-155
31440038-0	2019	Astragaloside IV protects endothelial progenitor cells from the damage of ox-LDL via the LOX-1/NLRP3 inflammasome pathway.	astragaloside A	0-16	NLR family pyrin domain containing 3	Homo sapiens	95-100
30641048-5	2019	Using NLRP3 as the prototypical member of the family, P-linked ATP Sepharose was determined to be a highly-effective capture agent.	p-linked atp sepharose	54-76	NLR family pyrin domain containing 3	Homo sapiens	6-11
30641048-6	2019	In subsequent examinations, P-linked ATP Sepharose was used as an enrichment tool to enable the effective profiling of NLRP3-biomarker signatures with selected reaction monitoring-mass spectrometry (SRM-MS).	Adenosine Triphosphate	37-40	NLR family pyrin domain containing 3	Homo sapiens	119-124
30641048-6	2019	In subsequent examinations, P-linked ATP Sepharose was used as an enrichment tool to enable the effective profiling of NLRP3-biomarker signatures with selected reaction monitoring-mass spectrometry (SRM-MS).	Sepharose	41-50	NLR family pyrin domain containing 3	Homo sapiens	119-124
30641048-7	2019	Finally, ATP Sepharose was used in combination with a fluorescence-linked enzyme chemoproteomic strategy (FLECS) screen to identify potential competitive inhibitors of NLRP3.	Adenosine Triphosphate	9-12	NLR family pyrin domain containing 3	Homo sapiens	168-173
30641048-7	2019	Finally, ATP Sepharose was used in combination with a fluorescence-linked enzyme chemoproteomic strategy (FLECS) screen to identify potential competitive inhibitors of NLRP3.	Sepharose	13-22	NLR family pyrin domain containing 3	Homo sapiens	168-173
30641048-8	2019	The identification of a novel benzo[d]imidazol-2-one inhibitor that specifically targets the ATP-binding and hydrolysis properties of the NLRP3 protein implies that ATP Sepharose and FLECS could be applied other NLRPs as well.	benzo[d]imidazol-2-one	30-52	NLR family pyrin domain containing 3	Homo sapiens	138-143
30641048-8	2019	The identification of a novel benzo[d]imidazol-2-one inhibitor that specifically targets the ATP-binding and hydrolysis properties of the NLRP3 protein implies that ATP Sepharose and FLECS could be applied other NLRPs as well.	Adenosine Triphosphate	93-96	NLR family pyrin domain containing 3	Homo sapiens	138-143
30641048-8	2019	The identification of a novel benzo[d]imidazol-2-one inhibitor that specifically targets the ATP-binding and hydrolysis properties of the NLRP3 protein implies that ATP Sepharose and FLECS could be applied other NLRPs as well.	Adenosine Triphosphate	165-168	NLR family pyrin domain containing 3	Homo sapiens	138-143
30641048-8	2019	The identification of a novel benzo[d]imidazol-2-one inhibitor that specifically targets the ATP-binding and hydrolysis properties of the NLRP3 protein implies that ATP Sepharose and FLECS could be applied other NLRPs as well.	Sepharose	169-178	NLR family pyrin domain containing 3	Homo sapiens	138-143
30807742-0	2019	The role of lysosomal cysteine cathepsins in NLRP3 inflammasome activation.	Cysteine	22-30	NLR family pyrin domain containing 3	Homo sapiens	45-50
30807742-3	2019	The cathepsins B, C, L, S and Z have been implicated in NLRP3 inflammasome activation following their activation with ATP, monosodium urate, silica crystals, or bacterial components, among others.	Adenosine Triphosphate	118-121	NLR family pyrin domain containing 3	Homo sapiens	56-61
30807742-3	2019	The cathepsins B, C, L, S and Z have been implicated in NLRP3 inflammasome activation following their activation with ATP, monosodium urate, silica crystals, or bacterial components, among others.	Uric Acid	123-139	NLR family pyrin domain containing 3	Homo sapiens	56-61
30807742-3	2019	The cathepsins B, C, L, S and Z have been implicated in NLRP3 inflammasome activation following their activation with ATP, monosodium urate, silica crystals, or bacterial components, among others.	Silicon Dioxide	141-147	NLR family pyrin domain containing 3	Homo sapiens	56-61
30807742-8	2019	Cathepsin Z is non-redundantly required for NLRP3 inflammasome activation following nigericin, ATP and monosodium urate activation.	Nigericin	84-93	NLR family pyrin domain containing 3	Homo sapiens	44-49
30807742-8	2019	Cathepsin Z is non-redundantly required for NLRP3 inflammasome activation following nigericin, ATP and monosodium urate activation.	Adenosine Triphosphate	95-98	NLR family pyrin domain containing 3	Homo sapiens	44-49
30807742-8	2019	Cathepsin Z is non-redundantly required for NLRP3 inflammasome activation following nigericin, ATP and monosodium urate activation.	Uric Acid	103-119	NLR family pyrin domain containing 3	Homo sapiens	44-49
30844378-7	2019	In silico modeling of NLRP3 is useful in predicting how Ser295 phosphorylation might impact upon the structural topology of the ATP-binding domain to influence catalytic activity.	Adenosine Triphosphate	128-131	NLR family pyrin domain containing 3	Homo sapiens	22-27
31440038-12	2019	Overexpression of LOX-1 in EPCs triggered NLRP3inflammasome activation, while inhibition of LOX-1 or treatment with ASV suppressed ox-LDL-induced NLRP3 inflammasome activation.	astragaloside A	116-119	NLR family pyrin domain containing 3	Homo sapiens	146-151
31396314-0	2019	Systematic understanding of the mechanism and effects of Arctigenin attenuates inflammation in dextran sulfate sodium-induced acute colitis through suppression of NLRP3 inflammasome by SIRT1.	Dextran Sulfate	95-117	NLR family pyrin domain containing 3	Homo sapiens	163-168
31315822-0	2019	Exogenous hydrogen sulfide mitigates NLRP3 inflammasome-mediated inflammation through promoting autophagy via the AMPK-mTOR pathway.	Hydrogen Sulfide	10-26	NLR family pyrin domain containing 3	Homo sapiens	37-42
31315822-1	2019	The aim of this study was to investigate whether exogenous hydrogen sulfide (H2S) could mitigate NLRP3 inflammasome-mediated inflammation through promoting autophagy via the AMPK-mTOR pathway in L02 cells.	Hydrogen Sulfide	59-75	NLR family pyrin domain containing 3	Homo sapiens	97-102
31315822-1	2019	The aim of this study was to investigate whether exogenous hydrogen sulfide (H2S) could mitigate NLRP3 inflammasome-mediated inflammation through promoting autophagy via the AMPK-mTOR pathway in L02 cells.	Hydrogen Sulfide	77-80	NLR family pyrin domain containing 3	Homo sapiens	97-102
31315822-4	2019	Exogenous H2S reduced the level of NLRP3, caspase-1, P62, IL-1beta and the ratio of P-mTOR/T-mTOR induced by OA and increased the ratio of LC3 II/I and the protein expression of Beclin1 suppressed by OA.	Hydrogen Sulfide	10-13	NLR family pyrin domain containing 3	Homo sapiens	35-40
31315822-5	2019	This study demonstrates for the first time that H2S might suppress NLRP3 inflammasome-mediated inflammation induced by OA through promoting autophagy via the AMPK-mTOR pathway.	Hydrogen Sulfide	48-51	NLR family pyrin domain containing 3	Homo sapiens	67-72
31357788-3	2019	Under the influence of ethanol, the damaged hepatocyte release uric acid, and adenosine triphosphate and induces NLRP3 inflammasome assembly and functional activation in Kupffer cells to promote the release of inflammatory mediators, such as interleukin-1beta and interleukin-18, that cascade mediates inflammation and drive alcoholic liver disease from steatosis to inflammation and fibrosis.	Ethanol	23-30	NLR family pyrin domain containing 3	Homo sapiens	113-118
31357788-3	2019	Under the influence of ethanol, the damaged hepatocyte release uric acid, and adenosine triphosphate and induces NLRP3 inflammasome assembly and functional activation in Kupffer cells to promote the release of inflammatory mediators, such as interleukin-1beta and interleukin-18, that cascade mediates inflammation and drive alcoholic liver disease from steatosis to inflammation and fibrosis.	Uric Acid	63-72	NLR family pyrin domain containing 3	Homo sapiens	113-118
31396314-9	2019	Arctigenin suppressed NLRP3 inflammasome by SIRT1 in DSS-induced acute colitis.	Dextran Sulfate	53-56	NLR family pyrin domain containing 3	Homo sapiens	22-27
31396314-13	2019	INF39, NLRP3 inhibitor also increased the effects of Arctigenin on inflammation in DSS-induced acute colitis.	Dextran Sulfate	83-86	NLR family pyrin domain containing 3	Homo sapiens	7-12
31396314-15	2019	Taken together our results demonstrated that Arctigenin attenuates inflammation in DSS-induced acute colitis through suppression of NLRP3 inflammasome by SIRT1.	Dextran Sulfate	83-86	NLR family pyrin domain containing 3	Homo sapiens	132-137
31285857-0	2019	Celastrol attenuates ox-LDL-induced mesangial cell proliferation via suppressing NLRP3 inflammasome activation.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	81-86
31285857-8	2019	As expected, celastrol pretreatment strikingly inhibited NLRP3 inflammasome activation and MC proliferation triggered by ox-LDL.	celastrol	13-22	NLR family pyrin domain containing 3	Homo sapiens	57-62
31284572-3	2019	The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation.	Oxygen	180-186	NLR family pyrin domain containing 3	Homo sapiens	4-9
31285857-9	2019	In summary, celastrol potently blocked ox-LDL-induced MC proliferation, possibly by inhibiting NLRP3 inflammasome activation.	celastrol	12-21	NLR family pyrin domain containing 3	Homo sapiens	95-100
31333677-0	2019	Tyrosine Dephosphorylation of ASC Modulates the Activation of the NLRP3 and AIM2 Inflammasomes.	Tyrosine	0-8	NLR family pyrin domain containing 3	Homo sapiens	66-71
31333677-2	2019	Tyrosine phosphorylation of the inflammasome sensors NLRP3, AIM2, NLRC4, and the adaptor protein, apoptosis-associated speck-like protein (ASC) has previously been demonstrated to be essential in the regulation of the inflammasome.	Tyrosine	0-8	NLR family pyrin domain containing 3	Homo sapiens	53-58
31333677-3	2019	By using the pharmacological protein tyrosine phosphatase (PTPase) inhibitor, phenylarsine oxide (PAO), we have demonstrated that tyrosine dephosphorylation is an essential step for the activation of the NLRP3 and AIM2 inflammasomes in human and murine macrophages.	oxophenylarsine	78-96	NLR family pyrin domain containing 3	Homo sapiens	204-209
31272469-8	2019	RESULTS: We show that ethanol increases the number of secreted nanovesicles and their content by raising the levels of both inflammatory-related proteins (TLR4, NFkappaB-p65, IL-1R, caspase-1, NLRP3) and by changing miRNAs (mir-146a, mir-182, and mir-200b) in the EVs from the WT-astrocytes compared with those from the untreated WT cells.	Ethanol	22-29	NLR family pyrin domain containing 3	Homo sapiens	193-198
31333677-3	2019	By using the pharmacological protein tyrosine phosphatase (PTPase) inhibitor, phenylarsine oxide (PAO), we have demonstrated that tyrosine dephosphorylation is an essential step for the activation of the NLRP3 and AIM2 inflammasomes in human and murine macrophages.	oxophenylarsine	98-101	NLR family pyrin domain containing 3	Homo sapiens	204-209
31333677-3	2019	By using the pharmacological protein tyrosine phosphatase (PTPase) inhibitor, phenylarsine oxide (PAO), we have demonstrated that tyrosine dephosphorylation is an essential step for the activation of the NLRP3 and AIM2 inflammasomes in human and murine macrophages.	Tyrosine	37-45	NLR family pyrin domain containing 3	Homo sapiens	204-209
31311035-10	2019	After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation.	Reactive Oxygen Species	55-78	NLR family pyrin domain containing 3	Homo sapiens	185-190
31030090-6	2019	These results indicated that ACD exhibited anti-inflammatory activity, which was associated with the inhibition of inflammatory mediator production via the downregulation of the NLRP3 inflammasome and TLR4-NF-kappaB/-MAPK signaling pathways, and the antioxidative effects of ACD were connected with GSH and SOD activation through upregulation of the Nrf2-mediated signaling pathways.	Glutathione	299-302	NLR family pyrin domain containing 3	Homo sapiens	178-183
30953761-0	2019	Saturated fatty acids induce NLRP3 activation in human macrophages through K+ efflux resulting from phospholipid saturation and Na, K-ATPase disruption.	Fatty Acids	0-21	NLR family pyrin domain containing 3	Homo sapiens	29-34
30953761-0	2019	Saturated fatty acids induce NLRP3 activation in human macrophages through K+ efflux resulting from phospholipid saturation and Na, K-ATPase disruption.	Phospholipids	100-112	NLR family pyrin domain containing 3	Homo sapiens	29-34
30953761-2	2019	Saturated fatty acids (SFAs) are sterile triggers able to induce the assembly of the NLRP3 inflammasome in macrophages, leading to IL-1beta secretion while unsaturated ones (UFAs) prevent SFAs-mediated NLRP3 activation.	Fatty Acids	0-21	NLR family pyrin domain containing 3	Homo sapiens	85-90
30953761-2	2019	Saturated fatty acids (SFAs) are sterile triggers able to induce the assembly of the NLRP3 inflammasome in macrophages, leading to IL-1beta secretion while unsaturated ones (UFAs) prevent SFAs-mediated NLRP3 activation.	Fatty Acids	0-21	NLR family pyrin domain containing 3	Homo sapiens	202-207
30953761-2	2019	Saturated fatty acids (SFAs) are sterile triggers able to induce the assembly of the NLRP3 inflammasome in macrophages, leading to IL-1beta secretion while unsaturated ones (UFAs) prevent SFAs-mediated NLRP3 activation.	ufas	174-178	NLR family pyrin domain containing 3	Homo sapiens	85-90
30953761-2	2019	Saturated fatty acids (SFAs) are sterile triggers able to induce the assembly of the NLRP3 inflammasome in macrophages, leading to IL-1beta secretion while unsaturated ones (UFAs) prevent SFAs-mediated NLRP3 activation.	ufas	174-178	NLR family pyrin domain containing 3	Homo sapiens	202-207
30953761-9	2019	This SFA-induced membrane remodeling promotes a disruption of the plasma membrane Na, K-ATPase, instigating a K+ efflux essential and sufficient for NLRP3 activation.	Fatty Acids	5-8	NLR family pyrin domain containing 3	Homo sapiens	149-154
31311035-10	2019	After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation.	Reactive Oxygen Species	80-83	NLR family pyrin domain containing 3	Homo sapiens	185-190
31311035-10	2019	After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation.	Reactive Oxygen Species	110-113	NLR family pyrin domain containing 3	Homo sapiens	185-190
31091351-6	2019	Moreover, heme itself stimulated significant Mphi pro-IL-1beta gene and protein expression via an S100A8-mediated mechanism and greatly amplified S100A8-driven NLRP3 inflammasome-mediated IL-1beta secretion.	Heme	10-14	NLR family pyrin domain containing 3	Homo sapiens	160-165
30878009-0	2019	The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells.	cooking oil	15-26	NLR family pyrin domain containing 3	Homo sapiens	94-99
31004077-0	2019	Pregnane X Receptor Activation Triggers Rapid ATP Release in Primed Macrophages That Mediates NLRP3 Inflammasome Activation.	Adenosine Triphosphate	46-49	NLR family pyrin domain containing 3	Homo sapiens	94-99
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Hydrogen Sulfide	76-79	NLR family pyrin domain containing 3	Homo sapiens	246-251
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Adenosine Triphosphate	147-150	NLR family pyrin domain containing 3	Homo sapiens	187-244
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Adenosine Triphosphate	147-150	NLR family pyrin domain containing 3	Homo sapiens	246-251
30877511-2	2019	We stimulated L02 cells with different concentrations of LPS, then the cell viability, cell apoptosis, and the protein level of NLRP3 inflammasome were detected by MTT and western blot to determine the appropriate LPS concentration used in this study.	monooxyethylene trimethylolpropane tristearate	164-167	NLR family pyrin domain containing 3	Homo sapiens	128-133
30877511-4	2019	Our results showed that exogenous H2S reduced the protein levels of NLRP3, cleaved caspase-1, TLR4, NF-kappaB, P62, and IL-1beta induced by LPS + ATP and increased the ratio of LC3-II/I and the protein levels of Beclin 1 suppressed by LPS + ATP.	Hydrogen Sulfide	34-37	NLR family pyrin domain containing 3	Homo sapiens	68-73
30877511-4	2019	Our results showed that exogenous H2S reduced the protein levels of NLRP3, cleaved caspase-1, TLR4, NF-kappaB, P62, and IL-1beta induced by LPS + ATP and increased the ratio of LC3-II/I and the protein levels of Beclin 1 suppressed by LPS + ATP.	Adenosine Triphosphate	146-149	NLR family pyrin domain containing 3	Homo sapiens	68-73
30877511-5	2019	This study demonstrated that H2S might suppress LPS + ATP-induced inflammation by inhibiting NLRP3 inflammasome and promoting autophagy.	Hydrogen Sulfide	29-32	NLR family pyrin domain containing 3	Homo sapiens	93-98
30877511-5	2019	This study demonstrated that H2S might suppress LPS + ATP-induced inflammation by inhibiting NLRP3 inflammasome and promoting autophagy.	Adenosine Triphosphate	54-57	NLR family pyrin domain containing 3	Homo sapiens	93-98
30877511-0	2019	Exogenous hydrogen sulfide mitigates LPS + ATP-induced inflammation by inhibiting NLRP3 inflammasome activation and promoting autophagy in L02 cells.	Hydrogen Sulfide	10-26	NLR family pyrin domain containing 3	Homo sapiens	82-87
30877511-0	2019	Exogenous hydrogen sulfide mitigates LPS + ATP-induced inflammation by inhibiting NLRP3 inflammasome activation and promoting autophagy in L02 cells.	Adenosine Triphosphate	43-46	NLR family pyrin domain containing 3	Homo sapiens	82-87
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Hydrogen Sulfide	58-74	NLR family pyrin domain containing 3	Homo sapiens	187-244
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Hydrogen Sulfide	58-74	NLR family pyrin domain containing 3	Homo sapiens	246-251
30877511-1	2019	The aim of this study is to investigate whether exogenous hydrogen sulfide (H2S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells.	Hydrogen Sulfide	76-79	NLR family pyrin domain containing 3	Homo sapiens	187-244
30976089-8	2019	Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP.	Phosphorylcholine	24-41	NLR family pyrin domain containing 3	Homo sapiens	75-80
30976089-8	2019	Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP.	Phosphorylcholine	24-41	NLR family pyrin domain containing 3	Homo sapiens	177-182
30976089-9	2019	Amoxicillin reduced bacterial populations in the lungs and reduced NLRP3 inflammasome protein levels, but did not reduce PAFR.	Amoxicillin	0-11	NLR family pyrin domain containing 3	Homo sapiens	67-72
30878009-0	2019	The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells.	ros	81-84	NLR family pyrin domain containing 3	Homo sapiens	94-99
30878009-3	2019	Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC).	ros	26-29	NLR family pyrin domain containing 3	Homo sapiens	39-44
30878009-13	2019	It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway.	ros	97-100	NLR family pyrin domain containing 3	Homo sapiens	110-115
31354329-3	2019	We and others have shown that high glucose can activate the NOD-like receptor family, pyrin domain containing family member 3 (NLRP3) pathway, leading to increased levels of cleaved caspase 1 and IL-1beta to activate a number of inflammatory pathways in the retina.	Glucose	35-42	NLR family pyrin domain containing 3	Homo sapiens	127-132
31244838-3	2019	If tissue damage occurs, danger signals released from necrotic cells, such as ATP, can activate NLRP3-inflammasomes (multiprotein complexes consisting of NLRP3, ASC, and active caspase-1) which cleaves and activates pro-IL-1beta.	Adenosine Triphosphate	78-81	NLR family pyrin domain containing 3	Homo sapiens	96-101
31244838-3	2019	If tissue damage occurs, danger signals released from necrotic cells, such as ATP, can activate NLRP3-inflammasomes (multiprotein complexes consisting of NLRP3, ASC, and active caspase-1) which cleaves and activates pro-IL-1beta.	Adenosine Triphosphate	78-81	NLR family pyrin domain containing 3	Homo sapiens	154-159
31244838-4	2019	NLRP3 activation also depends on NEK7 and mitochondrial ROS-production.	ros	56-59	NLR family pyrin domain containing 3	Homo sapiens	0-5
30851273-3	2019	This research aimed to elucidate whether and how metformin affects NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activity in oxidized low-density lipoprotein (ox-LDL) stimulated macrophages.	Metformin	49-58	NLR family pyrin domain containing 3	Homo sapiens	105-110
30851273-0	2019	Metformin reduced NLRP3 inflammasome activity in Ox-LDL stimulated macrophages through adenosine monophosphate activated protein kinase and protein phosphatase 2A.	Metformin	0-9	NLR family pyrin domain containing 3	Homo sapiens	18-23
30851273-10	2019	In the results, upregulation of NLRP3 protein expression and NLRP3 inflammasome activation induced by ox-LDL treatment in macrophages were significantly attenuated by metformin treatment.	Metformin	167-176	NLR family pyrin domain containing 3	Homo sapiens	32-37
30851273-3	2019	This research aimed to elucidate whether and how metformin affects NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activity in oxidized low-density lipoprotein (ox-LDL) stimulated macrophages.	Metformin	49-58	NLR family pyrin domain containing 3	Homo sapiens	67-103
30851273-10	2019	In the results, upregulation of NLRP3 protein expression and NLRP3 inflammasome activation induced by ox-LDL treatment in macrophages were significantly attenuated by metformin treatment.	Metformin	167-176	NLR family pyrin domain containing 3	Homo sapiens	61-66
30851273-12	2019	Inhibition of PP2A significantly restored NLRP3 and pro-IL-1beta protein expression level downregulated by metformin in ox-LDL-stimulated macrophages.	Metformin	107-116	NLR family pyrin domain containing 3	Homo sapiens	42-47
30851273-14	2019	Our data showed Metformin reduced NLRP3 protein expression and NLRP3 inflammasome activation in ox-LDL-stimulated macrophages through AMPK and PP2A.	Metformin	16-25	NLR family pyrin domain containing 3	Homo sapiens	34-39
30851273-14	2019	Our data showed Metformin reduced NLRP3 protein expression and NLRP3 inflammasome activation in ox-LDL-stimulated macrophages through AMPK and PP2A.	Metformin	16-25	NLR family pyrin domain containing 3	Homo sapiens	63-68
30982734-3	2019	Inhibition of CTL1 expression or choline phosphorylation attenuated NLRP3 inflammasome activation and IL-1beta and IL-18 production in stimulated macrophages.	Choline	33-40	NLR family pyrin domain containing 3	Homo sapiens	68-73
31231549-8	2019	Mechanistically, ORF8b interacts directly with the Leucine Rich Repeat domain of NLRP3 and localizes with NLRP3 and ASC in cytosolic dot-like structures.	Leucine	51-58	NLR family pyrin domain containing 3	Homo sapiens	81-86
31360100-0	2019	Caffeine Inhibits NLRP3 Inflammasome Activation by Suppressing MAPK/NF-kappaB and A2aR Signaling in LPS-Induced THP-1 Macrophages.	Caffeine	0-8	NLR family pyrin domain containing 3	Homo sapiens	18-23
31214205-7	2019	Here we explored the optimal imaging-based tools to measure ASC speck formation via imaging flow cytometry by using peripheral blood mononuclear cells (PBMCs) stimulated with the NLRP3 agonist Nigericin, as a positive control.	Nigericin	193-202	NLR family pyrin domain containing 3	Homo sapiens	179-184
31038962-1	2019	The nucleotide-binding domain and leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome is a key regulator of innate immune responses, and its aberrant activation is implicated in the pathogenesis of many diseases such as Alzheimer"s disease and type 2 diabetes.	Leucine	34-41	NLR family pyrin domain containing 3	Homo sapiens	100-105
31337974-4	2019	We demonstrated that MitoQ restored endothelial barrier integrity by preventing VE-cadherin disassembly and actin cytoskeleton remodeling, as well as decreased inflammation by the NF-kappaB and NLRP3 inflammasome pathways in endothelial cells.	mitoquinone	21-26	NLR family pyrin domain containing 3	Homo sapiens	194-199
31360100-4	2019	In the present study, we aimed to investigate the effects of caffeine on NLRP3 inflammasome activation in LPS-induced THP-1 macrophages and to explore the underlying the detailed mechanism.	Caffeine	61-69	NLR family pyrin domain containing 3	Homo sapiens	73-78
31360100-5	2019	We found that caffeine significantly reduced NLRP3 expression, ASC speck formation, and caspase 1 cleavage and therefore decreased IL-1beta and IL-18 secretion in THP-1 macrophages.	Caffeine	14-22	NLR family pyrin domain containing 3	Homo sapiens	45-50
31360100-8	2019	Given these findings, we conclude that caffeine inhibits NLRP3 inflammasome activation by suppressing MAPK/NF-kappaB signaling and A2aR-associated ROS production in LPS-induced THP-1 macrophages.	Caffeine	39-47	NLR family pyrin domain containing 3	Homo sapiens	57-62
31360100-8	2019	Given these findings, we conclude that caffeine inhibits NLRP3 inflammasome activation by suppressing MAPK/NF-kappaB signaling and A2aR-associated ROS production in LPS-induced THP-1 macrophages.	ros	147-150	NLR family pyrin domain containing 3	Homo sapiens	57-62
30853521-0	2019	N4-acetylcytidine is required for sustained NLRP3 inflammasome activation via HMGB1 pathway in microglia.	N-acetylcytidine	0-17	NLR family pyrin domain containing 3	Homo sapiens	44-49
33911592-10	2019	Finally, SAA markedly inhibited poly(I:C)-induced NLRP3 expression.	Poly I-C	32-41	NLR family pyrin domain containing 3	Homo sapiens	50-55
30853521-3	2019	Here we reported that N4-acetylcytidine (N4A), a nucleoside metabolite, activated microglia and sustained NLRP3 inflammasome activation by inducing HMGB1 signaling.	N-acetylcytidine	22-39	NLR family pyrin domain containing 3	Homo sapiens	106-111
30853521-3	2019	Here we reported that N4-acetylcytidine (N4A), a nucleoside metabolite, activated microglia and sustained NLRP3 inflammasome activation by inducing HMGB1 signaling.	CHEMBL3099812	41-44	NLR family pyrin domain containing 3	Homo sapiens	106-111
29385859-1	2019	OBJECTIVE: Previous studies have indicated that the nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3) inflammasome is activated by monosodium urate in the trophoblast of preeclampsia (PE) patients, leading to augmented placental IL-1beta levels.	Uric Acid	157-173	NLR family pyrin domain containing 3	Homo sapiens	121-126
30901677-0	2019	Genistein protects against DSS-induced colitis by inhibiting NLRP3 inflammasome via TGR5-cAMP signaling.	Genistein	0-9	NLR family pyrin domain containing 3	Homo sapiens	61-66
30901677-0	2019	Genistein protects against DSS-induced colitis by inhibiting NLRP3 inflammasome via TGR5-cAMP signaling.	Dextran Sulfate	27-30	NLR family pyrin domain containing 3	Homo sapiens	61-66
30901677-0	2019	Genistein protects against DSS-induced colitis by inhibiting NLRP3 inflammasome via TGR5-cAMP signaling.	Cyclic AMP	89-93	NLR family pyrin domain containing 3	Homo sapiens	61-66
30901677-8	2019	These protective effects of Genistein might be attributed by ubiquination of NLRP3 which was induced due to interaction of cAMP with NLRP3.	Genistein	28-37	NLR family pyrin domain containing 3	Homo sapiens	77-82
30901677-8	2019	These protective effects of Genistein might be attributed by ubiquination of NLRP3 which was induced due to interaction of cAMP with NLRP3.	Genistein	28-37	NLR family pyrin domain containing 3	Homo sapiens	133-138
30901677-8	2019	These protective effects of Genistein might be attributed by ubiquination of NLRP3 which was induced due to interaction of cAMP with NLRP3.	Cyclic AMP	123-127	NLR family pyrin domain containing 3	Homo sapiens	77-82
30901677-8	2019	These protective effects of Genistein might be attributed by ubiquination of NLRP3 which was induced due to interaction of cAMP with NLRP3.	Cyclic AMP	123-127	NLR family pyrin domain containing 3	Homo sapiens	133-138
30901677-9	2019	Furthermore, the effects of Genistein on NLRP3 inflammasome disappeared in TGR5-silenced U937 cells.	Genistein	28-37	NLR family pyrin domain containing 3	Homo sapiens	41-46
30901677-10	2019	In conclusion, our study unveils that Genistein was able to inhibit NLRP3 inflammasome via TGR5-cAMP signaling in macrophages.	Cyclic AMP	96-100	NLR family pyrin domain containing 3	Homo sapiens	68-73
30977640-8	2019	Then we found PCB29-pQ activates NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome that mediates caspase 1 activation.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	14-22	NLR family pyrin domain containing 3	Homo sapiens	33-76
30977640-8	2019	Then we found PCB29-pQ activates NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome that mediates caspase 1 activation.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	14-22	NLR family pyrin domain containing 3	Homo sapiens	78-83
30977640-10	2019	PCB29-pQ-induced high-mobility group box 1 (HMGB1) release and subsequent binding to its receptors [toll-like receptor 2 (TLR2), TLR4, TLR9, and receptor for advanced glycation end products (RAGE)] are essential for the activation of NLRP3 inflammasome.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	NLR family pyrin domain containing 3	Homo sapiens	234-239
31086327-3	2019	Here, we show that MCC950 directly interacts with the Walker B motif within the NLRP3 NACHT domain, thereby blocking ATP hydrolysis and inhibiting NLRP3 activation and inflammasome formation.	Adenosine Triphosphate	117-120	NLR family pyrin domain containing 3	Homo sapiens	80-85
30548648-0	2019	Polydatin suppresses the development of lung inflammation and fibrosis by inhibiting activation of the NACHT domain-, leucine-rich repeat-, and pyd-containing protein 3 inflammasome and the nuclear factor-kappaB pathway after Mycoplasma pneumoniae infection.	polydatin	0-9	NLR family pyrin domain containing 3	Homo sapiens	103-168
31129032-0	2019	Corrigendum to "Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis" [Redox Biology 16 (2018) 32-46].	Reactive Oxygen Species	16-39	NLR family pyrin domain containing 3	Homo sapiens	128-133
31129032-0	2019	Corrigendum to "Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis" [Redox Biology 16 (2018) 32-46].	Reactive Oxygen Species	118-121	NLR family pyrin domain containing 3	Homo sapiens	128-133
30912285-0	2019	Oral Ketone Supplementation Acutely Increases Markers of NLRP3 Inflammasome Activation in Human Monocytes.	Ketones	5-11	NLR family pyrin domain containing 3	Homo sapiens	57-62
30912285-1	2019	SCOPE: Cell culture studies indicate that the ketone beta-hydroxybutyrate (beta-OHB) directly inhibits the NLRP3 inflammasome, a key regulator of inflammation.	Ketones	46-52	NLR family pyrin domain containing 3	Homo sapiens	107-112
30912285-1	2019	SCOPE: Cell culture studies indicate that the ketone beta-hydroxybutyrate (beta-OHB) directly inhibits the NLRP3 inflammasome, a key regulator of inflammation.	3-Hydroxybutyric Acid	53-73	NLR family pyrin domain containing 3	Homo sapiens	107-112
30912285-1	2019	SCOPE: Cell culture studies indicate that the ketone beta-hydroxybutyrate (beta-OHB) directly inhibits the NLRP3 inflammasome, a key regulator of inflammation.	beta-ohb	75-83	NLR family pyrin domain containing 3	Homo sapiens	107-112
30912285-8	2019	CONCLUSION: Measures of NLRP3 activation increases when blood beta-OHB is elevated using ketone supplements, suggesting that increasing beta-OHB exogenously may have unintended effects that augment inflammatory activation.	beta-ohb	62-70	NLR family pyrin domain containing 3	Homo sapiens	24-29
30912285-8	2019	CONCLUSION: Measures of NLRP3 activation increases when blood beta-OHB is elevated using ketone supplements, suggesting that increasing beta-OHB exogenously may have unintended effects that augment inflammatory activation.	Ketones	89-95	NLR family pyrin domain containing 3	Homo sapiens	24-29
30912285-8	2019	CONCLUSION: Measures of NLRP3 activation increases when blood beta-OHB is elevated using ketone supplements, suggesting that increasing beta-OHB exogenously may have unintended effects that augment inflammatory activation.	beta-ohb	136-144	NLR family pyrin domain containing 3	Homo sapiens	24-29
31189953-1	2019	The NLRP3 inflammasome can be activated by stimuli that include nigericin, uric acid crystals, amyloid-beta fibrils and extracellular ATP.	Nigericin	64-73	NLR family pyrin domain containing 3	Homo sapiens	4-9
31189953-1	2019	The NLRP3 inflammasome can be activated by stimuli that include nigericin, uric acid crystals, amyloid-beta fibrils and extracellular ATP.	Uric Acid	75-84	NLR family pyrin domain containing 3	Homo sapiens	4-9
31189953-1	2019	The NLRP3 inflammasome can be activated by stimuli that include nigericin, uric acid crystals, amyloid-beta fibrils and extracellular ATP.	Adenosine Triphosphate	134-137	NLR family pyrin domain containing 3	Homo sapiens	4-9
31189953-4	2019	The earring-shaped NLRP3 consists of curved leucine-rich-repeat and globular NACHT domains, and the C-terminal lobe of NEK7 nestles against both NLRP3 domains.	Leucine	44-51	NLR family pyrin domain containing 3	Homo sapiens	19-24
30169827-5	2019	In experimental models using oxalate-enriched chow, CaOx crystals were bound to renal tubular cells, promoting a pro-inflammatory environment that led to fibrogenesis in the renal parenchyma by activation of a NACHT, LRR and PYD domains-containing protein 3 (NALP3)-dependent inflammasome in renal dendritic cells and macrophages.	Oxalates	29-36	NLR family pyrin domain containing 3	Homo sapiens	210-257
30169827-5	2019	In experimental models using oxalate-enriched chow, CaOx crystals were bound to renal tubular cells, promoting a pro-inflammatory environment that led to fibrogenesis in the renal parenchyma by activation of a NACHT, LRR and PYD domains-containing protein 3 (NALP3)-dependent inflammasome in renal dendritic cells and macrophages.	Oxalates	29-36	NLR family pyrin domain containing 3	Homo sapiens	259-264
31086329-2	2019	The molecule sulfonylurea MCC950 is a NLRP3 inflammasome inhibitor with potential clinical utility.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	26-32	NLR family pyrin domain containing 3	Homo sapiens	38-43
30771382-0	2019	Lysosomal regulation of extracellular vesicle excretion during d-ribose-induced NLRP3 inflammasome activation in podocytes.	Ribose	63-71	NLR family pyrin domain containing 3	Homo sapiens	80-85
30776465-7	2019	Interestingly, hsa-miR-6515-5p and its target genes NLRP3, UGP2 may regulate the Immune system and carbohydrate metabolism.	Carbohydrates	99-111	NLR family pyrin domain containing 3	Homo sapiens	52-57
31190807-0	2019	NLRP3 inflammasome-activating arginine-based liposomes promote antigen presentations in dendritic cells.	Arginine	30-38	NLR family pyrin domain containing 3	Homo sapiens	0-5
30896160-0	2019	Discovery of Quinazolin-4(3 H)-ones as NLRP3 Inflammasome Inhibitors: Computational Design, Metal-Free Synthesis, and in Vitro Biological Evaluation.	quinazolin-4(3 h)-ones	13-35	NLR family pyrin domain containing 3	Homo sapiens	39-44
30896160-0	2019	Discovery of Quinazolin-4(3 H)-ones as NLRP3 Inflammasome Inhibitors: Computational Design, Metal-Free Synthesis, and in Vitro Biological Evaluation.	Metals	92-97	NLR family pyrin domain containing 3	Homo sapiens	39-44
30771382-3	2019	In this study, we hypothesized that the NLRP3 inflammasome product, IL-1beta in response to exogenously administrated and endogenously produced d-ribose stimulation is released via extracellular vesicles including EVs via a sphingolipid-mediated molecular mechanisms controlling lysosome and multivesicular body (MVB) interaction.	Ribose	144-152	NLR family pyrin domain containing 3	Homo sapiens	40-45
30771382-3	2019	In this study, we hypothesized that the NLRP3 inflammasome product, IL-1beta in response to exogenously administrated and endogenously produced d-ribose stimulation is released via extracellular vesicles including EVs via a sphingolipid-mediated molecular mechanisms controlling lysosome and multivesicular body (MVB) interaction.	EVS	214-217	NLR family pyrin domain containing 3	Homo sapiens	40-45
30771382-3	2019	In this study, we hypothesized that the NLRP3 inflammasome product, IL-1beta in response to exogenously administrated and endogenously produced d-ribose stimulation is released via extracellular vesicles including EVs via a sphingolipid-mediated molecular mechanisms controlling lysosome and multivesicular body (MVB) interaction.	Sphingolipids	224-236	NLR family pyrin domain containing 3	Homo sapiens	40-45
30771382-4	2019	First, we demonstrated that both endogenous and exogenous d-ribose induced NLRP3 inflammasome activation to produce IL-1beta, which was released via EVs in podocytes.	Ribose	58-66	NLR family pyrin domain containing 3	Homo sapiens	75-80
30771382-4	2019	First, we demonstrated that both endogenous and exogenous d-ribose induced NLRP3 inflammasome activation to produce IL-1beta, which was released via EVs in podocytes.	EVS	149-152	NLR family pyrin domain containing 3	Homo sapiens	75-80
31010153-2	2019	The present study evaluated whether silibinin (SB) treatment of monocytes from preeclamptic women could modulate NLRP1 and NLRP3 inflammasomes as well as TLR4/NF-kappaB pathway activation.	Silybin	36-45	NLR family pyrin domain containing 3	Homo sapiens	123-128
31024004-0	2019	RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux.	Potassium	95-104	NLR family pyrin domain containing 3	Homo sapiens	38-43
31024004-4	2019	Here, we report that the replication of cytopathogenic RNA viruses such as vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) induced a lytic cell death leading to potassium efflux, the common trigger of NLRP3 inflammasome activation.	Potassium	183-192	NLR family pyrin domain containing 3	Homo sapiens	223-228
31178664-0	2019	Hydrogen Sulfide Attenuates High Glucose-Induced Human Retinal Pigment Epithelial Cell Inflammation by Inhibiting ROS Formation and NLRP3 Inflammasome Activation.	Hydrogen Sulfide	0-16	NLR family pyrin domain containing 3	Homo sapiens	132-137
31178664-6	2019	Furthermore, high glucose increased the mRNA expression levels of NLRP3, ACS, and caspase-1.	Glucose	18-25	NLR family pyrin domain containing 3	Homo sapiens	66-71
31178664-10	2019	Taken together, the findings of the present study have demonstrated that H2S protects cultured RPE cells from high glucose-induced damage through inhibiting ROS formation and NLRP3 inflammasome activation.	Deuterium	73-76	NLR family pyrin domain containing 3	Homo sapiens	175-180
30698909-12	2019	In conclusion, the cell model of inflammation-related lung cancer is set up successfully, and NLRP3 inflammasome activation may be involved in the malignant transformation of BEAS-2B cells which induced by CTPE alone or LPS combined with CTPE.	ctpe	206-210	NLR family pyrin domain containing 3	Homo sapiens	94-99
30698909-12	2019	In conclusion, the cell model of inflammation-related lung cancer is set up successfully, and NLRP3 inflammasome activation may be involved in the malignant transformation of BEAS-2B cells which induced by CTPE alone or LPS combined with CTPE.	ctpe	238-242	NLR family pyrin domain containing 3	Homo sapiens	94-99
30962589-6	2019	In monocytes, formation of GSDMD pores can induce activation of the NLRP3 inflammasome for maturation of the cytokines IL-1beta and IL-18.	gsdmd	27-32	NLR family pyrin domain containing 3	Homo sapiens	68-73
31035323-0	2019	Olive Leaf Extract (OleaVita) Suppresses Inflammatory Cytokine Production and NLRP3 Inflammasomes in Human Placenta.	oleavita	20-28	NLR family pyrin domain containing 3	Homo sapiens	78-83
31035323-9	2019	Thus, OleaVita is beneficial as an inhibitor of inflammation and NLRP3 inflammasome activation, and may be used as a supplement for the treatment and prevention of inflammatory diseases.	oleavita	6-14	NLR family pyrin domain containing 3	Homo sapiens	65-70
31027151-5	2019	Adsorption of serum proteins, and BSA on MSU, as well as upon m-CPPD crystals, inhibited their capacity to induce interleukin-1-beta secretions, along with a decreased ATP secretion, and a disturbance of mitochondrial membrane depolarization, suggesting an alteration of NLRP3 inflammasome activation.	m-cppd	62-68	NLR family pyrin domain containing 3	Homo sapiens	271-276
31010153-2	2019	The present study evaluated whether silibinin (SB) treatment of monocytes from preeclamptic women could modulate NLRP1 and NLRP3 inflammasomes as well as TLR4/NF-kappaB pathway activation.	Silybin	47-49	NLR family pyrin domain containing 3	Homo sapiens	123-128
31010153-8	2019	In vitro, SB treatment of monocytes from preeclamptic women reduced the basal activation of these cells by decreasing NLRP1/NLRP3 inflammasomes and p65NF-kappaB activity.	Silybin	10-12	NLR family pyrin domain containing 3	Homo sapiens	124-129
30658148-0	2019	Polysaccharides from chayote enhance lipid efflux and regulate NLRP3 inflammasome priming in macrophage-like THP-1 cells exposed to cholesterol crystals.	Polysaccharides	0-15	NLR family pyrin domain containing 3	Homo sapiens	63-68
30843539-4	2019	We found that polymers that demonstrated the most potent membrane-destabilizing activity at early endosomal pH values in an erythrocyte hemolysis assay were most efficient at delivery of siRNA, yet tended to be associated with the least amount of NOD-like related protein 3 (NLRP3) inflammasome activation.	Polymers	14-22	NLR family pyrin domain containing 3	Homo sapiens	247-273
30843539-4	2019	We found that polymers that demonstrated the most potent membrane-destabilizing activity at early endosomal pH values in an erythrocyte hemolysis assay were most efficient at delivery of siRNA, yet tended to be associated with the least amount of NOD-like related protein 3 (NLRP3) inflammasome activation.	Polymers	14-22	NLR family pyrin domain containing 3	Homo sapiens	275-280
30833078-0	2019	TXNIP-mediated nuclear factor-kappaB signaling pathway and intracellular shifting of TXNIP in uric acid-induced NLRP3 inflammasome.	Uric Acid	94-103	NLR family pyrin domain containing 3	Homo sapiens	112-117
30833078-1	2019	OBJECTIVE: The aim of this study was to assess the role of thioredoxin-interacting protein (TXNIP) in nuclear factor-kappaB (NF-kappaB) signaling and the interaction between TXNIP and NOD-like receptor protein 3 (NLRP3) in activation of the NLRP3 inflammasome in monosodium urate (MSU)-induced inflammation.	Uric Acid	263-279	NLR family pyrin domain containing 3	Homo sapiens	184-211
30833078-1	2019	OBJECTIVE: The aim of this study was to assess the role of thioredoxin-interacting protein (TXNIP) in nuclear factor-kappaB (NF-kappaB) signaling and the interaction between TXNIP and NOD-like receptor protein 3 (NLRP3) in activation of the NLRP3 inflammasome in monosodium urate (MSU)-induced inflammation.	Uric Acid	281-284	NLR family pyrin domain containing 3	Homo sapiens	184-211
30833078-7	2019	Binding between TXNIP and NLRP3 under oxidative stress caused by MSU crystals was observed and was blocked by quercetin or ascorbic acid.	Uric Acid	65-68	NLR family pyrin domain containing 3	Homo sapiens	26-31
30833078-7	2019	Binding between TXNIP and NLRP3 under oxidative stress caused by MSU crystals was observed and was blocked by quercetin or ascorbic acid.	Quercetin	110-119	NLR family pyrin domain containing 3	Homo sapiens	26-31
30833078-7	2019	Binding between TXNIP and NLRP3 under oxidative stress caused by MSU crystals was observed and was blocked by quercetin or ascorbic acid.	Ascorbic Acid	123-136	NLR family pyrin domain containing 3	Homo sapiens	26-31
30833078-8	2019	CONCLUSION: This study showed that activation of MSU-induced NLRP3 inflammasome requires TXNIP-mediated NF-kappaB signaling pathway and intracellular TXNIP shifting.	Uric Acid	49-52	NLR family pyrin domain containing 3	Homo sapiens	61-66
30658148-0	2019	Polysaccharides from chayote enhance lipid efflux and regulate NLRP3 inflammasome priming in macrophage-like THP-1 cells exposed to cholesterol crystals.	Cholesterol	132-143	NLR family pyrin domain containing 3	Homo sapiens	63-68
30658148-2	2019	Although macrophages are crucial for lipid clearance, the excessive uptake of cholesterol crystals (CC) by these cells induce NLRP3 inflammasome and foam cell formation.	Cholesterol	78-89	NLR family pyrin domain containing 3	Homo sapiens	126-131
30944389-6	2019	A mechanistic study revealed that GlcN inhibited the expression of NLRP3 and IL-1beta precursor by reducing reactive oxygen species generation and NF-kappaB activation in lipopolysaccharide-activated macrophages.	Glucosamine	34-38	NLR family pyrin domain containing 3	Homo sapiens	67-72
30971058-4	2019	We showed that Asiatic acid reduced intracellular production of mitochondrial reactive oxygen species and altered the mitochondrial membrane potential to regulate mitochondrial dysfunction, and suppressed the NLRP3 inflammasome in microglia cells.	asiatic acid	15-27	NLR family pyrin domain containing 3	Homo sapiens	209-214
30971058-6	2019	These data demonstrate that Asiatic acid both inhibits the activation of the NLRP3 inflammasome by downregulating mitochondrial reactive oxygen species directly to protect dopaminergic neurons from, and improves mitochondrial dysfunction in SH-SY5Y cells, which were established as a model of Parkinsons disease.	asiatic acid	28-40	NLR family pyrin domain containing 3	Homo sapiens	77-82
30971058-6	2019	These data demonstrate that Asiatic acid both inhibits the activation of the NLRP3 inflammasome by downregulating mitochondrial reactive oxygen species directly to protect dopaminergic neurons from, and improves mitochondrial dysfunction in SH-SY5Y cells, which were established as a model of Parkinsons disease.	Reactive Oxygen Species	128-151	NLR family pyrin domain containing 3	Homo sapiens	77-82
30971058-7	2019	Our finding reveals that Asiatic acid protects dopaminergic neurons from neuroinflammation by suppressing NLRP3 inflammasome activation in microglia cells as well as protecting dopaminergic neurons directly.	asiatic acid	25-37	NLR family pyrin domain containing 3	Homo sapiens	106-111
30963625-9	2019	Lidocaine dramatically reduced the protein expression of IL-1alpha, IL-6, THF-alpha, ELAVL1, NLRP3, caspase-1, and IL-1beta in adenovirus-infected thyroid follicular epithelial cells.	Lidocaine	0-9	NLR family pyrin domain containing 3	Homo sapiens	93-98
31011633-0	2019	Membrane fusogenic lysine type lipid assemblies possess enhanced NLRP3 inflammasome activation potency.	Lysine	19-25	NLR family pyrin domain containing 3	Homo sapiens	65-70
31011633-1	2019	Lysine (K) type cationic lipid with a propyl spacer and ditetradecyl hydrophobic moieties composing liposomes, K3C14, previously studied for gene delivery, were reported to activate the NLRP3 inflammasomes in human macrophages via the conventional phagolysosomal pathway.	Lysine	0-6	NLR family pyrin domain containing 3	Homo sapiens	186-191
31011633-1	2019	Lysine (K) type cationic lipid with a propyl spacer and ditetradecyl hydrophobic moieties composing liposomes, K3C14, previously studied for gene delivery, were reported to activate the NLRP3 inflammasomes in human macrophages via the conventional phagolysosomal pathway.	ditetradecyl	56-68	NLR family pyrin domain containing 3	Homo sapiens	186-191
31011633-6	2019	Even in the presence of endocytosis inhibitors, cytochalasin D or dynasore, K3C16 continued to activate the NLRP3 inflammasomes and to induce IL-1beta release.	Cytochalasin D	48-62	NLR family pyrin domain containing 3	Homo sapiens	108-113
31011633-6	2019	Even in the presence of endocytosis inhibitors, cytochalasin D or dynasore, K3C16 continued to activate the NLRP3 inflammasomes and to induce IL-1beta release.	N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide	66-74	NLR family pyrin domain containing 3	Homo sapiens	108-113
31011633-6	2019	Even in the presence of endocytosis inhibitors, cytochalasin D or dynasore, K3C16 continued to activate the NLRP3 inflammasomes and to induce IL-1beta release.	k3c16	76-81	NLR family pyrin domain containing 3	Homo sapiens	108-113
31011633-8	2019	It is demonstrated that the change in hydrophobic tail length by two hydrocarbons drastically changed a cellular entry route and potency in activating the NLRP3 inflammasomes.	Hydrocarbons	69-81	NLR family pyrin domain containing 3	Homo sapiens	155-160
30944389-6	2019	A mechanistic study revealed that GlcN inhibited the expression of NLRP3 and IL-1beta precursor by reducing reactive oxygen species generation and NF-kappaB activation in lipopolysaccharide-activated macrophages.	oxygen species	117-131	NLR family pyrin domain containing 3	Homo sapiens	67-72
30782482-6	2019	Real-time RT-PCR revealed that CD significantly increased NLRP3 and IL1B mRNA expression in different SMC cultures within 6 h of exposure.	Cadmium	31-33	NLR family pyrin domain containing 3	Homo sapiens	58-63
30782482-8	2019	Additional exposure of IFN-gamma-primed AAA-SMC to CD for 6-24 h, further augmented expression of AIM2, NLRP3, and Caspase-1 protein levels.	Cadmium	51-53	NLR family pyrin domain containing 3	Homo sapiens	104-109
30944389-7	2019	GlcN also suppressed mitochondrial reactive oxygen species generation and mitochondrial integrity loss in NLRP3-activated macrophages.	Glucosamine	0-4	NLR family pyrin domain containing 3	Homo sapiens	106-111
30944389-8	2019	Additionally, GlcN disrupted NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC.	Glucosamine	14-18	NLR family pyrin domain containing 3	Homo sapiens	29-34
30944389-8	2019	Additionally, GlcN disrupted NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC.	Glucosamine	14-18	NLR family pyrin domain containing 3	Homo sapiens	71-76
30983887-2	2019	Moreover, recent studies showed that accumulation of free cholesterol in macrophages leading to activation of NLRP3 inflammasome and production of interleukin-1beta (IL-1beta) has been linked to atherosclerosis-associated inflammation.	Cholesterol	58-69	NLR family pyrin domain containing 3	Homo sapiens	110-115
29634349-11	2019	CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2.	3-n-butylphthalide	12-18	NLR family pyrin domain containing 3	Homo sapiens	50-55
29634349-11	2019	CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2.	3-n-butylphthalide	12-18	NLR family pyrin domain containing 3	Homo sapiens	80-85
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Adenosine Triphosphate	172-175	NLR family pyrin domain containing 3	Homo sapiens	51-56
29475852-13	2019	Consequently, treatment of hepatocytes with ethanol resulted in TXNIP overexpression, activating NLRP3 inflammasome and caspase-1-mediated pyroptosis.	Ethanol	44-51	NLR family pyrin domain containing 3	Homo sapiens	97-102
29475852-16	2019	CONCLUSION: Alcohol decreases miR-148a expression in hepatocytes through FoxO1, facilitating TXNIP overexpression and NLRP3 inflammasome activation, which induces hepatocyte pyroptosis.	Alcohols	12-19	NLR family pyrin domain containing 3	Homo sapiens	118-123
30246378-0	2019	Angiotensin (1-7) inhibits arecoline-induced migration and collagen synthesis in human oral myofibroblasts via inhibiting NLRP3 inflammasome activation.	Arecoline	27-36	NLR family pyrin domain containing 3	Homo sapiens	122-127
30246378-7	2019	In vivo, activation of NLRP3 inflammasomes with an increase of Ang-II type 1 receptor (AT1R) protein level and ROS production in human oral fibrosis tissues.	Reactive Oxygen Species	111-114	NLR family pyrin domain containing 3	Homo sapiens	23-28
30246378-9	2019	In vitro, arecoline increased ROS along with upregulation of the angiotensin-converting enzyme (ACE)/Ang-II/AT1R axis and NLRP3 inflammasome/interleukin-1beta axis in human oral myofibroblasts, which were reduced by NOX4 inhibitor VAS2870, ROS scavenger N-acetylcysteine, and NOX4 small interfering RNA (siRNA).	Arecoline	10-19	NLR family pyrin domain containing 3	Homo sapiens	122-127
30962733-7	2019	Some types of ginsenosides, including Rh1, Rg3, Rb1, compound K, chikusetsu saponin IVa, Rg5, and Rg1, have been clearly demonstrated to inhibit inflammatory responses by suppressing the activation of various inflammasomes, including the NLRP3, NLRP1, and absent in melanoma 2 inflammasomes.	Ginsenosides	14-26	NLR family pyrin domain containing 3	Homo sapiens	238-243
30776150-7	2019	Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) was shown to be involved in the IL-1beta response of liver macrophages to HIV-1 infection and NLRP3 blocking experiments in primary CD68+ liver macrophages confirmed the contribution of the NLRP3-caspase 1 inflammatory signaling pathway in the IL-1beta response.	Leucine	27-34	NLR family pyrin domain containing 3	Homo sapiens	86-91
30776150-7	2019	Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) was shown to be involved in the IL-1beta response of liver macrophages to HIV-1 infection and NLRP3 blocking experiments in primary CD68+ liver macrophages confirmed the contribution of the NLRP3-caspase 1 inflammatory signaling pathway in the IL-1beta response.	Leucine	27-34	NLR family pyrin domain containing 3	Homo sapiens	187-192
30776150-7	2019	Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) was shown to be involved in the IL-1beta response of liver macrophages to HIV-1 infection and NLRP3 blocking experiments in primary CD68+ liver macrophages confirmed the contribution of the NLRP3-caspase 1 inflammatory signaling pathway in the IL-1beta response.	Leucine	27-34	NLR family pyrin domain containing 3	Homo sapiens	187-192
30847537-9	2019	Induction of IL-1beta is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1beta induction, and fibroblast activation and differentiation.	Reactive Oxygen Species	244-247	NLR family pyrin domain containing 3	Homo sapiens	60-65
30847537-9	2019	Induction of IL-1beta is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1beta induction, and fibroblast activation and differentiation.	Acetylcysteine	262-278	NLR family pyrin domain containing 3	Homo sapiens	60-65
30847537-10	2019	Therefore, fibrogenic CNTs and silica, but not CB, elicit robust macrophage-guided myofibroblast transformation, which depends on the induction of IL-1beta through the NLRP3 inflammasome pathway and the increased production of ROS in macrophages.	Silicon Dioxide	31-37	NLR family pyrin domain containing 3	Homo sapiens	168-173
30653357-1	2019	Activation of the NACHT, leucine-rich repeat, and pyrin domains-containing protein 3 (collectively known as NLRP3) inflammasome plays a key role in host immune response, which is the first line of defense against cellular stresses and pathogen infections.	Leucine	25-32	NLR family pyrin domain containing 3	Homo sapiens	108-113
30430362-0	2019	1,25-Dihydroxy Vitamin D3 Attenuates the Oxidative Stress-Mediated Inflammation Induced by PM2.5via the p38/NF-kappaB/NLRP3 Pathway.	Calcitriol	0-25	NLR family pyrin domain containing 3	Homo sapiens	118-123
30430362-8	2019	Taken together, our findings provided novel experimental evidences supporting that vitamin D3 could reduce the predominantly oxidative stress-mediated inflammation induced by PM2.5via the p38/NF-kappaB/NLRP3 signaling pathway.	Cholecalciferol	83-93	NLR family pyrin domain containing 3	Homo sapiens	202-207
30320900-4	2019	As an inhibitor of NLRP3, MCC950 (CP-456773) can regulate the activation of inflammasome.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	34-43	NLR family pyrin domain containing 3	Homo sapiens	19-24
30320900-8	2019	This study provides theoretical support to the therapeutic evaluation of RAPA and MCC950 to make the mammalian targets of RAPA and NLRP3 the therapeutic targets of MS.	Sirolimus	73-77	NLR family pyrin domain containing 3	Homo sapiens	131-136
30246378-10	2019	Furthermore, arecoline induced collagen synthesis or migration via the Smad or RhoA-ROCK pathway respectively, which could be inhibited by NLRP3 siRNA or caspase-1 blocker VX-765.	Arecoline	13-22	NLR family pyrin domain containing 3	Homo sapiens	139-144
30246378-11	2019	Ang-(1-7) shifted the balance of RAS toward the ACE2/Ang-(1-7)/Mas axis, inhibited arecoline-induced ROS and NLRP3 inflammasome activation, leading to attenuation of migration or collagen synthesis.	Arecoline	83-92	NLR family pyrin domain containing 3	Homo sapiens	109-114
30246378-12	2019	In summary, Ang-(1-7) attenuates arecoline-induced migration and collagen synthesis via inhibiting NLRP3 inflammasome in human oral myofibroblasts.	Arecoline	33-42	NLR family pyrin domain containing 3	Homo sapiens	99-104
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Nigericin	161-170	NLR family pyrin domain containing 3	Homo sapiens	51-56
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Nigericin	161-170	NLR family pyrin domain containing 3	Homo sapiens	62-67
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Nigericin	161-170	NLR family pyrin domain containing 3	Homo sapiens	62-67
30782961-4	2019	Cholesterol crystal uptake or formation in lysosomes may damage membranes and activate NLRP3 inflammasomes.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	87-92
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Adenosine Triphosphate	172-175	NLR family pyrin domain containing 3	Homo sapiens	62-67
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Adenosine Triphosphate	172-175	NLR family pyrin domain containing 3	Homo sapiens	62-67
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Urea	181-185	NLR family pyrin domain containing 3	Homo sapiens	51-56
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Urea	181-185	NLR family pyrin domain containing 3	Homo sapiens	62-67
30735689-3	2019	Undifferentiated THP1 cells constitutively express NLRP3, and NLRP3 inflammasome activation occurred in response to canonical NLRP3 activation stimuli including nigericin, ATP, and urea crystals, culminating in pro-IL-1beta cleavage, extracellular release of mature IL-1beta, and pyroptosis.	Urea	181-185	NLR family pyrin domain containing 3	Homo sapiens	62-67
30735689-4	2019	We used this THP1 cell system to investigate potential targets of the potent, NLRP3 inflammasome selective inhibitor CP-456,773.	cp-456	117-123	NLR family pyrin domain containing 3	Homo sapiens	78-83
30818045-0	2019	NLRP3 inflammasome inhibition with MCC950 improves diabetes-mediated cognitive impairment and vasoneuronal remodeling after ischemia.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	35-41	NLR family pyrin domain containing 3	Homo sapiens	0-5
30818045-9	2019	Saline or MCC950 (3 mg/kg), an inhibitor of NLRP3, was injected at 1 and 3 h after reperfusion.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	10-16	NLR family pyrin domain containing 3	Homo sapiens	44-49
30747229-5	2019	An in vitro model was used to analyze the effect of miR-223 downregulation on an ALI model, which increased inflammation, and induced the activation of the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome and Toll-like receptor 4 (TLR4)/nuclear factor (NF)-kappaB signaling pathway via rho-related GTP-binding protein RhoB (RHOB).	Guanosine Triphosphate	318-321	NLR family pyrin domain containing 3	Homo sapiens	205-210
30670444-5	2019	Furthermore, somatic gene mutations of varied functional classes license the NLRP3 inflammasome to generate a common phenotype with excess reactive oxygen species generation, Wnt/beta-catenin-induced proliferation, cation flux-induced cell swelling, and caspase-1 activation.	reactive	139-147	NLR family pyrin domain containing 3	Homo sapiens	77-82
30670444-5	2019	Furthermore, somatic gene mutations of varied functional classes license the NLRP3 inflammasome to generate a common phenotype with excess reactive oxygen species generation, Wnt/beta-catenin-induced proliferation, cation flux-induced cell swelling, and caspase-1 activation.	oxygen species	148-162	NLR family pyrin domain containing 3	Homo sapiens	77-82
30628668-0	2019	miRNA-20b inhibits cerebral ischemia-induced inflammation through targeting NLRP3.	mirna-20b	0-9	NLR family pyrin domain containing 3	Homo sapiens	76-81
30923255-0	2019	Saturated fatty acid-crystals activate NLRP3 inflammasome.	Fatty Acids	0-20	NLR family pyrin domain containing 3	Homo sapiens	39-44
30862067-5	2019	Melatonin can stimulate the release of proinflammatory cytokines and other mediators, but also, under different conditions, it can suppress inflammation-promoting processes such as NO release, activation of cyclooxygenase-2, inflammasome NLRP3, gasdermin D, toll-like receptor-4 and mTOR signaling, and cytokine release by SASP (senescence-associated secretory phenotype), and amyloid-beta toxicity.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	238-243
30911280-2	2019	Nucleotide-binding oligomerisation domain-like receptors (NLRs) Family Pyrin Domain Containing 3(NLRP3) inflammasome contributed to the pathogenesis of D-galactosamine and lipopolysaccharide-induced acute liver failure.	Galactosamine	152-167	NLR family pyrin domain containing 3	Homo sapiens	97-102
30633869-7	2019	In addition, inhibition of estrogen receptor signaling or ROS production markedly blocked leptin-induced activation of NLRP3 inflammasomes, suggesting that estrogen receptor signaling and ROS production mediate inflammasomes activation by leptin.	Reactive Oxygen Species	58-61	NLR family pyrin domain containing 3	Homo sapiens	119-124
30633869-7	2019	In addition, inhibition of estrogen receptor signaling or ROS production markedly blocked leptin-induced activation of NLRP3 inflammasomes, suggesting that estrogen receptor signaling and ROS production mediate inflammasomes activation by leptin.	Reactive Oxygen Species	188-191	NLR family pyrin domain containing 3	Homo sapiens	119-124
30664190-7	2019	It was observed that SUA significantly enhanced APN mRNA and protein expression (both P&lt;0.05) and increased NLRP3 (P&lt;0.001) and TNFalpha (P&lt;0.05) protein levels, as well as supernatant levels of IL-1beta (P&lt;0.01) and TNFalpha (P&lt;0.001) compared with untreated cells.	sua	21-24	NLR family pyrin domain containing 3	Homo sapiens	111-116
30628668-5	2019	The overexpression of miRNA-20b increased the levels of IL-1beta and IL-18 in the cerebral ischemia group through activation of the NLRP3 signaling pathway.	mirna-20b	22-31	NLR family pyrin domain containing 3	Homo sapiens	132-137
30628668-6	2019	Conversely, the downregulation of miRNA-20b suppressed IL-1beta and IL-18 levels in cerebral ischemia via suppression of the NLRP3 signaling pathway.	mirna-20b	34-43	NLR family pyrin domain containing 3	Homo sapiens	125-130
30628668-8	2019	The inhibition of NLRP3 decreased the pro-inflammatory effects of miRNA-20b in cerebral ischemia.	mirna-20b	66-75	NLR family pyrin domain containing 3	Homo sapiens	18-23
30637441-2	2019	In humans, the induction of IL-1beta production through MSU-induced NLRP3 inflammasome activation in monocytes/macrophages is responsible for pathogenesis of gouty arthritis.	Uric Acid	56-59	NLR family pyrin domain containing 3	Homo sapiens	68-73
30637441-7	2019	Resveratrol also inhibited NLRP3 inflammasome activation in MSU-stimulated monocytes by suppressing oligomerization of ASC.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	27-32
30628671-4	2019	In the present study, it was demonstrated that the disordered regulation of the NLRP3 inflammasome may induce the occurrence of RSA.	rabbit sperm membrane autoantigen	128-131	NLR family pyrin domain containing 3	Homo sapiens	80-85
30637441-7	2019	Resveratrol also inhibited NLRP3 inflammasome activation in MSU-stimulated monocytes by suppressing oligomerization of ASC.	Uric Acid	60-63	NLR family pyrin domain containing 3	Homo sapiens	27-32
30660990-0	2019	Anagliptin ameliorates high glucose- induced endothelial dysfunction via suppression of NLRP3 inflammasome activation mediated by SIRT1.	anagliptin	0-10	NLR family pyrin domain containing 3	Homo sapiens	88-93
30660990-7	2019	Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10).	anagliptin	13-23	NLR family pyrin domain containing 3	Homo sapiens	70-75
30597604-5	2019	Mechanistically, the roles of melatonin in macrophages are related to several cellular signaling pathways, such as NF-kappaB, STATs, and NLRP3/caspase-1.	Melatonin	30-39	NLR family pyrin domain containing 3	Homo sapiens	137-142
30628671-6	2019	Further investigation was performed to elucidate the mechanism of activation of the NLRP3 inflammasome in patients with RSA.	rabbit sperm membrane autoantigen	120-123	NLR family pyrin domain containing 3	Homo sapiens	84-89
30660990-7	2019	Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10).	anagliptin	13-23	NLR family pyrin domain containing 3	Homo sapiens	145-150
30660990-7	2019	Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10).	Glucose	53-60	NLR family pyrin domain containing 3	Homo sapiens	70-75
30628671-9	2019	The present study provides a potential future therapeutic target for RSA via the NLRP3 inflammasome.	rabbit sperm membrane autoantigen	69-72	NLR family pyrin domain containing 3	Homo sapiens	81-86
30660990-7	2019	Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10).	Glucose	53-60	NLR family pyrin domain containing 3	Homo sapiens	145-150
30496753-0	2019	Ketamine may exert antidepressant effects via suppressing NLRP3 inflammasome to upregulate AMPA receptors.	Ketamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	58-63
30660990-10	2019	Silencing of SIRT1 by transfection with SIRT1 siRNA abolished the inhibitory effects of anagliptin in NLRP3 inflammasome activation.	anagliptin	88-98	NLR family pyrin domain containing 3	Homo sapiens	102-107
29887266-5	2019	Elevated production of reactive oxygen species could be able to activate NLRP3 inflammasome representing new deregulated biological machinery and a novel therapeutic target in hemodialysis patients.	Reactive Oxygen Species	23-46	NLR family pyrin domain containing 3	Homo sapiens	73-78
30496753-4	2019	Thus, we postulated that NLRP3 inflammasome might play an important role in ketamine"s antidepressant effects.	Ketamine	76-84	NLR family pyrin domain containing 3	Homo sapiens	25-30
30496753-6	2019	Ketamine also abrogated LPS-induced over expression of IL-1beta and NLRP3 and reversed LPS-induced down-regulation of AMPA GluA1 subunits in hippocampi.	Ketamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	68-73
30496753-7	2019	The selective NLRP3 inflammasome inhibitor Ac-YVAD-CMK exhibited similar anti-inflammatory and antidepressant effects like ketamine.	ac-yvad	43-50	NLR family pyrin domain containing 3	Homo sapiens	14-19
30496753-7	2019	The selective NLRP3 inflammasome inhibitor Ac-YVAD-CMK exhibited similar anti-inflammatory and antidepressant effects like ketamine.	Ketamine	123-131	NLR family pyrin domain containing 3	Homo sapiens	14-19
30496753-9	2019	These results indicated that the NLRP3 inflammasome might be an important mediator, through which ketamine could regulate AMPA receptors to exert rapid antidepressant effects.	Ketamine	98-106	NLR family pyrin domain containing 3	Homo sapiens	33-38
30606476-7	2019	Meanwhile, BAY 11-7082 and IL4 were added with HMGB1 to observe the NLRP3 inflammasome and changes in NF-kappaB expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	11-22	NLR family pyrin domain containing 3	Homo sapiens	68-73
30582969-0	2019	Fusaric acid induces NRF2 as a cytoprotective response to prevent NLRP3 activation in the liver derived HepG2 cell line.	Fusaric Acid	0-12	NLR family pyrin domain containing 3	Homo sapiens	66-71
30873162-3	2019	The C-terminal conserves a leucine-rich repeats (LRRs) domain which can modulate NLRP3 activity and sense endogenous alarmins and microbial ligands.	Leucine	27-34	NLR family pyrin domain containing 3	Homo sapiens	81-86
30906223-10	2019	In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	30-41	NLR family pyrin domain containing 3	Homo sapiens	90-95
30906223-10	2019	In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression.	Glucose	58-65	NLR family pyrin domain containing 3	Homo sapiens	90-95
30906223-11	2019	In conclusion, this study suggested that As-IV could inhibit high glucose-induced NLRP3 inflammasome activation and subsequent secretion of proinflammatory cytokines via inhibiting TLR4/NF-kappaB signaling pathway and CaSR, which provides new insights into the anti-inflammatory activity of As-IV.	Glucose	66-73	NLR family pyrin domain containing 3	Homo sapiens	82-87
30899369-0	2019	Metformin induces the M2 macrophage polarization to accelerate the wound healing via regulating AMPK/mTOR/NLRP3 inflammasome singling pathway.	Metformin	0-9	NLR family pyrin domain containing 3	Homo sapiens	106-111
30899369-9	2019	We also found that the level of relative proteins of NLRP3 inflammasome was markedly decreased after metformin treatment.	Metformin	101-110	NLR family pyrin domain containing 3	Homo sapiens	53-58
30899369-10	2019	Furthermore, blockage of AMPK or activation of mTOR abolished the effects of metformin treatment on depressing NLRP3 inflammasome activation, M2 polarization and improving wound healing.	Metformin	77-86	NLR family pyrin domain containing 3	Homo sapiens	111-116
30899369-11	2019	It suggested that the treatment effects of metformin on wound healing were through regulating AMPK/mTOR/NLRP3 inflammasome signaling axis.	Metformin	43-52	NLR family pyrin domain containing 3	Homo sapiens	104-109
30899369-12	2019	CONCLUSION: Metformin regulated AMPK/mTOR singling pathway to inhibit NLRP3 inflammasome activation, which boosted M2 macrophage polarization to accelerate the wound healing.	Metformin	12-21	NLR family pyrin domain containing 3	Homo sapiens	70-75
30728075-5	2019	METHODS: Peripheral blood mononuclear cells (PBMCs) were cultured with a combination of monosodium urate crystals (MSU) and palmitic acid (C16.0) in order to activate the NLRP3 inflammasome and induce IL-1beta production.	Uric Acid	88-104	NLR family pyrin domain containing 3	Homo sapiens	171-176
30728075-5	2019	METHODS: Peripheral blood mononuclear cells (PBMCs) were cultured with a combination of monosodium urate crystals (MSU) and palmitic acid (C16.0) in order to activate the NLRP3 inflammasome and induce IL-1beta production.	msu	115-118	NLR family pyrin domain containing 3	Homo sapiens	171-176
30728075-5	2019	METHODS: Peripheral blood mononuclear cells (PBMCs) were cultured with a combination of monosodium urate crystals (MSU) and palmitic acid (C16.0) in order to activate the NLRP3 inflammasome and induce IL-1beta production.	Palmitic Acid	124-137	NLR family pyrin domain containing 3	Homo sapiens	171-176
30804327-6	2019	NLRP3 inflammasome activation by the bacterial toxin nigericin led to the proinflammatory interleukin-1beta (IL-1beta) release and to the induction of cell death by pyroptosis.	Nigericin	53-62	NLR family pyrin domain containing 3	Homo sapiens	0-5
30804327-8	2019	Especially, FADD, but not IL-1beta, secretion following NLRP3 inflammasome activation required extracellular glucose.	fadd	12-16	NLR family pyrin domain containing 3	Homo sapiens	56-61
30804327-8	2019	Especially, FADD, but not IL-1beta, secretion following NLRP3 inflammasome activation required extracellular glucose.	Glucose	109-116	NLR family pyrin domain containing 3	Homo sapiens	56-61
30804327-12	2019	Finally, we established human soluble FADD as a new marker of joint inflammation in gout and rheumatoid arthritis, two rheumatic diseases involving the NLRP3 inflammasome.	fadd	38-42	NLR family pyrin domain containing 3	Homo sapiens	152-157
30906223-0	2019	Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4/NF-kappaB and CaSR.	astragaloside A	0-16	NLR family pyrin domain containing 3	Homo sapiens	49-54
30906223-0	2019	Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4/NF-kappaB and CaSR.	Glucose	33-40	NLR family pyrin domain containing 3	Homo sapiens	49-54
30906223-7	2019	The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1beta (IL-1beta), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR.	Glucose	29-36	NLR family pyrin domain containing 3	Homo sapiens	119-124
30906223-9	2019	Meanwhile, NPS2143, BAY 11-7082, and INF39 could significantly abolish the high glucose-enhanced NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression in vitro.	Glucose	80-87	NLR family pyrin domain containing 3	Homo sapiens	97-102
30591217-0	2019	Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22.	Glucose	40-47	NLR family pyrin domain containing 3	Homo sapiens	104-109
30591217-9	2019	NLRP3 expression was significantly suppressed by transfection with a MALAT1-targeting antisense oligonucleotide (ASO).	Oligonucleotides	96-111	NLR family pyrin domain containing 3	Homo sapiens	0-5
30591217-9	2019	NLRP3 expression was significantly suppressed by transfection with a MALAT1-targeting antisense oligonucleotide (ASO).	Oligonucleotides, Antisense	113-116	NLR family pyrin domain containing 3	Homo sapiens	0-5
30591217-11	2019	Together, our results suggest that lncRNA MALAT1 promotes high glucose-induced pyroptosis of endothelial cells partly by affecting NLRP3 expression through competitively binding miR-22.	Glucose	63-70	NLR family pyrin domain containing 3	Homo sapiens	131-136
29486589-7	2019	The autophagy inhibitor 3-methyladenine reduced BLM-induced lung fibrosis and concurrently facilitated NLRP3 inflammasome activation and oxidation in fibroblasts.	3-methyladenine	24-39	NLR family pyrin domain containing 3	Homo sapiens	103-108
29486589-10	2019	Moreover, blocking autophagy with bafilomycin A1 or LC3B siRNA resulted in oxidant accumulation, NLRP3 inflammasome hyperactivation, and collagen deposition.	bafilomycin A1	34-48	NLR family pyrin domain containing 3	Homo sapiens	97-102
29486589-1	2019	AIMS: The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is activated by reactive oxygen species (ROS) and repressed by autophagy, has been identified as a novel agent of pulmonary fibrosis.	Reactive Oxygen Species	105-128	NLR family pyrin domain containing 3	Homo sapiens	62-67
29486589-1	2019	AIMS: The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is activated by reactive oxygen species (ROS) and repressed by autophagy, has been identified as a novel agent of pulmonary fibrosis.	Reactive Oxygen Species	130-133	NLR family pyrin domain containing 3	Homo sapiens	62-67
29486589-12	2019	Innovation and Conclusion: Autophagy attenuates pulmonary fibrosis by regulating NLRP3 inflammasome activation induced by AngII-mediated ROS via redox balance modulation.	Reactive Oxygen Species	137-140	NLR family pyrin domain containing 3	Homo sapiens	81-86
29486589-6	2019	Treatment with rapamycin promoted autophagy but inhibited oxidation, NLRP3 inflammasome, and lung fibrosis after bleomycin (BLM) infusion.	Sirolimus	15-24	NLR family pyrin domain containing 3	Homo sapiens	69-74
30354670-8	2019	Taken together, paricalcitol ameliorated EMT of HPMCs via modulating an NOX-dependent increase in the activity of NLRP3 inflammasome.	paricalcitol	16-28	NLR family pyrin domain containing 3	Homo sapiens	114-119
30347231-0	2019	LncRNA ANRIL promotes NLRP3 inflammasome activation in uric acid nephropathy through miR-122-5p/BRCC3 axis.	Uric Acid	55-64	NLR family pyrin domain containing 3	Homo sapiens	22-27
30600470-10	2019	In addition, the mRNA levels of NLRP3 and NF-kappaB p65 were regulated by resveratrol, but caspase-1 and IL-1beta were not.	Resveratrol	74-85	NLR family pyrin domain containing 3	Homo sapiens	32-37
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	36-43	NLR family pyrin domain containing 3	Homo sapiens	98-171
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	36-43	NLR family pyrin domain containing 3	Homo sapiens	173-178
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	215-222	NLR family pyrin domain containing 3	Homo sapiens	98-171
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	215-222	NLR family pyrin domain containing 3	Homo sapiens	173-178
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	215-222	NLR family pyrin domain containing 3	Homo sapiens	98-171
30447168-2	2019	In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain-like receptor pyrin domain-containing-3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure.	Ethanol	215-222	NLR family pyrin domain containing 3	Homo sapiens	173-178
30447168-3	2019	Purinergic receptors (especially the P2X7 receptor) are able to activate the NLRP3 inflammasome and are involved in many ethanol-related diseases (such as gout, pulmonary fibrosis, alcoholic steatohepatitis, and certain cancers).	Ethanol	121-128	NLR family pyrin domain containing 3	Homo sapiens	77-82
30447168-4	2019	We hypothesized that ethanol regulates purinergic receptors and thus modulates the NLRP3 inflammasome"s activity.	Ethanol	21-28	NLR family pyrin domain containing 3	Homo sapiens	83-88
29974310-5	2019	Further mechanistic studies showed that the reduction of pro-inflammatory cytokines by triptolide was mediated by the upregulation of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) and downregulation of caspase-1.	triptolide	87-97	NLR family pyrin domain containing 3	Homo sapiens	232-237
29974310-6	2019	Finally, we identified that hsa-miR-20b, a microRNA targeting the NLRP3 gene, was downregulated by triptolide.	triptolide	99-109	NLR family pyrin domain containing 3	Homo sapiens	66-71
30354670-0	2019	Paricalcitol attenuates TGF-beta1-induced phenotype transition of human peritoneal mesothelial cells (HPMCs) via modulation of oxidative stress and NLRP3 inflammasome.	paricalcitol	0-12	NLR family pyrin domain containing 3	Homo sapiens	148-153
30354670-7	2019	Paricalcitol alleviated TGF-beta1-induced EMT and the NLRP3 inflammasome, which was associated with a down-regulation of NOX activity by interfering with p47phox and p22phox interaction and mitochondrial NOX4 production in HPMCs.	paricalcitol	0-12	NLR family pyrin domain containing 3	Homo sapiens	54-59
30447168-8	2019	Taken as a whole, our results suggest that ethanol induces NLRP3 inflammasome activation by upregulating the P2X7 receptor.	Ethanol	43-50	NLR family pyrin domain containing 3	Homo sapiens	59-64
30761138-12	2019	Inhibition of ROS by N-Acetyl Cysteine inhibited TLR2-induced priming of the NLRP3 inflammasome, but had no effect on MSU-induced activation.	Reactive Oxygen Species	14-17	NLR family pyrin domain containing 3	Homo sapiens	77-82
30594776-3	2019	The nucleotide-binding oligomerization domain-, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome is an inflammatory complex existing in microglia.	Leucine	48-55	NLR family pyrin domain containing 3	Homo sapiens	99-104
30699285-8	2019	Third, TAM signaling can induce autophagy which is an important mechanism to inhibit NLRP3 inflammasome activation in macrophages.	Tamoxifen	7-10	NLR family pyrin domain containing 3	Homo sapiens	85-90
30761006-12	2019	CRP not only increased the expression of pro-IL-1beta and NLRP3 via the FcgammaRs/NF-kappaB pathway, but also promoted NLRP3 inflammasome activation and IL-1beta maturation by upregulation of reactive oxygen species (ROS) levels, purinergic receptor signaling, and activation of cysteine proteases.	Reactive Oxygen Species	192-215	NLR family pyrin domain containing 3	Homo sapiens	119-124
30761006-12	2019	CRP not only increased the expression of pro-IL-1beta and NLRP3 via the FcgammaRs/NF-kappaB pathway, but also promoted NLRP3 inflammasome activation and IL-1beta maturation by upregulation of reactive oxygen species (ROS) levels, purinergic receptor signaling, and activation of cysteine proteases.	Reactive Oxygen Species	217-220	NLR family pyrin domain containing 3	Homo sapiens	119-124
30761102-8	2019	K+ efflux and mitochondrial reactive oxygen species were important for SARS-CoV 3a-induced NLRP3 inflammasome activation.	Reactive Oxygen Species	28-51	NLR family pyrin domain containing 3	Homo sapiens	91-96
30611121-0	2019	Calcitriol inhibits ROS-NLRP3-IL-1beta signaling axis via activation of Nrf2-antioxidant signaling in hyperosmotic stress stimulated human corneal epithelial cells.	Calcitriol	0-10	NLR family pyrin domain containing 3	Homo sapiens	24-29
30611121-0	2019	Calcitriol inhibits ROS-NLRP3-IL-1beta signaling axis via activation of Nrf2-antioxidant signaling in hyperosmotic stress stimulated human corneal epithelial cells.	ros	20-23	NLR family pyrin domain containing 3	Homo sapiens	24-29
30611121-1	2019	PURPOSE: The activation of ROS-NLRP3-IL-1beta signaling axis induced by hyperosmotic stress (HS) has been recognized as a key priming stage of epithelial inflammation in dry eye pathogenesis.	ros	27-30	NLR family pyrin domain containing 3	Homo sapiens	31-36
30611121-8	2019	RESULTS: Calcitriol could protect cells against HS-induced injury through inhibiting ROS-NLRP3-IL-1beta signaling axis.	Calcitriol	9-19	NLR family pyrin domain containing 3	Homo sapiens	89-94
30611121-8	2019	RESULTS: Calcitriol could protect cells against HS-induced injury through inhibiting ROS-NLRP3-IL-1beta signaling axis.	ros	85-88	NLR family pyrin domain containing 3	Homo sapiens	89-94
30611121-9	2019	Calcitriol remarkably suppressed the expression of NLRP3 inflammasome related genes and the production of IL-1beta in cells that were exposed to HS.	Calcitriol	0-10	NLR family pyrin domain containing 3	Homo sapiens	51-56
30761138-12	2019	Inhibition of ROS by N-Acetyl Cysteine inhibited TLR2-induced priming of the NLRP3 inflammasome, but had no effect on MSU-induced activation.	Acetylcysteine	21-38	NLR family pyrin domain containing 3	Homo sapiens	77-82
30666218-8	2018	In this study, we discovered: (i) that activation of NLRP3 inflammasome was involved in the depressive-like behaviors induced by SD; (ii) decrease in BDNF following SD required the activation of NLRP3 inflammasomes; (iii) leptin augmented the anti-depressive action of fluoxetine through an increase in expression of astrocytic 5-HT2B receptors.	Fluoxetine	269-279	NLR family pyrin domain containing 3	Homo sapiens	53-58
30459218-9	2019	Our results suggest that AII and A17 amacrines express clustered, extrasynaptic NMDA receptors, with different and complementary subunits that are likely to contribute differentially to signal processing and plasticity.SIGNIFICANCE STATEMENT Glutamate is the most important excitatory neurotransmitter in the CNS, but not all glutamate receptors transmit fast excitatory signals at synapses.	Glutamic Acid	242-251	NLR family pyrin domain containing 3	Homo sapiens	25-28
30666218-8	2018	In this study, we discovered: (i) that activation of NLRP3 inflammasome was involved in the depressive-like behaviors induced by SD; (ii) decrease in BDNF following SD required the activation of NLRP3 inflammasomes; (iii) leptin augmented the anti-depressive action of fluoxetine through an increase in expression of astrocytic 5-HT2B receptors.	Fluoxetine	269-279	NLR family pyrin domain containing 3	Homo sapiens	195-200
30315709-0	2019	Role and mechanism of ROS scavengers in alleviating NLRP3-mediated inflammation.	Reactive Oxygen Species	22-25	NLR family pyrin domain containing 3	Homo sapiens	52-57
30612459-0	2019	Rhein, An Anthraquinone Drug, Suppresses the NLRP3 Inflammasome and Macrophage Activation in Urate Crystal-Induced Gouty Inflammation.	Anthraquinones	10-23	NLR family pyrin domain containing 3	Homo sapiens	45-50
30612459-3	2019	Gouty arthritis is an inflammatory disease characterized by urate crystal-induced NLRP3 inflammasome activation with up-regulated caspase-1 protease and IL-1 beta in macrophages.	Uric Acid	60-65	NLR family pyrin domain containing 3	Homo sapiens	82-87
30740538-0	2019	Niclosamide activates the NLRP3 inflammasome by intracellular acidification and mitochondrial inhibition.	Niclosamide	0-11	NLR family pyrin domain containing 3	Homo sapiens	26-31
30740538-3	2019	Here we identified niclosamide, a mitochondrial uncoupler, as an activator of NLRP3 inflammasome.	Niclosamide	19-30	NLR family pyrin domain containing 3	Homo sapiens	78-83
30740538-5	2019	Intracellular acidification, by inhibiting glycolysis, works together with mitochondrial inhibition to induce intracellular ATP loss, which compromises intracellular potassium maintenance, a key event to NLRP3 inflammasome activation.	Adenosine Triphosphate	124-127	NLR family pyrin domain containing 3	Homo sapiens	204-209
30740538-5	2019	Intracellular acidification, by inhibiting glycolysis, works together with mitochondrial inhibition to induce intracellular ATP loss, which compromises intracellular potassium maintenance, a key event to NLRP3 inflammasome activation.	Potassium	166-175	NLR family pyrin domain containing 3	Homo sapiens	204-209
30740538-7	2019	Our work illustrates how energy metabolism converges upon intracellular potassium to activate NLRP3 inflammasome and highlights a biphasic relationship between cellular physiology and IL-1beta release.	Potassium	72-81	NLR family pyrin domain containing 3	Homo sapiens	94-99
30315709-3	2019	Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model.	Reactive Oxygen Species	29-52	NLR family pyrin domain containing 3	Homo sapiens	59-64
30315709-3	2019	Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model.	Reactive Oxygen Species	29-52	NLR family pyrin domain containing 3	Homo sapiens	100-105
30315709-3	2019	Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model.	Reactive Oxygen Species	54-57	NLR family pyrin domain containing 3	Homo sapiens	59-64
30315709-3	2019	Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model.	Reactive Oxygen Species	54-57	NLR family pyrin domain containing 3	Homo sapiens	100-105
30315709-5	2019	This article, at first, briefly overviews how ROS may mediate the regulation of NLRP3 inflammasome activation.	Reactive Oxygen Species	46-49	NLR family pyrin domain containing 3	Homo sapiens	80-85
30315709-6	2019	Then, preclinical researches of various ROS scavengers for treating NLRP3 inflammasome-associated diseases are focused on and critically analyzed.	Reactive Oxygen Species	40-43	NLR family pyrin domain containing 3	Homo sapiens	68-73
30389501-12	2019	In summary, we have demonstrated that SREBP-1 could be a key player in oxLDL-induced excessive lipid accumulation leading to macrophage FCF via ROS-mediated NLRP3/IL-1beta/SREBP-1 pathway.	Reactive Oxygen Species	144-147	NLR family pyrin domain containing 3	Homo sapiens	157-162
31663353-7	2019	RESULTS: Based on our findings using western blotting and immunohistochemistry assay, overexpression of NLRP1 and NLRP3 proteins in the hippocampal region of Meth addicts was observed.	Methamphetamine	158-162	NLR family pyrin domain containing 3	Homo sapiens	114-119
31663353-10	2019	CONCLUSION: Chronic Meth abuse could result in increases of NLRP1 and NLRP3 and induction of inflammation and apoptosis in the hippocampus in Meth groups (Tab.	Methamphetamine	20-24	NLR family pyrin domain containing 3	Homo sapiens	70-75
31594217-0	2019	Stavudine Reduces NLRP3 Inflammasome Activation and Modulates Amyloid-beta Autophagy.	Stavudine	0-9	NLR family pyrin domain containing 3	Homo sapiens	18-23
30591286-11	2019	Recent demonstration that cholesterol crystals trigger the NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3) inflammasome and the release of inflammatory cytokines that also drive uric acid crystal-induced inflammation indicates that the multiple actions of colchicine that make it effective in gout may be relevant to preventing inflammation and limiting inflammatory injury in atherosclerosis.	Cholesterol	26-37	NLR family pyrin domain containing 3	Homo sapiens	59-64
30591286-11	2019	Recent demonstration that cholesterol crystals trigger the NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3) inflammasome and the release of inflammatory cytokines that also drive uric acid crystal-induced inflammation indicates that the multiple actions of colchicine that make it effective in gout may be relevant to preventing inflammation and limiting inflammatory injury in atherosclerosis.	Leucine	102-109	NLR family pyrin domain containing 3	Homo sapiens	59-64
30591286-11	2019	Recent demonstration that cholesterol crystals trigger the NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3) inflammasome and the release of inflammatory cytokines that also drive uric acid crystal-induced inflammation indicates that the multiple actions of colchicine that make it effective in gout may be relevant to preventing inflammation and limiting inflammatory injury in atherosclerosis.	Uric Acid	234-243	NLR family pyrin domain containing 3	Homo sapiens	59-64
30591286-11	2019	Recent demonstration that cholesterol crystals trigger the NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3) inflammasome and the release of inflammatory cytokines that also drive uric acid crystal-induced inflammation indicates that the multiple actions of colchicine that make it effective in gout may be relevant to preventing inflammation and limiting inflammatory injury in atherosclerosis.	Colchicine	312-322	NLR family pyrin domain containing 3	Homo sapiens	59-64
30471618-2	2019	Our previous study has demonstrated that in human peritoneal mesothelial cells (HPMCs), exposure to high glucose-based peritoneal dialysis (PD) solutions induced mitochondrial reactive oxygen species (ROS) production, activation of NLRP3 inflammasome and IL-1beta expression.	Glucose	105-112	NLR family pyrin domain containing 3	Homo sapiens	232-237
30471618-3	2019	This study aimed to investigate the effect of high glucose-based PD fluids on the TXNIP expression and the underlying mechanisms by which TXNIP-NLRP3 interaction mediates the inflammatory injury to HPMCs in high glucose-based PD fluids conditions.	Glucose	51-58	NLR family pyrin domain containing 3	Homo sapiens	144-149
30471618-3	2019	This study aimed to investigate the effect of high glucose-based PD fluids on the TXNIP expression and the underlying mechanisms by which TXNIP-NLRP3 interaction mediates the inflammatory injury to HPMCs in high glucose-based PD fluids conditions.	Glucose	212-219	NLR family pyrin domain containing 3	Homo sapiens	144-149
30471618-8	2019	We also found that ROS generation induced by high glucose-based PD solutions disrupts the TRX1-TXNIP association, while promoting the binding of TXNIP to NLRP3 in HPMCs.	Reactive Oxygen Species	19-22	NLR family pyrin domain containing 3	Homo sapiens	154-159
30471618-8	2019	We also found that ROS generation induced by high glucose-based PD solutions disrupts the TRX1-TXNIP association, while promoting the binding of TXNIP to NLRP3 in HPMCs.	Glucose	50-57	NLR family pyrin domain containing 3	Homo sapiens	154-159
30471618-9	2019	Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1beta expression.	Reactive Oxygen Species	34-37	NLR family pyrin domain containing 3	Homo sapiens	121-126
30471618-9	2019	Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1beta expression.	Ammonium pyrrolidyldithiocarbamate	49-53	NLR family pyrin domain containing 3	Homo sapiens	121-126
30471618-9	2019	Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1beta expression.	Glucose	81-88	NLR family pyrin domain containing 3	Homo sapiens	121-126
29857009-9	2019	In Study 2 the saturated fatty acid meal led to increases in sputum neutrophil percentages and sputum cell gene expression of Toll-like receptor 4 (TLR4) and NLRP3 at 4 hours in nonobese asthmatic patients.	Fatty Acids	15-35	NLR family pyrin domain containing 3	Homo sapiens	158-163
30246263-0	2019	Evaluation on the effect of hydrogen sulfide on the NLRP3 signaling pathway and its involvement in the pathogenesis of atherosclerosis.	Hydrogen Sulfide	28-44	NLR family pyrin domain containing 3	Homo sapiens	52-57
30246263-8	2019	Furthermore, upregulation of H 2 S synthesis by treating the cells with NaHS also reduced the protein levels of TXNIP, NLRP3, ASC, caspase-1, and IL-1beta.	Hydrogen Sulfide	29-34	NLR family pyrin domain containing 3	Homo sapiens	119-124
30842373-7	2019	CD54 expression, induced by OA and SA, was suppressed by potassium chloride, a typical inhibitor of NLRP3 inflammasome activation.	Potassium Chloride	57-75	NLR family pyrin domain containing 3	Homo sapiens	100-105
30246263-8	2019	Furthermore, upregulation of H 2 S synthesis by treating the cells with NaHS also reduced the protein levels of TXNIP, NLRP3, ASC, caspase-1, and IL-1beta.	sodium bisulfide	72-76	NLR family pyrin domain containing 3	Homo sapiens	119-124
30391945-4	2019	Using inhibitor-based approaches, we show that NLRP3 activation by T. vaginalis involves host cell detection of extracellular ATP via P2X7 receptors and potassium efflux.	Adenosine Triphosphate	126-129	NLR family pyrin domain containing 3	Homo sapiens	47-52
30391945-4	2019	Using inhibitor-based approaches, we show that NLRP3 activation by T. vaginalis involves host cell detection of extracellular ATP via P2X7 receptors and potassium efflux.	Potassium	153-162	NLR family pyrin domain containing 3	Homo sapiens	47-52
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	Dinitrochlorobenzene	126-130	NLR family pyrin domain containing 3	Homo sapiens	231-236
30439413-0	2019	Cyclo(His-Pro) inhibits NLRP3 inflammasome cascade in ALS microglial cells.	histidyl-proline diketopiperazine	0-13	NLR family pyrin domain containing 3	Homo sapiens	24-29
30825154-0	2019	The LPS/D-Galactosamine-Induced Fulminant Hepatitis Model to Assess the Role of Ligand-Activated Nuclear Receptors on the NLRP3 Inflammasome Pathway In Vivo.	Galactosamine	10-23	NLR family pyrin domain containing 3	Homo sapiens	122-127
30825154-1	2019	The NLRP3 inflammasome is a cellular sensor of danger signals such as extracellular ATP or abnormally accumulating molecules like crystals.	Adenosine Triphosphate	84-87	NLR family pyrin domain containing 3	Homo sapiens	4-9
30439413-5	2019	We found that cyclo(His-Pro) inhibits NLRP3 inflammasome activation by reducing protein nitration via reduction in NO and ROS levels, indicative of lower peroxynitrite generation by LPS.	histidyl-proline diketopiperazine	14-27	NLR family pyrin domain containing 3	Homo sapiens	38-43
30439413-5	2019	We found that cyclo(His-Pro) inhibits NLRP3 inflammasome activation by reducing protein nitration via reduction in NO and ROS levels, indicative of lower peroxynitrite generation by LPS.	ros	122-125	NLR family pyrin domain containing 3	Homo sapiens	38-43
30439413-5	2019	We found that cyclo(His-Pro) inhibits NLRP3 inflammasome activation by reducing protein nitration via reduction in NO and ROS levels, indicative of lower peroxynitrite generation by LPS.	Peroxynitrous Acid	154-167	NLR family pyrin domain containing 3	Homo sapiens	38-43
30560887-8	2018	On the other hand, EP reduced the LPS/ATP-induced proliferation and migration of A549 cells through attenuated NLRP3 inflammasome activity.	Adenosine Triphosphate	38-41	NLR family pyrin domain containing 3	Homo sapiens	111-116
30496979-7	2019	These effects was consistent with the in vitro data revealing that palmatine inhibited the activation of NLRP3 inflammasomes, while promoted the expression and mitochondrial recruitment of PINK1 and Parkin in THP-1 cell differentiated macrophages.	palmatine	67-76	NLR family pyrin domain containing 3	Homo sapiens	105-110
30788452-0	2019	Fish Oil Derived Omega 3 Fatty Acids Suppress Adipose NLRP3 Inflammasome Signaling in Human Obesity.	Fatty Acids, Omega-3	17-36	NLR family pyrin domain containing 3	Homo sapiens	54-59
30483776-7	2019	In addition, bile acids, including deoxycholic acid and chenodeoxycholic acid, are able to activate the NLRP3 inflammasome in macrophages; however, bile acids have the potential to exert the opposite role by interacting with the membrane-bound Takeda G-protein receptor 5 or by activating nuclear farnesoid-X receptor.	Bile Acids and Salts	13-23	NLR family pyrin domain containing 3	Homo sapiens	104-109
30483776-7	2019	In addition, bile acids, including deoxycholic acid and chenodeoxycholic acid, are able to activate the NLRP3 inflammasome in macrophages; however, bile acids have the potential to exert the opposite role by interacting with the membrane-bound Takeda G-protein receptor 5 or by activating nuclear farnesoid-X receptor.	Deoxycholic Acid	35-51	NLR family pyrin domain containing 3	Homo sapiens	104-109
30483776-7	2019	In addition, bile acids, including deoxycholic acid and chenodeoxycholic acid, are able to activate the NLRP3 inflammasome in macrophages; however, bile acids have the potential to exert the opposite role by interacting with the membrane-bound Takeda G-protein receptor 5 or by activating nuclear farnesoid-X receptor.	Chenodeoxycholic Acid	56-77	NLR family pyrin domain containing 3	Homo sapiens	104-109
30483776-7	2019	In addition, bile acids, including deoxycholic acid and chenodeoxycholic acid, are able to activate the NLRP3 inflammasome in macrophages; however, bile acids have the potential to exert the opposite role by interacting with the membrane-bound Takeda G-protein receptor 5 or by activating nuclear farnesoid-X receptor.	Bile Acids and Salts	148-158	NLR family pyrin domain containing 3	Homo sapiens	104-109
31814545-5	2019	Some flavonoids exert anti-inflammatory effects through: Blockade of NF-kappaB, and NLRP3 inflammasome, inhibition of pro-inflammatory cytokine production, IL-1beta, IL-2, IL-6, TNF-alpha, IL-17A, down regulation of chemokines, and reduction of reactive oxygen and nitrogen species.	Flavonoids	5-15	NLR family pyrin domain containing 3	Homo sapiens	84-89
30378427-0	2018	Atypical Gasdermin D and Mixed Lineage Kinase Domain-like Protein Leakage Aggravates Tetrachlorobenzoquinone-Induced Nod-like Receptor Protein 3 Inflammasome Activation.	tetrachlorobenzoquinone	85-108	NLR family pyrin domain containing 3	Homo sapiens	117-144
29932955-3	2018	Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	227-232
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	tetrachlorobenzoquinone	31-54	NLR family pyrin domain containing 3	Homo sapiens	89-116
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	tetrachlorobenzoquinone	31-54	NLR family pyrin domain containing 3	Homo sapiens	118-123
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	tetrachlorobenzoquinone	56-60	NLR family pyrin domain containing 3	Homo sapiens	89-116
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	tetrachlorobenzoquinone	56-60	NLR family pyrin domain containing 3	Homo sapiens	118-123
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	Reactive Oxygen Species	165-188	NLR family pyrin domain containing 3	Homo sapiens	89-116
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	Reactive Oxygen Species	165-188	NLR family pyrin domain containing 3	Homo sapiens	118-123
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	Reactive Oxygen Species	190-193	NLR family pyrin domain containing 3	Homo sapiens	89-116
30378427-1	2018	Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage.	Reactive Oxygen Species	190-193	NLR family pyrin domain containing 3	Homo sapiens	118-123
30378427-2	2018	In addition, TCBQ down-regulates NLRP3 ubiquitination and promotes the activation of NLRP3 inflammasome.	tetrachlorobenzoquinone	13-17	NLR family pyrin domain containing 3	Homo sapiens	33-38
30378427-2	2018	In addition, TCBQ down-regulates NLRP3 ubiquitination and promotes the activation of NLRP3 inflammasome.	tetrachlorobenzoquinone	13-17	NLR family pyrin domain containing 3	Homo sapiens	85-90
29932955-3	2018	Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	227-232
29932955-3	2018	Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3.	Reactive Oxygen Species	60-63	NLR family pyrin domain containing 3	Homo sapiens	227-232
29932955-4	2018	Lysosomal destabilization, efflux of cytosolic potassium ions and influx of calcium ions, signals from damaged mitochondria, both translational and post-translational controls, and prion-like polymerization have increasingly clear roles in regulating NLRP3 activation.	Potassium	47-56	NLR family pyrin domain containing 3	Homo sapiens	251-256
29932955-4	2018	Lysosomal destabilization, efflux of cytosolic potassium ions and influx of calcium ions, signals from damaged mitochondria, both translational and post-translational controls, and prion-like polymerization have increasingly clear roles in regulating NLRP3 activation.	Calcium	76-83	NLR family pyrin domain containing 3	Homo sapiens	251-256
30218857-0	2018	Polydatin suppresses proliferation and metastasis of non-small cell lung cancer cells by inhibiting NLRP3 inflammasome activation via NF-kappaB pathway.	polydatin	0-9	NLR family pyrin domain containing 3	Homo sapiens	100-105
30544610-6	2018	Furthermore, cinnamaldehyde and 2-methoxy cinnamaldehyde diminished expressions of NLRP3 and pro-IL-1beta.	cinnamaldehyde	13-27	NLR family pyrin domain containing 3	Homo sapiens	83-88
30544610-6	2018	Furthermore, cinnamaldehyde and 2-methoxy cinnamaldehyde diminished expressions of NLRP3 and pro-IL-1beta.	2-methoxycinnamaldehyde	32-56	NLR family pyrin domain containing 3	Homo sapiens	83-88
30544610-8	2018	In conclusion, for cinnamaldehyde-related compounds to suppress NLRP3 inflammasome-mediated IL-1beta secretion, the propenal group of the side chain was essential, while the substituted group of the aromatic ring played a modifying role.	cinnamaldehyde	19-33	NLR family pyrin domain containing 3	Homo sapiens	64-69
30218857-11	2018	The anti-tumor effect of polydatin was possibly related to the inhibition of NLRP3 inflammation via the NF-kappaB pathway.	polydatin	25-34	NLR family pyrin domain containing 3	Homo sapiens	77-82
30218857-7	2018	In addition, polydatin suppressed the expression of NLRP3, ASC and pro-caspase-1in NSCLC cells.	polydatin	13-22	NLR family pyrin domain containing 3	Homo sapiens	52-57
30218857-8	2018	Activation of NLRP3 inflammasome counteracted the inhibitory effect of polydatin on proliferation and migration of NSCLC cells, suggesting that polydatin suppressed progression of NSCLC through inhibiting NLRP3 inflammasome activation.	polydatin	71-80	NLR family pyrin domain containing 3	Homo sapiens	14-19
30218857-8	2018	Activation of NLRP3 inflammasome counteracted the inhibitory effect of polydatin on proliferation and migration of NSCLC cells, suggesting that polydatin suppressed progression of NSCLC through inhibiting NLRP3 inflammasome activation.	polydatin	71-80	NLR family pyrin domain containing 3	Homo sapiens	205-210
30218857-8	2018	Activation of NLRP3 inflammasome counteracted the inhibitory effect of polydatin on proliferation and migration of NSCLC cells, suggesting that polydatin suppressed progression of NSCLC through inhibiting NLRP3 inflammasome activation.	polydatin	144-153	NLR family pyrin domain containing 3	Homo sapiens	14-19
30218857-8	2018	Activation of NLRP3 inflammasome counteracted the inhibitory effect of polydatin on proliferation and migration of NSCLC cells, suggesting that polydatin suppressed progression of NSCLC through inhibiting NLRP3 inflammasome activation.	polydatin	144-153	NLR family pyrin domain containing 3	Homo sapiens	205-210
30427314-12	2018	RESULTS: Compared with titanium particles with adherent bacterial debris, endotoxin-free titanium particles induced 86% less NLRP3 mRNA (0.05 +- 0.03 versus 0.35 +- 0.01 NLRP3/GAPDH, p &lt; 0.001) and 91% less IL1beta mRNA (0.02 +- 0.01 versus 0.22 +- 0.03 IL1beta/GAPDH, p &lt; 0.001).	Titanium	89-97	NLR family pyrin domain containing 3	Homo sapiens	125-130
30236770-9	2018	The inhibition of ROS production decreased NLRP3 inflammasome activation and IL-1beta production in CD4 T cells, leading to the suppression of Th17 differentiation.	ros	18-21	NLR family pyrin domain containing 3	Homo sapiens	43-48
30427314-12	2018	RESULTS: Compared with titanium particles with adherent bacterial debris, endotoxin-free titanium particles induced 86% less NLRP3 mRNA (0.05 +- 0.03 versus 0.35 +- 0.01 NLRP3/GAPDH, p &lt; 0.001) and 91% less IL1beta mRNA (0.02 +- 0.01 versus 0.22 +- 0.03 IL1beta/GAPDH, p &lt; 0.001).	Titanium	89-97	NLR family pyrin domain containing 3	Homo sapiens	170-175
30427314-22	2018	In contrast, activation of the NLRP3 inflammasome by titanium particles is not dependent on adherent PAMPs.	Titanium	53-61	NLR family pyrin domain containing 3	Homo sapiens	31-36
30323145-8	2018	We found that H2O2 treatment activated NLRP3 inflammasomes and decreased phosphorylation of signal transduction and STAT3 serine 727.	Hydrogen Peroxide	14-18	NLR family pyrin domain containing 3	Homo sapiens	39-44
30003820-8	2018	In contrast, supplementation with CoQ10 significantly recovered mitochondrial function and concurrently decreased the generation of reactive oxygen species and lipid peroxides, inhibited the accumulation of lipid droplets and the formation of the NOD-like receptor family pyrin domain-containing three (NLRP3) inflammasome, and reduced interleukin-1beta release and cell death.	coenzyme Q10	34-39	NLR family pyrin domain containing 3	Homo sapiens	303-308
30320338-10	2018	Although NLR family pyrin domain containing 3 (NLRP3)-inflammasome-caspase-1 activation is required for the maturation of IL-1beta, and DHMEQ reduced the NLRP3 mRNA expression and caspase-1 activity; a caspase-1 inhibitor did not influence the A50-induced IL-1beta production.	dehydroxymethylepoxyquinomicin	136-141	NLR family pyrin domain containing 3	Homo sapiens	47-52
30320338-10	2018	Although NLR family pyrin domain containing 3 (NLRP3)-inflammasome-caspase-1 activation is required for the maturation of IL-1beta, and DHMEQ reduced the NLRP3 mRNA expression and caspase-1 activity; a caspase-1 inhibitor did not influence the A50-induced IL-1beta production.	dehydroxymethylepoxyquinomicin	136-141	NLR family pyrin domain containing 3	Homo sapiens	154-159
30487600-0	2018	PtdIns4P on dispersed trans-Golgi network mediates NLRP3 inflammasome activation.	phosphatidylinositol 4-phosphate	0-8	NLR family pyrin domain containing 3	Homo sapiens	51-56
30323145-8	2018	We found that H2O2 treatment activated NLRP3 inflammasomes and decreased phosphorylation of signal transduction and STAT3 serine 727.	Serine	122-128	NLR family pyrin domain containing 3	Homo sapiens	39-44
30487600-4	2018	NLRP3 is recruited to the dispersed TGN (dTGN) through ionic bonding between its conserved polybasic region and negatively charged phosphatidylinositol-4-phosphate (PtdIns4P) on the dTGN.	phosphatidylinositol 4-phosphate	131-163	NLR family pyrin domain containing 3	Homo sapiens	0-5
30487600-4	2018	NLRP3 is recruited to the dispersed TGN (dTGN) through ionic bonding between its conserved polybasic region and negatively charged phosphatidylinositol-4-phosphate (PtdIns4P) on the dTGN.	phosphatidylinositol 4-phosphate	165-173	NLR family pyrin domain containing 3	Homo sapiens	0-5
30323145-9	2018	BAPTA-AM pretreatment abolished the H2O2-induced activation of NLRP3 inflammasomes, caspase-1 expression, interleukin-1beta expression and apoptosis in SHSY5Y cells, and had no effect in cells with downregulated STAT3 expression by RNAi.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	0-8	NLR family pyrin domain containing 3	Homo sapiens	63-68
30487600-6	2018	Disruption of the interaction between NLRP3 and PtdIns4P on the dTGN blocked NLRP3 aggregation and downstream signalling.	phosphatidylinositol 4-phosphate	48-56	NLR family pyrin domain containing 3	Homo sapiens	77-82
30323145-9	2018	BAPTA-AM pretreatment abolished the H2O2-induced activation of NLRP3 inflammasomes, caspase-1 expression, interleukin-1beta expression and apoptosis in SHSY5Y cells, and had no effect in cells with downregulated STAT3 expression by RNAi.	Hydrogen Peroxide	36-40	NLR family pyrin domain containing 3	Homo sapiens	63-68
30281174-0	2018	Licochalcone A attenuates acne symptoms mediated by suppression of NLRP3 inflammasome.	licochalcone A	0-14	NLR family pyrin domain containing 3	Homo sapiens	67-72
30513737-9	2018	Moreover, this strong reduction of pro-inflammatory IL-1beta is associated with a decrease of NLRP3 and, in J774A, ASC protein expression, which depends on the choice of activator ATP or nigericin.	Adenosine Triphosphate	180-183	NLR family pyrin domain containing 3	Homo sapiens	94-99
30513737-9	2018	Moreover, this strong reduction of pro-inflammatory IL-1beta is associated with a decrease of NLRP3 and, in J774A, ASC protein expression, which depends on the choice of activator ATP or nigericin.	Nigericin	187-196	NLR family pyrin domain containing 3	Homo sapiens	94-99
30281174-3	2018	We found that licochalcone A, a chalconoid isolated from the root of Glycyrrhiza inflate, was an effective inhibitor for P. acnes-induced NLRP3 inflammasome activation.	licochalcone A	14-28	NLR family pyrin domain containing 3	Homo sapiens	138-143
30281174-3	2018	We found that licochalcone A, a chalconoid isolated from the root of Glycyrrhiza inflate, was an effective inhibitor for P. acnes-induced NLRP3 inflammasome activation.	Chalcones	32-42	NLR family pyrin domain containing 3	Homo sapiens	138-143
30281174-4	2018	Licochalcone A blocked P. acnes-induced production of caspase-1(p10) and IL-1beta in primary mouse macrophages and human SZ95 sebocytes, indicating the suppression of NLRP3 inflammasome.	licochalcone	0-12	NLR family pyrin domain containing 3	Homo sapiens	167-172
30281174-8	2018	This study demonstrated that licochalcone A is effective in the control of P. acnes-induced skin inflammation as an efficient inhibitor for NLRP3 inflammasome.	licochalcone A	29-43	NLR family pyrin domain containing 3	Homo sapiens	140-145
30515160-3	2018	For IL-1beta production, betaine affects canonical and non-canonical inflammasome-mediated processing of IL-1beta through signaling pathways, such as NF-kappaB, NLRP3 and caspase-8/11.	Betaine	25-32	NLR family pyrin domain containing 3	Homo sapiens	161-166
30486377-0	2018	Pterostilbene Attenuates Hexavalent Chromium-Induced Allergic Contact Dermatitis by Preventing Cell Apoptosis and Inhibiting IL-1beta-Related NLRP3 Inflammasome Activation.	pterostilbene	0-13	NLR family pyrin domain containing 3	Homo sapiens	142-147
30486377-11	2018	Furthermore, our current findings demonstrated that the NLRP3 inflammasome could be involved in the Cr(VI)-mediated inflammation and apoptosis of ACD.	chromium hexavalent ion	100-106	NLR family pyrin domain containing 3	Homo sapiens	56-61
30415294-2	2018	Extracellular ATP is a danger signal which is known to activate the NLRP3 inflammasome in various cell systems.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	68-73
30415294-7	2018	Cell culture in 0.2% O2 induced expression of NLRP3 and pro-IL-1beta genes but not of the pro-IL-18 gene.	Oxygen	21-23	NLR family pyrin domain containing 3	Homo sapiens	46-51
30205151-0	2018	Acrolein induces NLRP3 inflammasome-mediated pyroptosis and suppresses migration via ROS-dependent autophagy in vascular endothelial cells.	Acrolein	0-8	NLR family pyrin domain containing 3	Homo sapiens	17-22
30205151-4	2018	In addition, exposure to acrolein resulted in NLRP3 inflammasome activation as evidenced by cleavage of caspase-1 and downstream mature interleukin (IL)-1beta and IL-18 secretion.	Acrolein	25-33	NLR family pyrin domain containing 3	Homo sapiens	46-51
30205151-5	2018	Knockdown of NLRP3 by small interfering RNA remarkably suppressed acrolein-induced pyroptosis and increased cell migration.	Acrolein	66-74	NLR family pyrin domain containing 3	Homo sapiens	13-18
30205151-6	2018	Moreover, the scavenging ROS relieved the autophagy, NLRP3 inflammasome activation and pyroptosis.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	53-58
30205151-8	2018	In our study, 3-methyladenine (3-MA), an autophagy inhibitor, aggravated NLRP3 inflammasome activation, pyroptosis and decreased cell migration, rapamycin (Rapa), an autophagy inducer, alleviated aforementioned phenomenon under acrolein stress.	3-methyladenine	14-29	NLR family pyrin domain containing 3	Homo sapiens	73-78
30205151-8	2018	In our study, 3-methyladenine (3-MA), an autophagy inhibitor, aggravated NLRP3 inflammasome activation, pyroptosis and decreased cell migration, rapamycin (Rapa), an autophagy inducer, alleviated aforementioned phenomenon under acrolein stress.	3-methyladenine	31-35	NLR family pyrin domain containing 3	Homo sapiens	73-78
30205151-9	2018	Besides, we found damaged mitochondrion accentuated NLRP3 inflammasome and pyroptosis in acrolein-treated cells.	Acrolein	89-97	NLR family pyrin domain containing 3	Homo sapiens	52-57
30555323-11	2018	In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1beta production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation.	Nigericin	40-49	NLR family pyrin domain containing 3	Homo sapiens	72-77
30555323-11	2018	In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1beta production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation.	Rifaximin	93-102	NLR family pyrin domain containing 3	Homo sapiens	72-77
30485804-3	2018	Furthermore, BAX/BAK signaling induces a parallel pathway to NLRP3 inflammasome-mediated caspase-1-dependent IL-1beta maturation that requires potassium efflux.	Potassium	143-152	NLR family pyrin domain containing 3	Homo sapiens	61-66
30366764-0	2018	Cholesterol Homeostatic Regulator SCAP-SREBP2 Integrates NLRP3 Inflammasome Activation and Cholesterol Biosynthetic Signaling in Macrophages.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	57-62
30366764-2	2018	Here, we have shown that NLRP3 inflammasome activation is integrated with the maturation of cholesterol master transcription factor SREBP2.	Cholesterol	92-103	NLR family pyrin domain containing 3	Homo sapiens	25-30
30450301-9	2018	Moreover, ligation of GPR91 with succinate promoted the lipopolysaccharide-induced production of NLRP3, IL-1beta, VEGF and MMP-13 in PBMCs through increased phosphorylation of p65.	Succinic Acid	33-42	NLR family pyrin domain containing 3	Homo sapiens	97-102
30422993-0	2018	Delayed oseltamivir plus sirolimus treatment attenuates H1N1 virus-induced severe lung injury correlated with repressed NLRP3 inflammasome activation and inflammatory cell infiltration.	Oseltamivir	8-19	NLR family pyrin domain containing 3	Homo sapiens	120-125
30092543-4	2018	PM2.5 was found capable of causing weak cell death but potent IL-1beta secretion in THP-1 cells, which was involved in NLRP3 inflammasome activation as evidenced by Z-YVAD-FMK inhibited IL-1beta secretion and overexpressed ASC and NLRP3 protein in PM2.5 treated cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	165-175	NLR family pyrin domain containing 3	Homo sapiens	119-124
30092543-4	2018	PM2.5 was found capable of causing weak cell death but potent IL-1beta secretion in THP-1 cells, which was involved in NLRP3 inflammasome activation as evidenced by Z-YVAD-FMK inhibited IL-1beta secretion and overexpressed ASC and NLRP3 protein in PM2.5 treated cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	165-175	NLR family pyrin domain containing 3	Homo sapiens	231-236
30422993-0	2018	Delayed oseltamivir plus sirolimus treatment attenuates H1N1 virus-induced severe lung injury correlated with repressed NLRP3 inflammasome activation and inflammatory cell infiltration.	Sirolimus	25-34	NLR family pyrin domain containing 3	Homo sapiens	120-125
30422993-7	2018	It was noted that decreased NLRP3 inflammasome activation was associated with inhibited nuclear factor (NF)-kappaB activation, reduced reactive oxygen species production and increased autophagy.	Reactive Oxygen Species	135-158	NLR family pyrin domain containing 3	Homo sapiens	28-33
30422993-10	2018	These results demonstrated that combined treatment with sirolimus and oseltamivir attenuates pH1N1-induced severe lung injury, which is correlated with suppressed mTOR-NLRP3-IL-1beta axis and reduced viral titer.	Sirolimus	56-65	NLR family pyrin domain containing 3	Homo sapiens	168-173
30422993-10	2018	These results demonstrated that combined treatment with sirolimus and oseltamivir attenuates pH1N1-induced severe lung injury, which is correlated with suppressed mTOR-NLRP3-IL-1beta axis and reduced viral titer.	Oseltamivir	70-81	NLR family pyrin domain containing 3	Homo sapiens	168-173
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	3-Hydroxybutyric Acid	0-20	NLR family pyrin domain containing 3	Homo sapiens	129-172
30459926-5	2018	Although reactive oxygen species from mitochondria have been reported to be involved in the activation of the NLRP3 inflammasome in microglial cells upon the deposition of Abeta, whether Abeta directly or indirectly activates the NLRP3 inflammasome remains unclear.	Reactive Oxygen Species	9-32	NLR family pyrin domain containing 3	Homo sapiens	110-115
30404007-0	2018	Shiga Toxin/Lipopolysaccharide Activates Caspase-4 and Gasdermin D to Trigger Mitochondrial Reactive Oxygen Species Upstream of the NLRP3 Inflammasome.	Reactive Oxygen Species	92-115	NLR family pyrin domain containing 3	Homo sapiens	132-137
30404007-6	2018	Together, these data show that Stx2/LPS complex activates the non-canonical inflammasome and mitochondrial ROS upstream of the NLRP3 inflammasome to promote cytokine maturation and pyroptosis.	Reactive Oxygen Species	107-110	NLR family pyrin domain containing 3	Homo sapiens	127-132
30099341-5	2018	Additionally, leucodin suppressed P2x7R, TLR4 and NLRP3 expression in LPS/ATP-stimulated macrophages.	Adenosine Triphosphate	74-77	NLR family pyrin domain containing 3	Homo sapiens	50-55
30218403-8	2018	Our results suggested that BHB inhibits the activation of NLRP3 inflammasome in C6 glioma cells and consequently suppressed the C6 cell migration.	3-Hydroxybutyric Acid	27-30	NLR family pyrin domain containing 3	Homo sapiens	58-63
30218403-9	2018	These findings also implicated that by inhibiting NLRP3 inflammasome, BHB reduced the inflammatory microenvironment which provided ancillary therapeutic benefits for the intervention of glioma.	3-Hydroxybutyric Acid	70-73	NLR family pyrin domain containing 3	Homo sapiens	50-55
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	3-Hydroxybutyric Acid	0-20	NLR family pyrin domain containing 3	Homo sapiens	174-179
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	3-Hydroxybutyric Acid	22-25	NLR family pyrin domain containing 3	Homo sapiens	129-172
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	3-Hydroxybutyric Acid	22-25	NLR family pyrin domain containing 3	Homo sapiens	174-179
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	Ketones	32-38	NLR family pyrin domain containing 3	Homo sapiens	129-172
30218403-2	2018	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.	Ketones	32-38	NLR family pyrin domain containing 3	Homo sapiens	174-179
30218403-4	2018	Our results indicated that administration of BHB suppressed C6 cells migration and NLRP3 inflammasome activation, reducing the levels of activated cysteinyl aspartate-specific proteinase 1 (caspase-1) and mature Interleukin 1beta (IL-1beta).	3-Hydroxybutyric Acid	45-48	NLR family pyrin domain containing 3	Homo sapiens	83-88
30218403-5	2018	Fully activation of NLRP3 inflammasome was induced by lipopolysaccharide (LPS) prime plus adenosine triphosphate (ATP) stimulation in C6 cells, which promoted in vitro migration of C6 cell.	Adenosine Triphosphate	90-112	NLR family pyrin domain containing 3	Homo sapiens	20-25
30138619-9	2018	Treatment of cultured PBMCs with 10 ng of lipopolysaccharide induced NLRP3, caspase-1, ASC, IL-1beta, IL-17A, and IL-23 expression, which was marked suppressed by treatment with ascorbic acid.	Ascorbic Acid	178-191	NLR family pyrin domain containing 3	Homo sapiens	69-74
30218403-5	2018	Fully activation of NLRP3 inflammasome was induced by lipopolysaccharide (LPS) prime plus adenosine triphosphate (ATP) stimulation in C6 cells, which promoted in vitro migration of C6 cell.	Adenosine Triphosphate	114-117	NLR family pyrin domain containing 3	Homo sapiens	20-25
29764192-4	2018	Cholesterol crystal-induced NLRP3 inflammasome activation was used to trigger maturation and release of IL-1beta in PBMCs.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	28-33
29105345-0	2018	Estradiol inhibits NLRP3 inflammasome in fibroblast-like synoviocytes activated by lipopolysaccharide and adenosine triphosphate.	Estradiol	0-9	NLR family pyrin domain containing 3	Homo sapiens	19-24
29105345-0	2018	Estradiol inhibits NLRP3 inflammasome in fibroblast-like synoviocytes activated by lipopolysaccharide and adenosine triphosphate.	Adenosine Triphosphate	106-128	NLR family pyrin domain containing 3	Homo sapiens	19-24
29105345-2	2018	This study was performed to identify whether NLRP3 inflammasome can be triggered by lipopolysaccharides (LPS) and adenosine triphos adenine (ATP), which are positively related with knee OA severity in joint-spaces, in human fibroblast-like synoviocytes (FLS), and to identify whether estrogen would inhibit the activation of NLRP3 inflammasome.	adenosine triphos adenine	114-139	NLR family pyrin domain containing 3	Homo sapiens	45-50
29105345-2	2018	This study was performed to identify whether NLRP3 inflammasome can be triggered by lipopolysaccharides (LPS) and adenosine triphos adenine (ATP), which are positively related with knee OA severity in joint-spaces, in human fibroblast-like synoviocytes (FLS), and to identify whether estrogen would inhibit the activation of NLRP3 inflammasome.	adenosine triphos adenine	114-139	NLR family pyrin domain containing 3	Homo sapiens	325-330
29105345-2	2018	This study was performed to identify whether NLRP3 inflammasome can be triggered by lipopolysaccharides (LPS) and adenosine triphos adenine (ATP), which are positively related with knee OA severity in joint-spaces, in human fibroblast-like synoviocytes (FLS), and to identify whether estrogen would inhibit the activation of NLRP3 inflammasome.	Adenosine Triphosphate	141-144	NLR family pyrin domain containing 3	Homo sapiens	45-50
29105345-2	2018	This study was performed to identify whether NLRP3 inflammasome can be triggered by lipopolysaccharides (LPS) and adenosine triphos adenine (ATP), which are positively related with knee OA severity in joint-spaces, in human fibroblast-like synoviocytes (FLS), and to identify whether estrogen would inhibit the activation of NLRP3 inflammasome.	Adenosine Triphosphate	141-144	NLR family pyrin domain containing 3	Homo sapiens	325-330
29105345-7	2018	RESULTS: Our results demonstrated that treatment with LPS and ATP increased significantly both in mRNA and protein levels of all the NLRP3 inflammasome components, and triggered the NLRP3 inflammasome, followed by upregulated IL-1beta and IL-18 in the cell supernatant.	Adenosine Triphosphate	62-65	NLR family pyrin domain containing 3	Homo sapiens	133-138
29105345-7	2018	RESULTS: Our results demonstrated that treatment with LPS and ATP increased significantly both in mRNA and protein levels of all the NLRP3 inflammasome components, and triggered the NLRP3 inflammasome, followed by upregulated IL-1beta and IL-18 in the cell supernatant.	Adenosine Triphosphate	62-65	NLR family pyrin domain containing 3	Homo sapiens	182-187
29105345-9	2018	CONCLUSION: These results suggested the increased LPS and ATP in joint-space may promote knee OA by NLRP3 inflammasome and E2 may exert a protective effect by inhibiting the activation of NLRP3 inflammasome in FLS.	Adenosine Triphosphate	58-61	NLR family pyrin domain containing 3	Homo sapiens	100-105
29105345-9	2018	CONCLUSION: These results suggested the increased LPS and ATP in joint-space may promote knee OA by NLRP3 inflammasome and E2 may exert a protective effect by inhibiting the activation of NLRP3 inflammasome in FLS.	Adenosine Triphosphate	58-61	NLR family pyrin domain containing 3	Homo sapiens	188-193
30295793-3	2018	The nucleotide-binding domain, leucine-rich repeats-containing family, pyrin domain-containing-3 (NLRP3) inflammasome complex, comprising NLRP3, apoptotic speck protein containing a caspase recruitment domain (ASC), and cysteine aspartic acid protease 1 (Caspase 1), regulates microglial inflammation in several neurodegenerative diseases.	Leucine	31-38	NLR family pyrin domain containing 3	Homo sapiens	98-103
30356764-10	2018	Results: In vitro, IL-1beta production induced by m- and t-CPPD and m-CPPTbeta crystals was NLRP3 inflammasome dependent.	m-cpptbeta	68-78	NLR family pyrin domain containing 3	Homo sapiens	92-97
30301855-9	2018	Because NLRP3-dependent production of IL-1beta and nitric oxide (NO) in Toxoplasma-infected human cells is involved in the GRA15-dependent virulence mechanism, blocking NO or IL-1beta production in the host could represent a novel therapeutic approach for treating human toxoplasmosis.	Nitric Oxide	51-63	NLR family pyrin domain containing 3	Homo sapiens	8-13
30305631-3	2018	Here we show, using CTLs from patients with CD46 deficiency or with constitutively-active NLRP3, that CD46 delivers co-stimulatory signals for optimal CTL activity by augmenting nutrient-influx and fatty acid synthesis.	Fatty Acids	198-208	NLR family pyrin domain containing 3	Homo sapiens	90-95
30232264-0	2018	Chloride regulates dynamic NLRP3-dependent ASC oligomerization and inflammasome priming.	Chlorides	0-8	NLR family pyrin domain containing 3	Homo sapiens	27-32
30349539-6	2018	Several kinases and phosphatases have been shown to control NLRP3 inflammasome activation in response to either exogenous pathogen infections or endogenous molecules, such as bile acids.	Bile Acids and Salts	175-185	NLR family pyrin domain containing 3	Homo sapiens	60-65
29951874-6	2018	The maturation of IL-1beta, induced by H2O2, depends on the activation of the NLRP3 inflammasome.	Hydrogen Peroxide	39-43	NLR family pyrin domain containing 3	Homo sapiens	78-83
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glycyrrhizic Acid	27-39	NLR family pyrin domain containing 3	Homo sapiens	95-100
30119194-13	2018	The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells.	Glucose	117-124	NLR family pyrin domain containing 3	Homo sapiens	95-100
30119194-14	2018	In summary, the results suggested that FMN exhibited the protective effect on STZ-induced cognitive impairment possibly via the mediation of HMGB1/TLR4/NF-kappaB signaling and NLRP3 inflammasome.	Streptozocin	78-81	NLR family pyrin domain containing 3	Homo sapiens	176-181
29951874-7	2018	Cyclic stretching enhances the maturation of IL-1beta via promoting H2O2-induced NLRP3 inflammasome activation in tenocytes.	Hydrogen Peroxide	68-72	NLR family pyrin domain containing 3	Homo sapiens	81-86
30270565-2	2018	Our results show that the mRNA levels of IL-1beta, IL-18, NLRP3, ASC, and caspase-1 in the DSS+ZEA-treated group are lower than those in either the DSS or ZEA group, and the protein expression trends are similar.	Dextran Sulfate	91-94	NLR family pyrin domain containing 3	Homo sapiens	58-63
30270565-2	2018	Our results show that the mRNA levels of IL-1beta, IL-18, NLRP3, ASC, and caspase-1 in the DSS+ZEA-treated group are lower than those in either the DSS or ZEA group, and the protein expression trends are similar.	Zearalenone	95-98	NLR family pyrin domain containing 3	Homo sapiens	58-63
30249062-9	2018	Results showed that treating with methotrexate could alleviate the inflammatory condition, downregulate the activation of NF-kappaB and NLRP3/Caspase-1 inflammatory pathways and reduce the level of related cytokines.	Methotrexate	34-46	NLR family pyrin domain containing 3	Homo sapiens	136-141
30307163-2	2018	In this study, we explored the role of NLRP3 inflammasome on high glucose (HG) or transforming growth factor-B1 (TGFB1)-induced EMT in HK-2 cells.	Glucose	66-73	NLR family pyrin domain containing 3	Homo sapiens	39-44
30307163-6	2018	We found that NLRP3 interference could inhibit HG-induced ROS.	Reactive Oxygen Species	58-61	NLR family pyrin domain containing 3	Homo sapiens	14-19
30307163-9	2018	Besides, TGFB1 induced the activation of NLRP3 inflammasome and the generation of ROS, which were blocked by NLRP3 interference or NAC.	Reactive Oxygen Species	82-85	NLR family pyrin domain containing 3	Homo sapiens	109-114
30307163-9	2018	Besides, TGFB1 induced the activation of NLRP3 inflammasome and the generation of ROS, which were blocked by NLRP3 interference or NAC.	Acetylcysteine	131-134	NLR family pyrin domain containing 3	Homo sapiens	41-46
30307163-11	2018	These results indicated that knockdown of NLRP3 antagonized HG-induced EMT by inhibiting ROS production, phosphorylation of SMAD3, P38MAPK and ERK1/2, highlighting NLRP3 as a potential therapy target for diabetic nephropathy.	Reactive Oxygen Species	89-92	NLR family pyrin domain containing 3	Homo sapiens	42-47
30527115-12	2018	Treatment with Glybenclamide at 200 muM was used to prevent NLRP3 inflammasome activation.	Glyburide	15-28	NLR family pyrin domain containing 3	Homo sapiens	60-65
30054450-0	2018	Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation.	Cholesterol	15-26	NLR family pyrin domain containing 3	Homo sapiens	53-58
30054450-4	2018	By using pharmacological and genetic approaches targeting NPC1, we reveal that blockade of cholesterol trafficking through the late endosome-lysosome pathway blunts NLRP3 inflammasome activation.	Cholesterol	91-102	NLR family pyrin domain containing 3	Homo sapiens	165-170
30054450-6	2018	However, the inability to activate the NLRP3 inflammasome was traced to perturbed cholesterol trafficking to the ER but not the PM.	Cholesterol	82-93	NLR family pyrin domain containing 3	Homo sapiens	39-44
30054450-7	2018	Accordingly, acute cholesterol depletion in the ER membranes by statins abrogated casp-1 activation and IL-1beta secretion and ablated NLRP3 inflammasome assembly.	Cholesterol	19-30	NLR family pyrin domain containing 3	Homo sapiens	135-140
30054450-9	2018	Together, this study reveals ER sterol levels as a metabolic rheostat for the activation of the NLRP3 inflammasome.	Sterols	32-38	NLR family pyrin domain containing 3	Homo sapiens	96-101
30307163-0	2018	Knockdown of NLRP3 alleviates high glucose or TGFB1-induced EMT in human renal tubular cells Tubular injury is one of the crucial determinants of progressive renal failure in diabetic nephropathy (DN), while epithelial-to-mesenchymal transition (EMT) of tubular cells contributes to the accumulation of matrix protein in the diabetic kidney.	Glucose	35-42	NLR family pyrin domain containing 3	Homo sapiens	13-18
30249062-12	2018	These findings indicated that methotrexate could inhibit the onset of inflammation in joint tissue by suppressing the activation of NF-kappaB and NLRP3/Caspase-1 pathways and regulating the inflammation related metabolic networks.	Methotrexate	30-42	NLR family pyrin domain containing 3	Homo sapiens	146-151
30237538-6	2018	In HepG2 cells, we found that As2O3-induced pyroptotic cell death was dependent upon the activation of NLRP3 inflammasome, which was CTSB-dependent.	Arsenic Trioxide	30-35	NLR family pyrin domain containing 3	Homo sapiens	103-108
30237538-7	2018	In addition, inhibiting autophagy alleviated the As2O3-induced increase of cytosolic CTSB expression and subsequent release of LDH, activation of the NLRP3 inflammasome, and pyroptosis.	Arsenic Trioxide	49-54	NLR family pyrin domain containing 3	Homo sapiens	150-155
30237538-8	2018	Moreover, we found that Tau alleviated As2O3-induced elevation of autophagy, CTSB expression, and activation of the NLRP3 inflammasome, and reduced the release of LDH, pyroptotic cell death, and inflammation.	Arsenic Trioxide	39-44	NLR family pyrin domain containing 3	Homo sapiens	116-121
30237538-11	2018	These results demonstrated that As2O3-induced pyroptosis involves autophagy, CTSB, and the NLRP3 inflammasome cascade, and that Tau alleviates As2O3-induced liver inflammation by inhibiting the autophagic-CTSB-NLRP3 inflammasomal pathway rather than decreasing lipid accumulation.	Arsenic Trioxide	32-37	NLR family pyrin domain containing 3	Homo sapiens	91-96
30237538-11	2018	These results demonstrated that As2O3-induced pyroptosis involves autophagy, CTSB, and the NLRP3 inflammasome cascade, and that Tau alleviates As2O3-induced liver inflammation by inhibiting the autophagic-CTSB-NLRP3 inflammasomal pathway rather than decreasing lipid accumulation.	Arsenic Trioxide	32-37	NLR family pyrin domain containing 3	Homo sapiens	210-215
30217191-0	2018	NLRP3 inflammasome-dependent pyroptosis is proposed to be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment.	Isoflurane	101-111	NLR family pyrin domain containing 3	Homo sapiens	0-5
29960001-0	2018	Flavonoids interfere with NLRP3 inflammasome activation.	Flavonoids	0-10	NLR family pyrin domain containing 3	Homo sapiens	26-31
29960001-3	2018	To elucidate the effects on NLRP3 inflammasome pathway and to determine the structure-activity relationships, NLRP3 inflammasome in differentiated THP-1 cells was activated via treatment with monosodium urate (MSU) crystals.	Uric Acid	192-208	NLR family pyrin domain containing 3	Homo sapiens	28-33
29960001-3	2018	To elucidate the effects on NLRP3 inflammasome pathway and to determine the structure-activity relationships, NLRP3 inflammasome in differentiated THP-1 cells was activated via treatment with monosodium urate (MSU) crystals.	Uric Acid	192-208	NLR family pyrin domain containing 3	Homo sapiens	110-115
29960001-3	2018	To elucidate the effects on NLRP3 inflammasome pathway and to determine the structure-activity relationships, NLRP3 inflammasome in differentiated THP-1 cells was activated via treatment with monosodium urate (MSU) crystals.	Uric Acid	210-213	NLR family pyrin domain containing 3	Homo sapiens	28-33
29960001-3	2018	To elucidate the effects on NLRP3 inflammasome pathway and to determine the structure-activity relationships, NLRP3 inflammasome in differentiated THP-1 cells was activated via treatment with monosodium urate (MSU) crystals.	Uric Acid	210-213	NLR family pyrin domain containing 3	Homo sapiens	110-115
29960001-10	2018	The present study, for the first time, demonstrated the structure-activity profiles of flavonoids in NLRP3 inflammasome activation and mechanisms of cellular action.	Flavonoids	87-97	NLR family pyrin domain containing 3	Homo sapiens	101-106
29960001-11	2018	Certain flavonoids including apigenin are expected to ameliorate the inflammatory symptoms in autoinflammatory diseases associated with NLRP3 inflammasome activation.	Flavonoids	8-18	NLR family pyrin domain containing 3	Homo sapiens	136-141
30126633-0	2018	Tannic acid inhibits NLRP3 inflammasome-mediated IL-1beta production via blocking NF-kappaB signaling in macrophages.	Tannins	0-11	NLR family pyrin domain containing 3	Homo sapiens	21-26
30126633-3	2018	Here, we reported that tannic acid inhibited NLRP3 inflammasome activation by blocking NF-kappaB signaling to suppress IL-1beta secretion.	Tannins	23-34	NLR family pyrin domain containing 3	Homo sapiens	45-50
30126633-4	2018	We found that the BMDMs (bone marrow-derived macrophages cells) pre-treated with tannic acid blocked caspase-1 cleavage and inhibited IL-1beta secretion in a NLRP3-dependent manner, and suppressed NF-kappaB signaling activation by inhibiting NF-kappaB/P65 nuclear localization, suggesting that tannic acid inhibited NLRP3 inflammasome activation.	Tannins	81-92	NLR family pyrin domain containing 3	Homo sapiens	158-163
30126633-4	2018	We found that the BMDMs (bone marrow-derived macrophages cells) pre-treated with tannic acid blocked caspase-1 cleavage and inhibited IL-1beta secretion in a NLRP3-dependent manner, and suppressed NF-kappaB signaling activation by inhibiting NF-kappaB/P65 nuclear localization, suggesting that tannic acid inhibited NLRP3 inflammasome activation.	Tannins	81-92	NLR family pyrin domain containing 3	Homo sapiens	316-321
30126633-5	2018	These investigations revealed that tannic acid inhibited NLRP3 inflammasome activation via blocking NF-kappaB signaling in macrophages, providing us with evidence that tannic acid may be a potent inhibitor for NLRP3-driven diseases.	Tannins	35-46	NLR family pyrin domain containing 3	Homo sapiens	57-62
30126633-5	2018	These investigations revealed that tannic acid inhibited NLRP3 inflammasome activation via blocking NF-kappaB signaling in macrophages, providing us with evidence that tannic acid may be a potent inhibitor for NLRP3-driven diseases.	Tannins	35-46	NLR family pyrin domain containing 3	Homo sapiens	210-215
30126633-5	2018	These investigations revealed that tannic acid inhibited NLRP3 inflammasome activation via blocking NF-kappaB signaling in macrophages, providing us with evidence that tannic acid may be a potent inhibitor for NLRP3-driven diseases.	Tannins	168-179	NLR family pyrin domain containing 3	Homo sapiens	57-62
30126633-5	2018	These investigations revealed that tannic acid inhibited NLRP3 inflammasome activation via blocking NF-kappaB signaling in macrophages, providing us with evidence that tannic acid may be a potent inhibitor for NLRP3-driven diseases.	Tannins	168-179	NLR family pyrin domain containing 3	Homo sapiens	210-215
30217146-8	2018	Moreover, the process of NLRP3 inflammasome activation and IL-1beta production in macrophages in response to T. pallidum infection involves K+ efflux, mitochondrial ROS production and cathepsin release.	ros	165-168	NLR family pyrin domain containing 3	Homo sapiens	25-30
30217191-2	2018	recently published a paper, titled "Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment".	Isoflurane	94-104	NLR family pyrin domain containing 3	Homo sapiens	53-58
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	Isoflurane	112-122	NLR family pyrin domain containing 3	Homo sapiens	22-27
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	Isoflurane	112-122	NLR family pyrin domain containing 3	Homo sapiens	180-185
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	233-239	NLR family pyrin domain containing 3	Homo sapiens	22-27
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	233-239	NLR family pyrin domain containing 3	Homo sapiens	180-185
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	Isoflurane	269-279	NLR family pyrin domain containing 3	Homo sapiens	22-27
30217191-4	2018	Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.	Isoflurane	269-279	NLR family pyrin domain containing 3	Homo sapiens	180-185
29794149-6	2018	Using the direct NLRP3 inhibitor, CY-09, we demonstrated significantly reduced human platelet aggregation in response to threshold concentrations of collagen and ADP, as well as impaired clot retraction in CY-09-treated human platelets, supporting a role for NLRP3 also in regulating human platelet alphaIIbbeta3 outside-in signaling.	CY5.5 cyanine dye	34-39	NLR family pyrin domain containing 3	Homo sapiens	17-22
30297978-0	2018	Corrigendum to "Formononetin Administration Ameliorates Dextran Sulfate Sodium-Induced Acute Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway".	formononetin	16-28	NLR family pyrin domain containing 3	Homo sapiens	115-120
30297978-0	2018	Corrigendum to "Formononetin Administration Ameliorates Dextran Sulfate Sodium-Induced Acute Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway".	Dextran Sulfate	56-78	NLR family pyrin domain containing 3	Homo sapiens	115-120
30185776-7	2018	Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly.	Potassium	72-81	NLR family pyrin domain containing 3	Homo sapiens	105-110
29906464-0	2018	Inflammatory mediators ATP and S100A12 activate the NLRP3 inflammasome to induce MUC5AC production in airway epithelial cells.	Adenosine Triphosphate	23-26	NLR family pyrin domain containing 3	Homo sapiens	52-57
29906464-8	2018	NLRP3 siRNA or inhibitors of NF-kappaB, NLRP3 inflammasome oligomerization, or caspase-1 nearly completely inhibited ATP- and S100A12-mediated MUC5AC production.	Adenosine Triphosphate	117-120	NLR family pyrin domain containing 3	Homo sapiens	0-5
29906464-8	2018	NLRP3 siRNA or inhibitors of NF-kappaB, NLRP3 inflammasome oligomerization, or caspase-1 nearly completely inhibited ATP- and S100A12-mediated MUC5AC production.	Adenosine Triphosphate	117-120	NLR family pyrin domain containing 3	Homo sapiens	40-45
29906464-9	2018	Furthermore, S100A12-as well as ATP-mediated MUC5AC production was almost equally blunted by both nonspecific and specific antagonists of the purinergic receptor P2X7, a principal receptor mediating NLRP3 inflammasome activation by ATP.	Adenosine Triphosphate	32-35	NLR family pyrin domain containing 3	Homo sapiens	199-204
29976096-2	2018	Among the multiple mechanisms of inflammation, the arterial deposition of lipids and particularly of cholesterol crystals is the one responsible for the activation of inflammasome NLRP3, followed by the rise of circulating markers, mainly C-reactive protein (CRP).	Cholesterol	101-112	NLR family pyrin domain containing 3	Homo sapiens	180-185
29794149-6	2018	Using the direct NLRP3 inhibitor, CY-09, we demonstrated significantly reduced human platelet aggregation in response to threshold concentrations of collagen and ADP, as well as impaired clot retraction in CY-09-treated human platelets, supporting a role for NLRP3 also in regulating human platelet alphaIIbbeta3 outside-in signaling.	CY5.5 cyanine dye	34-39	NLR family pyrin domain containing 3	Homo sapiens	259-264
29794149-6	2018	Using the direct NLRP3 inhibitor, CY-09, we demonstrated significantly reduced human platelet aggregation in response to threshold concentrations of collagen and ADP, as well as impaired clot retraction in CY-09-treated human platelets, supporting a role for NLRP3 also in regulating human platelet alphaIIbbeta3 outside-in signaling.	Adenosine Diphosphate	162-165	NLR family pyrin domain containing 3	Homo sapiens	17-22
29794149-6	2018	Using the direct NLRP3 inhibitor, CY-09, we demonstrated significantly reduced human platelet aggregation in response to threshold concentrations of collagen and ADP, as well as impaired clot retraction in CY-09-treated human platelets, supporting a role for NLRP3 also in regulating human platelet alphaIIbbeta3 outside-in signaling.	CY5.5 cyanine dye	206-211	NLR family pyrin domain containing 3	Homo sapiens	17-22
30142638-0	2018	Prostaglandin E2 Activates NLRP3 Inflammasome in Endothelial Cells to Promote Diabetic Retinopathy.	Dinoprostone	0-16	NLR family pyrin domain containing 3	Homo sapiens	27-32
30159395-3	2018	NLRP3 has been shown to be activated by diverse stimuli including microbial toxins, ATP, particulate matter, etc.	Adenosine Triphosphate	84-87	NLR family pyrin domain containing 3	Homo sapiens	0-5
30142638-2	2018	Prostaglandin E2 (PGE2) and nucleotide-binding domain and Leucine-rich repeat Receptor containing a Pyrin domain 3 (NLRP3) inflammasomes have been long considered to be associated with PDR.	Dinoprostone	0-16	NLR family pyrin domain containing 3	Homo sapiens	116-121
30142638-9	2018	PGE2 upregulated the expression of NLRP3 inflammasome components and inflammatory chemokines.	Dinoprostone	0-4	NLR family pyrin domain containing 3	Homo sapiens	35-40
30142638-10	2018	Knockdown of NLRP3 attenuated the expression of NLRP3 inflammasome components and inhibited the effect of PGE2.	Dinoprostone	106-110	NLR family pyrin domain containing 3	Homo sapiens	13-18
29946988-3	2018	This study was undertaken to evaluate whether NLRP3 gene transcript variants are involved in the occurrence of PG.	pg	111-113	NLR family pyrin domain containing 3	Homo sapiens	46-51
29946988-10	2018	Here, we show that NLRP3-4 transcript variant may be closely related to the occurrence of PG.	pg	90-92	NLR family pyrin domain containing 3	Homo sapiens	19-24
29946988-11	2018	Thus, NLRP3-4 gene transcript variant may provide a novel target for the diagnosis and therapy of PG.	pg	98-100	NLR family pyrin domain containing 3	Homo sapiens	6-13
30021766-5	2018	However, steroid-naive mild asthmatics showed fasting-dependent blunting of the NLRP3 inflammasome.	Steroids	9-16	NLR family pyrin domain containing 3	Homo sapiens	80-85
30021766-7	2018	This pilot study shows that prolonged fasting blunts the NLRP3 inflammasome and Th2 cell activation in steroid-naive asthmatics as well as diminishes airway epithelial cell cytokine production.	Steroids	103-110	NLR family pyrin domain containing 3	Homo sapiens	57-62
30157949-0	2018	Tofacitinib inhibits granulocyte-macrophage colony-stimulating factor-induced NLRP3 inflammasome activation in human neutrophils.	tofacitinib	0-11	NLR family pyrin domain containing 3	Homo sapiens	78-83
30157949-11	2018	Although tofacitinib pretreatment marginally inhibited GM-CSF-induced pro-IL-1beta mRNA expression, tofacitinib completely abrogated NLRP3 protein expression in neutrophils.	tofacitinib	100-111	NLR family pyrin domain containing 3	Homo sapiens	133-138
29746940-4	2018	RESULTS: Our results demonstrated that the NLRP3 inflammasome activation and cytokines production by DCs are dependent on ROS generation, endosome acidification, and K+ efflux and involve the Pb recognition by dectin-1 and Syk phosphorylation.	Reactive Oxygen Species	122-125	NLR family pyrin domain containing 3	Homo sapiens	43-48
29993075-10	2018	In conclusion, quercetin can preserve the function of the liver in acute alcoholic injury by upregulating the expression of IL-10 and HO-1 and thus inhibiting NLRP3 inflammasome activation and inflammatory factor secretion.	Quercetin	15-24	NLR family pyrin domain containing 3	Homo sapiens	159-164
30126430-11	2018	In THP-1 cells, RIP3 and NLRP3 interaction was enhanced by LPS/ATP stimulation resulting in IL-1beta and IL-18 production.	Adenosine Triphosphate	63-66	NLR family pyrin domain containing 3	Homo sapiens	25-30
29993075-0	2018	Targeting heme oxygenase-1 by quercetin ameliorates alcohol-induced acute liver injury via inhibiting NLRP3 inflammasome activation.	Quercetin	30-39	NLR family pyrin domain containing 3	Homo sapiens	102-107
29993075-0	2018	Targeting heme oxygenase-1 by quercetin ameliorates alcohol-induced acute liver injury via inhibiting NLRP3 inflammasome activation.	Alcohols	52-59	NLR family pyrin domain containing 3	Homo sapiens	102-107
29993075-8	2018	The underlying mechanism of quercetin"s benefit on the liver may be explained by its anti-oxidant properties and inhibitory effect on the ROS/NF-kappaB/NLRP3 inflammasome/IL-1beta and IL-18 pathway by inducing HO-1.	Quercetin	28-37	NLR family pyrin domain containing 3	Homo sapiens	152-157
29993075-8	2018	The underlying mechanism of quercetin"s benefit on the liver may be explained by its anti-oxidant properties and inhibitory effect on the ROS/NF-kappaB/NLRP3 inflammasome/IL-1beta and IL-18 pathway by inducing HO-1.	ros	138-141	NLR family pyrin domain containing 3	Homo sapiens	152-157
30078841-6	2018	In particular, the S. mutans-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage.	Adenosine Triphosphate	72-94	NLR family pyrin domain containing 3	Homo sapiens	37-42
30078841-6	2018	In particular, the S. mutans-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage.	Adenosine Triphosphate	96-99	NLR family pyrin domain containing 3	Homo sapiens	37-42
30078841-6	2018	In particular, the S. mutans-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage.	Potassium	110-119	NLR family pyrin domain containing 3	Homo sapiens	37-42
29746940-4	2018	RESULTS: Our results demonstrated that the NLRP3 inflammasome activation and cytokines production by DCs are dependent on ROS generation, endosome acidification, and K+ efflux and involve the Pb recognition by dectin-1 and Syk phosphorylation.	Lead	192-194	NLR family pyrin domain containing 3	Homo sapiens	43-48
29957361-0	2018	Gamma-tocotrienol attenuates the aberrant lipid mediator production in NLRP3 inflammasome-stimulated macrophages.	plastochromanol 8	0-17	NLR family pyrin domain containing 3	Homo sapiens	71-76
29957361-1	2018	The activation of NLRP3 inflammasome in innate immune cells is associated with enhanced production of pro-inflammatory lipid mediator eicosanoids that play a crucial role in propagating inflammation.	Eicosanoids	134-145	NLR family pyrin domain containing 3	Homo sapiens	18-23
30069026-5	2018	Defective NLRP3 sumoylation, either by NLRP3 mutation of SUMO acceptor lysines or depletion of MAPL, results in enhanced caspase-1 activation and IL-1beta release.	Lysine	71-78	NLR family pyrin domain containing 3	Homo sapiens	10-15
29957361-2	2018	Gamma-tocotrienol (gammaT3) is an unsaturated vitamin E that has been demonstrated to attenuate NLRP3-inflammasome.	plastochromanol 8	0-17	NLR family pyrin domain containing 3	Homo sapiens	96-101
29957361-2	2018	Gamma-tocotrienol (gammaT3) is an unsaturated vitamin E that has been demonstrated to attenuate NLRP3-inflammasome.	gammat3	19-26	NLR family pyrin domain containing 3	Homo sapiens	96-101
29957361-2	2018	Gamma-tocotrienol (gammaT3) is an unsaturated vitamin E that has been demonstrated to attenuate NLRP3-inflammasome.	unsaturated vitamin e	34-55	NLR family pyrin domain containing 3	Homo sapiens	96-101
30065091-6	2018	Since the mammalian sterol cholesterol triggers NLRP3-mediated pyroptosis, we hypothesized that ergosterol may also do so.	Sterols	20-26	NLR family pyrin domain containing 3	Homo sapiens	48-53
29345311-6	2018	We assessed NLRP3 inflammasome priming and assembly after cinacalcet-induced CaSR activation and evaluated if this activation is mediated by downstream ERK1/2 signaling in LS14 preadipocytes.	Cinacalcet	58-68	NLR family pyrin domain containing 3	Homo sapiens	12-17
29345311-7	2018	Exposure to 2 muM cinacalcet elevated mRNA expression of NLRP3, CASP-1, and IL-1beta, as well as an increase in pro-IL-1beta protein.	Cinacalcet	18-28	NLR family pyrin domain containing 3	Homo sapiens	57-62
29345311-10	2018	Upstream ERK pathway inhibition decreased cinacalcet-dependent activation of NLRP3 inflammasome.	Cinacalcet	42-52	NLR family pyrin domain containing 3	Homo sapiens	77-82
30065091-6	2018	Since the mammalian sterol cholesterol triggers NLRP3-mediated pyroptosis, we hypothesized that ergosterol may also do so.	Cholesterol	27-38	NLR family pyrin domain containing 3	Homo sapiens	48-53
30065091-6	2018	Since the mammalian sterol cholesterol triggers NLRP3-mediated pyroptosis, we hypothesized that ergosterol may also do so.	Ergosterol	96-106	NLR family pyrin domain containing 3	Homo sapiens	48-53
30108544-8	2018	therefore, in this experimental model of TBI we evaluated whether the treatment with artesunate at the dose of 30 mg\Kg, had an efficacy in reducing the neuroinflammatory process after TBI injury, and in inhibiting the NLRP3 inflammasome pathway, which plays a key role in the inflammatory process.	Artesunate	85-95	NLR family pyrin domain containing 3	Homo sapiens	219-224
30108544-10	2018	our results show that artesunate was able to reduce the TBI-induced lesion, it also showed an anti-inflammatory action through the inhibition of Nf-kb, release of proinflammatory cytokines IL-1beta and TNF-alpha and through the inhibition NLRP3 inflammasome complex, furthermore was able to reduce the activation of astrocytes and microglia (GFAP, Iba-1).	Artesunate	22-32	NLR family pyrin domain containing 3	Homo sapiens	239-244
30101125-0	2018	Inhibiting the NLRP3 Inflammasome With Methylene Blue as Treatment Adjunct in Myelodysplasia.	Methylene Blue	39-53	NLR family pyrin domain containing 3	Homo sapiens	15-20
30101125-10	2018	If as in rodents, methylene blue also inhibits NLRP3 inflammasome function in human myelodysplasia a trial of adjunctive methylene blue treatment in transfusion dependent, low risk myelodysplasia where marrow inflammation and apoptosis predominates, would be worth trying.	Methylene Blue	18-32	NLR family pyrin domain containing 3	Homo sapiens	47-52
30101125-11	2018	HIGHLIGHTS - Cytogenetic abnormalities and innate immune activation are seen in myelodysplasia- The NLRP3 inflammasome is a core element generating marrow failure of myelodysplasia- In April 2018 methylene blue was reported to potently inhibit NLRP3 inflammasome function- Methylene blue has benign side effects and has been in human use for a century- Study of methylene blue treatment of myelodysplasia would be a low-risk intervention.	Methylene Blue	196-210	NLR family pyrin domain containing 3	Homo sapiens	100-105
30101125-11	2018	HIGHLIGHTS - Cytogenetic abnormalities and innate immune activation are seen in myelodysplasia- The NLRP3 inflammasome is a core element generating marrow failure of myelodysplasia- In April 2018 methylene blue was reported to potently inhibit NLRP3 inflammasome function- Methylene blue has benign side effects and has been in human use for a century- Study of methylene blue treatment of myelodysplasia would be a low-risk intervention.	Methylene Blue	196-210	NLR family pyrin domain containing 3	Homo sapiens	244-249
30101125-11	2018	HIGHLIGHTS - Cytogenetic abnormalities and innate immune activation are seen in myelodysplasia- The NLRP3 inflammasome is a core element generating marrow failure of myelodysplasia- In April 2018 methylene blue was reported to potently inhibit NLRP3 inflammasome function- Methylene blue has benign side effects and has been in human use for a century- Study of methylene blue treatment of myelodysplasia would be a low-risk intervention.	Methylene Blue	273-287	NLR family pyrin domain containing 3	Homo sapiens	100-105
30101125-11	2018	HIGHLIGHTS - Cytogenetic abnormalities and innate immune activation are seen in myelodysplasia- The NLRP3 inflammasome is a core element generating marrow failure of myelodysplasia- In April 2018 methylene blue was reported to potently inhibit NLRP3 inflammasome function- Methylene blue has benign side effects and has been in human use for a century- Study of methylene blue treatment of myelodysplasia would be a low-risk intervention.	Methylene Blue	362-376	NLR family pyrin domain containing 3	Homo sapiens	100-105
30042332-8	2018	Specifically, mitochondrial-targeted peptides such as elamipretide have the potential to mitigate mitochondrial dysfunction and aberrant inflammatory response through activation of nucleotide-binding oligomerization domain (NOD)-like family receptors, such as the pyrin domain containing 3 (NLRP3) inflammasome, nuclear factor-kappa B (NF-kappaB) signaling pathway inhibition, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	54-66	NLR family pyrin domain containing 3	Homo sapiens	291-296
29663696-6	2018	In the work reported here, we examined the roles of the different beta-tubulin isotypes in response to glutamate/glycine treatment, and found that both betaII and betaIII bind to glutathione in the presence of ROS, especially betaIII.	Glutamic Acid	103-112	NLR family pyrin domain containing 3	Homo sapiens	152-170
29976873-0	2018	Targeting the NLRP3 Inflammasome-Related Pathways via Tianeptine Treatment-Suppressed Microglia Polarization to the M1 Phenotype in Lipopolysaccharide-Stimulated Cultures.	tianeptine	54-64	NLR family pyrin domain containing 3	Homo sapiens	14-19
29971445-7	2018	Similarly, H2O2 upregulated TRPM2 protein expression by 80%, and induced both NLRP3 inflammasome activation and increased bioactive IL-1beta secretion (P &lt;= 0.036), whereas ACA pretreatment suppressed these effects (P &lt;= 0.029).	Hydrogen Peroxide	11-15	NLR family pyrin domain containing 3	Homo sapiens	78-83
29730525-5	2018	These cholesterol crystals induce a dose-dependent secretion of mature Interleukin 1-beta (IL-1beta) from human monocytes and macrophages (an NLRP3 inflammasome-mediated pathway).	Cholesterol	6-17	NLR family pyrin domain containing 3	Homo sapiens	142-147
29763636-5	2018	In addition, leonurine decreased representative M1 marker (iNOS and CD86) expression, NLRP3 inflammasome activation and M1 cytokine (TNF-alpha and IL-1beta) production.	leonurine	13-22	NLR family pyrin domain containing 3	Homo sapiens	86-91
29763636-6	2018	In the in vitro cultured RAW264.7 and human monocyte-derived macrophages (MDMs), blockade of COX-2/mPGES-1 and 5-LOX by leonurine inhibited macrophage M1 polarization and NLRP3 inflammasome activation in response to MSU crystals, and thus down-regulated IL-1beta and TNF-alpha with STAT1 and NF-kappaB inactivation.	leonurine	120-129	NLR family pyrin domain containing 3	Homo sapiens	171-176
29677537-0	2018	The rescue effect of mesenchymal stem cell on sodium iodate-induced retinal pigment epithelial cell death through deactivation of NF-kappaB-mediated NLRP3 inflammasome.	sodium iodate	46-59	NLR family pyrin domain containing 3	Homo sapiens	149-154
29677537-8	2018	Taken together, MSC protected against NaIO3-triggered RPE death via deactivating NF-kappaB-mediated NLRP3 inflammasome and maintaining mitochondrial integrity.	sodium iodate	38-43	NLR family pyrin domain containing 3	Homo sapiens	100-105
29683202-2	2018	Crystalline cholesterol and uric acid activate the PRR Nod-like receptor protein (NLRP)3 inflammasome to release interleukin (IL)-1beta and result in vigorous inflammation.	Cholesterol	12-23	NLR family pyrin domain containing 3	Homo sapiens	51-88
29683202-2	2018	Crystalline cholesterol and uric acid activate the PRR Nod-like receptor protein (NLRP)3 inflammasome to release interleukin (IL)-1beta and result in vigorous inflammation.	Uric Acid	28-37	NLR family pyrin domain containing 3	Homo sapiens	51-88
29663696-6	2018	In the work reported here, we examined the roles of the different beta-tubulin isotypes in response to glutamate/glycine treatment, and found that both betaII and betaIII bind to glutathione in the presence of ROS, especially betaIII.	Glycine	113-120	NLR family pyrin domain containing 3	Homo sapiens	152-170
29663696-6	2018	In the work reported here, we examined the roles of the different beta-tubulin isotypes in response to glutamate/glycine treatment, and found that both betaII and betaIII bind to glutathione in the presence of ROS, especially betaIII.	Glutathione	179-190	NLR family pyrin domain containing 3	Homo sapiens	152-170
29663696-6	2018	In the work reported here, we examined the roles of the different beta-tubulin isotypes in response to glutamate/glycine treatment, and found that both betaII and betaIII bind to glutathione in the presence of ROS, especially betaIII.	ros	210-213	NLR family pyrin domain containing 3	Homo sapiens	152-170
29663696-9	2018	In view of the high levels of betaII and betaIII expressed in the nervous system it is conceivable that these tubulin isotypes may use their sulfhydryl groups to scavenge ROS and protect neuronal cells against oxidative stress.	ros	171-174	NLR family pyrin domain containing 3	Homo sapiens	30-48
29959312-0	2018	Oridonin is a covalent NLRP3 inhibitor with strong anti-inflammasome activity.	oridonin	0-8	NLR family pyrin domain containing 3	Homo sapiens	23-28
29896237-6	2018	It was demonstrated that IL-1beta secretion was suppressed by IL-31 treatment from LPS-challenged peritoneal macrophages following adenosine triphosphate stimulation, which is an activator of NLR family, pyrin domain-containing 3 (NLRP3).	Adenosine Triphosphate	131-153	NLR family pyrin domain containing 3	Homo sapiens	231-236
29959312-4	2018	Ori forms a covalent bond with the cysteine 279 of NLRP3 in NACHT domain to block the interaction between NLRP3 and NEK7, thereby inhibiting NLRP3 inflammasome assembly and activation.	Cysteine	35-43	NLR family pyrin domain containing 3	Homo sapiens	51-56
29959312-4	2018	Ori forms a covalent bond with the cysteine 279 of NLRP3 in NACHT domain to block the interaction between NLRP3 and NEK7, thereby inhibiting NLRP3 inflammasome assembly and activation.	Cysteine	35-43	NLR family pyrin domain containing 3	Homo sapiens	106-111
29959312-4	2018	Ori forms a covalent bond with the cysteine 279 of NLRP3 in NACHT domain to block the interaction between NLRP3 and NEK7, thereby inhibiting NLRP3 inflammasome assembly and activation.	Cysteine	35-43	NLR family pyrin domain containing 3	Homo sapiens	106-111
29891674-6	2018	A GSDMD-derived inhibitor, N-acetyl-Phe-Leu-Thr-Asp-chloromethylketone (Ac-FLTD-CMK), inhibits GSDMD cleavage by caspases-1, -4, -5, and -11 in vitro, suppresses pyroptosis downstream of both canonical and noncanonical inflammasomes, as well as reduces IL-1beta release following activation of the NLRP3 inflammasome in macrophages.	n-acetyl-phe-leu-thr-asp-chloromethylketone	27-70	NLR family pyrin domain containing 3	Homo sapiens	298-303
29877709-0	2018	Structural Insights of Benzenesulfonamide Analogues as NLRP3 Inflammasome Inhibitors: Design, Synthesis, and Biological Characterization.	benzenesulfonamide	23-41	NLR family pyrin domain containing 3	Homo sapiens	55-60
29891674-6	2018	A GSDMD-derived inhibitor, N-acetyl-Phe-Leu-Thr-Asp-chloromethylketone (Ac-FLTD-CMK), inhibits GSDMD cleavage by caspases-1, -4, -5, and -11 in vitro, suppresses pyroptosis downstream of both canonical and noncanonical inflammasomes, as well as reduces IL-1beta release following activation of the NLRP3 inflammasome in macrophages.	ac-fltd	72-79	NLR family pyrin domain containing 3	Homo sapiens	298-303
29792697-2	2018	Inhaled and ingested TiO2 particles enter the bloodstream, are phagocytized by macrophages and neutrophils, are inflammatory, and activate the NLRP3 inflammasome.	titanium dioxide	21-25	NLR family pyrin domain containing 3	Homo sapiens	143-148
29940605-10	2018	Moreover, BK-induced up-regulation of p-p38, NF-kappaB p-p65, NLRP3, ASC, caspase-1, and COX-2 was dose-dependently down-regulated by propofol treatment.	Propofol	134-142	NLR family pyrin domain containing 3	Homo sapiens	62-67
29940605-11	2018	CONCLUSIONS Propofol prevents inflammation in MG-63 cells by regulating p38MAPK-NF-kappaB pathway, NLRP3 inflammasome, and COX-2 expression.	Propofol	12-20	NLR family pyrin domain containing 3	Homo sapiens	99-104
29775050-5	2018	These water-suspended PU NPs reduce the nuclear factor-kappaB (NF-kappaB) activation and suppress the subsequent NLR family pyrin domain containing 3 (NLRP3) inflammasome signals.	Water	6-11	NLR family pyrin domain containing 3	Homo sapiens	151-156
29903983-0	2018	4"-Methoxyresveratrol Alleviated AGE-Induced Inflammation via RAGE-Mediated NF-kappaB and NLRP3 Inflammasome Pathway.	4'-methoxyresveratrol	0-21	NLR family pyrin domain containing 3	Homo sapiens	90-95
29723525-4	2018	Pharmacologic or genetic inhibition of ALK through targeted drugs (ceritinib and lorlatinib) or RNAi blocked extracellular ATP-induced NLRP3 inflammasome activation in macrophages.	ceritinib	67-76	NLR family pyrin domain containing 3	Homo sapiens	135-140
29723525-4	2018	Pharmacologic or genetic inhibition of ALK through targeted drugs (ceritinib and lorlatinib) or RNAi blocked extracellular ATP-induced NLRP3 inflammasome activation in macrophages.	lorlatinib	81-91	NLR family pyrin domain containing 3	Homo sapiens	135-140
29723525-4	2018	Pharmacologic or genetic inhibition of ALK through targeted drugs (ceritinib and lorlatinib) or RNAi blocked extracellular ATP-induced NLRP3 inflammasome activation in macrophages.	Adenosine Triphosphate	123-126	NLR family pyrin domain containing 3	Homo sapiens	135-140
29904810-2	2018	RECENT FINDINGS: Recent evidence about therapeutic targets on pericarditis has demonstrated that NALP3 inflammasome blockade is the cornerstone in the clinical benefits of colchicine.	Colchicine	172-182	NLR family pyrin domain containing 3	Homo sapiens	97-102
29655789-5	2018	Finally, by generating a THP-1 cell line stably expressing ILF2 protein using the lentivirus infection system, we demonstrate that ILF2 represses ATP-induced activation of endogenous NLRP3 inflammasome in macrophages.	Adenosine Triphosphate	146-149	NLR family pyrin domain containing 3	Homo sapiens	183-188
29880500-6	2018	NLRP3 is activated by various endogenous danger signals abundantly present in atherosclerotic lesions, such as oxidized low-density lipoprotein and cholesterol crystals.	Cholesterol	148-159	NLR family pyrin domain containing 3	Homo sapiens	0-5
29915584-8	2018	In vitro analysis demonstrated that the blockade of autophagy with 3-methyladenine (3-MA) in Mycobacterium leprae-stimulated human primary monocytes increased the assembly of NLRP3 specks assembly, and it was associated with an increase of IL-1beta and IL-6 production.	3-methyladenine	67-82	NLR family pyrin domain containing 3	Homo sapiens	175-180
29915584-8	2018	In vitro analysis demonstrated that the blockade of autophagy with 3-methyladenine (3-MA) in Mycobacterium leprae-stimulated human primary monocytes increased the assembly of NLRP3 specks assembly, and it was associated with an increase of IL-1beta and IL-6 production.	3-methyladenine	84-88	NLR family pyrin domain containing 3	Homo sapiens	175-180
29219210-6	2018	These effects are mediated through CtBP, an NADH-sensitive transcriptional co-repressor; through effects on NLRP3 inflammasome assembly and caspase-1 activation; through formation of advanced glycation end-products; and by less well-defined mechanisms.	ctbp	35-39	NLR family pyrin domain containing 3	Homo sapiens	108-113
29183866-4	2018	Using the NLRP3 inflammasome specific inhibitor MCC950, we were able to measure the activity of canonical or alternative NLRP3 pathways, AIM2 and NLRC4 inflammasomes in whole blood.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	48-54	NLR family pyrin domain containing 3	Homo sapiens	10-15
29183866-4	2018	Using the NLRP3 inflammasome specific inhibitor MCC950, we were able to measure the activity of canonical or alternative NLRP3 pathways, AIM2 and NLRC4 inflammasomes in whole blood.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	48-54	NLR family pyrin domain containing 3	Homo sapiens	121-126
28437591-0	2018	Fluorofenidone attenuates interleukin-1beta production by interacting with NLRP3 inflammasome in unilateral ureteral obstruction.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	0-14	NLR family pyrin domain containing 3	Homo sapiens	75-80
29947341-0	2018	Hemin Induces the Activation of NLRP3 Inflammasome in N9 Microglial Cells.	Hemin	0-5	NLR family pyrin domain containing 3	Homo sapiens	32-37
29947341-1	2018	BACKGROUND: Hemin is an important sterile component that induces a neuroinflammatory response after intracerebral hemorrhage, in which NLRP3 inflammasome activation has also proved to be involved.	Hemin	12-17	NLR family pyrin domain containing 3	Homo sapiens	135-140
29947341-4	2018	METHODS: In this study, N9 microglial cells were treated with hemin, and subsequently used to detect the production of caspase-1 p10 and NLRP3 inflammasome assembly.	Hemin	62-67	NLR family pyrin domain containing 3	Homo sapiens	137-142
29947341-7	2018	Moreover, hemin was observed to be capable of inducing the assembly of the NLRP3 inflammasome without any increase in IL-1beta.	Hemin	10-15	NLR family pyrin domain containing 3	Homo sapiens	75-80
29947341-9	2018	Furthermore, hemin-induced NLRP3 inflammasome activation did not significantly affect pyroptosis.	Hemin	13-18	NLR family pyrin domain containing 3	Homo sapiens	27-32
29492824-6	2018	It is our hypothesis that Meth activates NLRP3 inflammasome in microglia and promotes the processing and release of interleukin (IL)-1beta, resulting in neurotoxic activity.	Methamphetamine	26-30	NLR family pyrin domain containing 3	Homo sapiens	41-46
29159877-15	2018	Cell death induced by dental calculus was significantly inhibited by cytochalasin D, z-YVAD-fmk and glyburide, indicating NLRP3 inflammasome involvement.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	85-95	NLR family pyrin domain containing 3	Homo sapiens	122-127
29159877-15	2018	Cell death induced by dental calculus was significantly inhibited by cytochalasin D, z-YVAD-fmk and glyburide, indicating NLRP3 inflammasome involvement.	Glyburide	100-109	NLR family pyrin domain containing 3	Homo sapiens	122-127
29620210-0	2018	Saikosaponin-d alleviates carbon-tetrachloride induced acute hepatocellular injury by inhibiting oxidative stress and NLRP3 inflammasome activation in the HL-7702 cell line.	saikosaponin D	0-14	NLR family pyrin domain containing 3	Homo sapiens	118-123
28437591-1	2018	AIM: We explored whether Fluorofenidone reduced interleukin-1beta (IL-1beta) production by interacting with NLRP3 inflammasome in unilateral ureteral obstruction (UUO).	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	25-39	NLR family pyrin domain containing 3	Homo sapiens	108-113
28437591-9	2018	Interestingly, Fluorofenidone inhibited the activation of NLRP3 inflammasome, downregulated Caspase-1 levels and thereby decreased the cleavage of pro-IL-1beta into IL-1beta in vivo and in vitro.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	15-29	NLR family pyrin domain containing 3	Homo sapiens	58-63
28437591-10	2018	Fluorofenidone treatment distinctively weakened the interaction between NLRP3 and ASC, as well as ASC and pro-Caspase-1 in vivo.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	0-14	NLR family pyrin domain containing 3	Homo sapiens	72-77
28437591-12	2018	CONCLUSION: Fluorofenidone serves as a novel anti-inflammatory agent that attenuates IL-1beta production in UUO model by interacting with NLRP3 inflammasome.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	12-26	NLR family pyrin domain containing 3	Homo sapiens	138-143
29475133-0	2018	Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	112-117
29950247-2	2018	The recent studies showed that all of S100A9/TLR4, S100A9/CD33 and Nox/ROS signaling pathways can activate oxygen-sensitivity NLRP3 inflammasome and then induce the pyroptosis of hematopoeitic stem cells (HSC) / hematopeitic pregenitor cells (HPC), resulting in ineffective hematopoiesis in patients with MDS.	nicotine 1-N-oxide	67-70	NLR family pyrin domain containing 3	Homo sapiens	126-131
29950247-2	2018	The recent studies showed that all of S100A9/TLR4, S100A9/CD33 and Nox/ROS signaling pathways can activate oxygen-sensitivity NLRP3 inflammasome and then induce the pyroptosis of hematopoeitic stem cells (HSC) / hematopeitic pregenitor cells (HPC), resulting in ineffective hematopoiesis in patients with MDS.	ros	71-74	NLR family pyrin domain containing 3	Homo sapiens	126-131
29950247-2	2018	The recent studies showed that all of S100A9/TLR4, S100A9/CD33 and Nox/ROS signaling pathways can activate oxygen-sensitivity NLRP3 inflammasome and then induce the pyroptosis of hematopoeitic stem cells (HSC) / hematopeitic pregenitor cells (HPC), resulting in ineffective hematopoiesis in patients with MDS.	Oxygen	107-113	NLR family pyrin domain containing 3	Homo sapiens	126-131
29475133-9	2018	These results suggest that mitochondrial ROS-TXNIP/NLRP3/IL-1beta axis activation is responsible for tubular oxidative injury, which can be ameliorated by MitoQ via the inhibition of mtROS overproduction.	mitoquinone	155-160	NLR family pyrin domain containing 3	Homo sapiens	51-56
29475133-0	2018	Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis.	Reactive Oxygen Species	102-105	NLR family pyrin domain containing 3	Homo sapiens	112-117
29475133-7	2018	Treating HK-2 cells with MitoQ suppressed the dissociation of TRX from TXNIP and subsequently blocked the interaction between TXNIP and NLRP3, leading to the inhibition of NLRP3 inflammasome activation and IL-1beta maturation.	mitoquinone	25-30	NLR family pyrin domain containing 3	Homo sapiens	136-141
29475133-7	2018	Treating HK-2 cells with MitoQ suppressed the dissociation of TRX from TXNIP and subsequently blocked the interaction between TXNIP and NLRP3, leading to the inhibition of NLRP3 inflammasome activation and IL-1beta maturation.	mitoquinone	25-30	NLR family pyrin domain containing 3	Homo sapiens	172-177
29475133-9	2018	These results suggest that mitochondrial ROS-TXNIP/NLRP3/IL-1beta axis activation is responsible for tubular oxidative injury, which can be ameliorated by MitoQ via the inhibition of mtROS overproduction.	Reactive Oxygen Species	41-44	NLR family pyrin domain containing 3	Homo sapiens	51-56
29706079-0	2018	Amelioration of Alcoholic Liver Steatosis by Dihydroquercetin through the Modulation of AMPK-Dependent Lipogenesis Mediated by P2X7R-NLRP3-Inflammasome Activation.	taxifolin	45-61	NLR family pyrin domain containing 3	Homo sapiens	133-138
29881379-4	2018	Mechanistically, betaine ameliorates sulfur amino acid metabolism against oxidative stress, inhibits nuclear factor-kappaB activity and NLRP3 inflammasome activation, regulates energy metabolism, and mitigates endoplasmic reticulum stress and apoptosis.	Betaine	17-24	NLR family pyrin domain containing 3	Homo sapiens	136-141
29780394-2	2018	Uric acid was shown to be one of the "danger" signals involved in the activation of NLRP3 inflammasome; notably, the concentration of uric acid is increased in the serum and in the cerebrospinal fluid of MS individuals.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	84-89
30701884-4	2018	The mechanisms of atherosclerosis associated with IL-1beta determine the ability of cholesterol crystals and other "Pro-atherogenic" factors to induce the synthesis of IL-1beta by activating NLRP3 inflammasome.	Cholesterol	84-95	NLR family pyrin domain containing 3	Homo sapiens	191-196
30701884-5	2018	The mechanisms of atherosclerosis associated with IL-1beta determine the ability of cholesterol crystals and other "proatherogenic" factors to induce the synthesis of IL-1beta by activating NLRP3 inflammasome.	Cholesterol	84-95	NLR family pyrin domain containing 3	Homo sapiens	190-195
29780394-2	2018	Uric acid was shown to be one of the "danger" signals involved in the activation of NLRP3 inflammasome; notably, the concentration of uric acid is increased in the serum and in the cerebrospinal fluid of MS individuals.	Uric Acid	134-143	NLR family pyrin domain containing 3	Homo sapiens	84-89
29780394-7	2018	Results showed that uric acid serum concentration was significantly increased in PPMS; in these and in AMS patients, mRNA for NLRP3, ASC, and IL-18 was upregulated as well, but caspase-8 mRNA was upregulated only in PPMS.	Uric Acid	20-29	NLR family pyrin domain containing 3	Homo sapiens	126-131
29720213-11	2018	ROS was required for PM2.5-induced IL-1beta production and NLRP3 inflammasome activation in oAbeta-stimulated microglia.	ros	0-3	NLR family pyrin domain containing 3	Homo sapiens	59-64
29716544-4	2018	Immunohistochemistry was used to examine the expression of NLRP3 and IL-1beta in the paraffin-embedded OSCC tissues.	Paraffin	85-93	NLR family pyrin domain containing 3	Homo sapiens	59-64
29716544-9	2018	Obvious expression of NLRP3 and IL-1beta was found in the paraffin-embedded OSCC tissues, and the NLRP3 expression levels were correlated with the tumor size, lymphonode metastatic status and IL-1beta expression.	Paraffin	58-66	NLR family pyrin domain containing 3	Homo sapiens	22-27
29720213-13	2018	CONCLUSIONS: For the first time, these results suggested that the effects of PM2.5 under AD context were possibly mediated by NLRP3 inflammasome activation, which was triggered by ROS.	ros	180-183	NLR family pyrin domain containing 3	Homo sapiens	126-131
29338075-8	2018	Suppression of P2X7 receptor-NLRP3 activation by gentiopicroside inhibited IL-1beta production.	gentiopicroside	49-64	NLR family pyrin domain containing 3	Homo sapiens	29-34
29338075-9	2018	In ethanol-exposed HepG2 cells, gentiopicroside reduced lipogenesis and promoted lipid oxidation via activation of P2X7 receptor-NLRP3 inflammasomes.	gentiopicroside	32-47	NLR family pyrin domain containing 3	Homo sapiens	129-134
29472126-4	2018	More importantly, (E)-1-(6-methoxybenzo[d]oxazol-2-yl)-2-(4-methoxyphenyl)ethanone oxime (5d) exhibited anti-hyperuricemic and anti-acute gouty arthritis activities through regulating XOD, NLRP3 and TLR4.	(e)-1-(6-methoxybenzo[d]oxazol-2-yl)-2-(4-methoxyphenyl)ethanone oxime	18-88	NLR family pyrin domain containing 3	Homo sapiens	189-194
29338075-9	2018	In ethanol-exposed HepG2 cells, gentiopicroside reduced lipogenesis and promoted lipid oxidation via activation of P2X7 receptor-NLRP3 inflammasomes.	Ethanol	3-10	NLR family pyrin domain containing 3	Homo sapiens	129-134
29338075-14	2018	CONCLUSIONS AND IMPLICATIONS: Activation of LKB1/AMPK signalling by gentiopicroside was mediated by the P2X7 receptor-NLRP3 inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of alcoholic hepatosteatosis.	gentiopicroside	68-83	NLR family pyrin domain containing 3	Homo sapiens	118-123
29735414-2	2018	In this study, Homocysteine (Hcy) is revealed to be a DAMP that activates adipocyte NLRP3 inflammasomes, participating in insulin resistance.	Homocysteine	29-32	NLR family pyrin domain containing 3	Homo sapiens	84-89
29438905-2	2018	The study evaluated the involvement of molecular structures called damage-associated molecular patterns (DAMPs), such as hyaluronan (HA) and heat shock proteins (Hsp) on NLRP1 and NLRP3 inflammasomes activation in peripheral blood monocytes.	Hyaluronic Acid	121-131	NLR family pyrin domain containing 3	Homo sapiens	180-185
29735414-3	2018	Hcy-induced activation of NLRP3 inflammasomes were observed in both adipocytes and adipose tissue macrophages (ATMs) and mediated insulin resistance.	Homocysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	26-31
29735414-4	2018	Lysophosphatidylcholine (lyso-PC) acted as a second signal activator, mediating Hcy-induced adipocyte NLRP3 inflammasome activation.	Lysophosphatidylcholines	0-23	NLR family pyrin domain containing 3	Homo sapiens	102-107
29735414-4	2018	Lysophosphatidylcholine (lyso-PC) acted as a second signal activator, mediating Hcy-induced adipocyte NLRP3 inflammasome activation.	Lysophosphatidylcholines	25-32	NLR family pyrin domain containing 3	Homo sapiens	102-107
29735414-4	2018	Lysophosphatidylcholine (lyso-PC) acted as a second signal activator, mediating Hcy-induced adipocyte NLRP3 inflammasome activation.	Homocysteine	80-83	NLR family pyrin domain containing 3	Homo sapiens	102-107
29735414-7	2018	This study demonstrated that Hcy activates adipose NLRP3 inflammasomes in an adipocyte lyso-PC-dependent manner and highlights the importance of the adipocyte NLRP3 inflammasome in insulin resistance.	Homocysteine	29-32	NLR family pyrin domain containing 3	Homo sapiens	51-56
29313961-7	2018	Sustained monocyte activation, induced by fungal beta-glucan particles upon actin cytoskeleton disruption, relies on Dectin-1 and results in the classical caspase-1 inflammasome formation through NLRP3, generation of an oxidative burst, NF-kappaB activation, and increased inflammatory cytokine release.	beta-Glucans	49-60	NLR family pyrin domain containing 3	Homo sapiens	196-201
29735414-7	2018	This study demonstrated that Hcy activates adipose NLRP3 inflammasomes in an adipocyte lyso-PC-dependent manner and highlights the importance of the adipocyte NLRP3 inflammasome in insulin resistance.	Homocysteine	29-32	NLR family pyrin domain containing 3	Homo sapiens	159-164
29477360-3	2018	Here we demonstrated that the Nod-like receptor protein 3 (NLRP3) inflammasome is activated by mitochondrial reactive oxygen species (mROS) during I/R injury via direct interactions between the inflammasome and thioredoxin-interacting protein (TXNIP).	Reactive Oxygen Species	109-132	NLR family pyrin domain containing 3	Homo sapiens	30-57
29477360-3	2018	Here we demonstrated that the Nod-like receptor protein 3 (NLRP3) inflammasome is activated by mitochondrial reactive oxygen species (mROS) during I/R injury via direct interactions between the inflammasome and thioredoxin-interacting protein (TXNIP).	Reactive Oxygen Species	109-132	NLR family pyrin domain containing 3	Homo sapiens	59-64
29366884-3	2018	The glucans inhibited lipid-induced inflammation, but only the beta-1,3-d-glucan regulated both the NLRP3 inflammasome activation and the expression of genes involved on lipid efflux in acLDL- or CC-pretreated cells, thereby reducing foam cell formation.	(1----3)-beta-d-glucan	63-80	NLR family pyrin domain containing 3	Homo sapiens	100-105
29477360-8	2018	MitoTEMPO treatment also inhibited NLRP3 inflammasome activation and co-localization of NLRP3 and TXNIP after simulated ischemia/reperfusion (SI/R) injury.	MitoTEMPO	0-9	NLR family pyrin domain containing 3	Homo sapiens	35-40
29477360-8	2018	MitoTEMPO treatment also inhibited NLRP3 inflammasome activation and co-localization of NLRP3 and TXNIP after simulated ischemia/reperfusion (SI/R) injury.	MitoTEMPO	0-9	NLR family pyrin domain containing 3	Homo sapiens	88-93
28880687-1	2018	OBJECTIVE: Monosodium urate (MSU) has been shown to promote interleukin-1beta (IL-1beta) secretion in human monocytes, but the priming signals for NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway remains elusive.	Uric Acid	11-27	NLR family pyrin domain containing 3	Homo sapiens	199-204
29921379-5	2018	This finding highlights the possible molecular pathways involving NLRP3 activation for management of ROS and insulin IR.	Reactive Oxygen Species	101-104	NLR family pyrin domain containing 3	Homo sapiens	66-71
29854843-0	2018	Cyanidin-3-glucoside Alleviates 4-Hydroxyhexenal-Induced NLRP3 Inflammasome Activation via JNK-c-Jun/AP-1 Pathway in Human Retinal Pigment Epithelial Cells.	cyanidin-3-o-glucoside	0-20	NLR family pyrin domain containing 3	Homo sapiens	57-62
29325899-4	2018	Specifically, beta-hydroxybutyrate has been shown to interact with multiple novel molecular targets such as histone deacetylases, hydroxycarboxylic acid receptors on immune cells, and the NLRP3 inflammasome.	3-Hydroxybutyric Acid	14-34	NLR family pyrin domain containing 3	Homo sapiens	188-193
29712950-6	2018	IL-1alpha-primed ARPE-19 cells, human embryonal stem cell (hESC)-derived RPE cells, and primary human RPE cells were exposed to MG-132 and bafilomycin A to activate NLRP3 via the inhibition of proteasomes and autophagy, respectively.	bafilomycin A	139-152	NLR family pyrin domain containing 3	Homo sapiens	165-170
29854843-0	2018	Cyanidin-3-glucoside Alleviates 4-Hydroxyhexenal-Induced NLRP3 Inflammasome Activation via JNK-c-Jun/AP-1 Pathway in Human Retinal Pigment Epithelial Cells.	4-hydroxyhexenal	32-48	NLR family pyrin domain containing 3	Homo sapiens	57-62
29650946-7	2018	The patient completed a course of daunorubicin, cytarabine, and AII trans-retinoic acid (ATRA) with complete remission.	Tretinoin	89-93	NLR family pyrin domain containing 3	Homo sapiens	64-67
29676014-5	2018	In addition, the successful use of macrolide antibiotics to treat lung infections in these conditions further confirms that the innate immune system is the key conductor of inflammation in these pulmonary diseases, as there is a strong body of evidence that macrolides are able to modulate the NLRP3 inflammasome and interleukin-1beta and interleukin-18 secretion, both of which are central players in the innate immune response.	Macrolides	35-44	NLR family pyrin domain containing 3	Homo sapiens	294-299
29676014-5	2018	In addition, the successful use of macrolide antibiotics to treat lung infections in these conditions further confirms that the innate immune system is the key conductor of inflammation in these pulmonary diseases, as there is a strong body of evidence that macrolides are able to modulate the NLRP3 inflammasome and interleukin-1beta and interleukin-18 secretion, both of which are central players in the innate immune response.	Macrolides	258-268	NLR family pyrin domain containing 3	Homo sapiens	294-299
29550474-9	2018	IL-18 secretion was inhibited by PGE2 treatment, and PGE2 inhibited inflammasome complex (ASC/Cas-1/NLRP3) formation in THP-1 cells.	Dinoprostone	53-57	NLR family pyrin domain containing 3	Homo sapiens	100-105
29850543-12	2018	Conclusions: The NLRP3 rs4612666 gene polymorphism may be related to the occurrence of LAA IS and MES, suggesting that the NLRP3 gene polymorphism increases the susceptibility of LAA IS by changing the plaque vulnerability.	2-(N-morpholino)ethanesulfonic acid	98-101	NLR family pyrin domain containing 3	Homo sapiens	17-22
29850543-12	2018	Conclusions: The NLRP3 rs4612666 gene polymorphism may be related to the occurrence of LAA IS and MES, suggesting that the NLRP3 gene polymorphism increases the susceptibility of LAA IS by changing the plaque vulnerability.	2-(N-morpholino)ethanesulfonic acid	98-101	NLR family pyrin domain containing 3	Homo sapiens	123-128
29393464-0	2018	NLRP1 and NLRP3 inflammasomes mediate LPS/ATP-induced pyroptosis in knee osteoarthritis.	Adenosine Triphosphate	42-45	NLR family pyrin domain containing 3	Homo sapiens	10-15
29551284-0	2018	Atractylodin attenuates lipopolysaccharide-induced acute lung injury by inhibiting NLRP3 inflammasome and TLR4 pathways.	atractylodin	0-12	NLR family pyrin domain containing 3	Homo sapiens	83-88
29393464-9	2018	However, LPS+ATP-induced pyroptosis was attenuated by NLRP1 and NLRP3 siRNAs.	Adenosine Triphosphate	13-16	NLR family pyrin domain containing 3	Homo sapiens	64-69
29446486-0	2018	Interleukin-17A participates in podocyte injury by inducing IL-1beta secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.	ros	87-90	NLR family pyrin domain containing 3	Homo sapiens	91-96
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	Glyburide	33-46	NLR family pyrin domain containing 3	Homo sapiens	82-87
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	Glyburide	33-46	NLR family pyrin domain containing 3	Homo sapiens	217-222
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	n-benzyloxycarbony	117-135	NLR family pyrin domain containing 3	Homo sapiens	217-222
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	Alanine	140-143	NLR family pyrin domain containing 3	Homo sapiens	217-222
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	fluoromethylketone	159-177	NLR family pyrin domain containing 3	Homo sapiens	217-222
29432801-10	2018	This study suggests that L. interrogans infection leads to reactive oxygen species (ROS)- and cathepsin B-dependent NLRP3 inflammasome activation, which subsequently mediates caspase-1 activation and IL-1beta and IL-18 release.	Reactive Oxygen Species	59-82	NLR family pyrin domain containing 3	Homo sapiens	116-121
29446486-8	2018	Blockade of intracellular ROS or inhibition of caspase-1 prevented activation of the NLRP3 inflammasome, thereby restoring podocyte morphology.	ros	26-29	NLR family pyrin domain containing 3	Homo sapiens	85-90
29594175-8	2018	This was inhibited by Z-YVAD-FMK (a caspase-1 selective inhibitor) and by MCC950 (a NLRP3 selective inhibitor).	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	74-80	NLR family pyrin domain containing 3	Homo sapiens	84-89
29386291-11	2018	Moreover, we identified two target lysine residues, K110 and K140, which are essential for both porcine ASC ubiquitination and NLRP3 inflammasome-mediated IL-1beta production.	Lysine	35-41	NLR family pyrin domain containing 3	Homo sapiens	127-132
29594175-9	2018	In PBB BAL macrophages inflammasome complexes were visualised as fluorescence specks of NLRP3 or AIM2 colocalised with cleaved caspase-1 and cleaved IL-1beta.	pbb	3-6	NLR family pyrin domain containing 3	Homo sapiens	88-93
29594175-10	2018	NTHi stimulation induced formation of specks of cleaved IL-1beta, NLRP3 and AIM2 in PBMCs, blood monocytes and monocyte-derived macrophages.	nthi	0-4	NLR family pyrin domain containing 3	Homo sapiens	66-71
29743981-0	2018	Induction of NLRP3 Inflammasome Activation by Heme in Human Endothelial Cells.	Heme	46-50	NLR family pyrin domain containing 3	Homo sapiens	13-18
29743866-8	2018	These results suggest that Dex inhibiting c-Fos nuclear protein levels promoted by LPS/ATP blocks the up-regulation of NLRP3.	Dexmedetomidine	27-30	NLR family pyrin domain containing 3	Homo sapiens	119-124
29743866-8	2018	These results suggest that Dex inhibiting c-Fos nuclear protein levels promoted by LPS/ATP blocks the up-regulation of NLRP3.	Adenosine Triphosphate	87-90	NLR family pyrin domain containing 3	Homo sapiens	119-124
29743866-9	2018	This suggestion is supported by co-immunoprecipitation and PCR studies, in which Dex decreased the amount of c-Fos that binds to NLRP3 under the stimulation of LPS/ATP.	Dexmedetomidine	81-84	NLR family pyrin domain containing 3	Homo sapiens	129-134
29743866-9	2018	This suggestion is supported by co-immunoprecipitation and PCR studies, in which Dex decreased the amount of c-Fos that binds to NLRP3 under the stimulation of LPS/ATP.	Adenosine Triphosphate	164-167	NLR family pyrin domain containing 3	Homo sapiens	129-134
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Dexmedetomidine	32-35	NLR family pyrin domain containing 3	Homo sapiens	119-124
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Adenosine Triphosphate	106-109	NLR family pyrin domain containing 3	Homo sapiens	119-124
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Dexmedetomidine	212-215	NLR family pyrin domain containing 3	Homo sapiens	119-124
29743866-0	2018	Dexmedetomidine inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades.	Dexmedetomidine	0-15	NLR family pyrin domain containing 3	Homo sapiens	99-104
29743866-0	2018	Dexmedetomidine inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades.	Adenosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	99-104
29743866-3	2018	The present study was aimed to investigate effect of Dex on NLRP3 activity in activated microglia and reveal the underlying mechanisms.	Dexmedetomidine	53-56	NLR family pyrin domain containing 3	Homo sapiens	60-65
29743866-5	2018	Data from ELISA and Western blot assays showed that Dex abrogated the promoting effects of LPS/ATP on the release of pro-inflammatory cytokines including IL-1beta and IL-18 in the cell medium and the expression of NLRP3 and its downstream target caspase-1 in HMC3 cells.	Dexmedetomidine	52-55	NLR family pyrin domain containing 3	Homo sapiens	214-219
29743866-5	2018	Data from ELISA and Western blot assays showed that Dex abrogated the promoting effects of LPS/ATP on the release of pro-inflammatory cytokines including IL-1beta and IL-18 in the cell medium and the expression of NLRP3 and its downstream target caspase-1 in HMC3 cells.	Adenosine Triphosphate	95-98	NLR family pyrin domain containing 3	Homo sapiens	214-219
29743981-11	2018	Our results identified endothelial cells as a target of heme-mediated NLRP3 activation that can contribute to the inflammation triggered by sterile hemolysis.	Heme	56-60	NLR family pyrin domain containing 3	Homo sapiens	70-75
29743981-3	2018	Heme, released from RBCs, is a DAMP and induces IL-1beta production through the activation of the nucleotide-binding domain and leucine-rich repeat-containing family and pyrin domain containing 3 (NLRP3) in macrophages; however, other cellular targets of heme-mediated inflammasome activation were not investigated.	Heme	0-4	NLR family pyrin domain containing 3	Homo sapiens	197-202
29743981-3	2018	Heme, released from RBCs, is a DAMP and induces IL-1beta production through the activation of the nucleotide-binding domain and leucine-rich repeat-containing family and pyrin domain containing 3 (NLRP3) in macrophages; however, other cellular targets of heme-mediated inflammasome activation were not investigated.	Heme	255-259	NLR family pyrin domain containing 3	Homo sapiens	197-202
29743981-5	2018	We found that heme upregulated NLRP3 expression and induced active IL-1beta production in human umbilical vein endothelial cells (HUVECs).	Heme	14-18	NLR family pyrin domain containing 3	Homo sapiens	31-36
29743981-8	2018	Unfettered production of reactive oxygen species played a critical role in heme-mediated NLRP3 activation.	Reactive Oxygen Species	25-48	NLR family pyrin domain containing 3	Homo sapiens	89-94
29743981-8	2018	Unfettered production of reactive oxygen species played a critical role in heme-mediated NLRP3 activation.	Heme	75-79	NLR family pyrin domain containing 3	Homo sapiens	89-94
29743981-9	2018	Activation of NLRP3 by heme required structural integrity of the heme molecule, as neither protoporphyrin IX nor iron-induced IL-1beta production.	Heme	23-27	NLR family pyrin domain containing 3	Homo sapiens	14-19
29743981-9	2018	Activation of NLRP3 by heme required structural integrity of the heme molecule, as neither protoporphyrin IX nor iron-induced IL-1beta production.	Heme	65-69	NLR family pyrin domain containing 3	Homo sapiens	14-19
29545514-5	2018	RESULTS The results of SP showed that NLRP3 and caspase-1 were mainly expressed in the cytoplasm of epithelial cells, mesenchymal cells, and trophoblast cells in fetal membranes, and the cytoplasm of placental syncytiotrophoblasts and vascular endothelial cells in placental tissues.	sp	23-25	NLR family pyrin domain containing 3	Homo sapiens	38-43
29277324-8	2018	In parallel, SIRT3 overexpression in THP-1 cells decreased the palmitate-induced generation of mitochondrial reactive oxygen species, restored autophagy, and attenuated NLRP3 inflammasome activation.	Palmitates	63-72	NLR family pyrin domain containing 3	Homo sapiens	169-174
29374549-11	2018	AGEs induced HAEC injury by inducing reactive oxygen species -mediated NLRP3 inflammasome activation.	Reactive Oxygen Species	37-60	NLR family pyrin domain containing 3	Homo sapiens	71-76
29374549-12	2018	Matrine recovered HAEC viability by inhibiting reactive oxygen species -mediated NLRP3 inflammasome activation.	Reactive Oxygen Species	47-70	NLR family pyrin domain containing 3	Homo sapiens	81-86
29500339-0	2018	Hydroxychloroquine attenuates renal ischemia/reperfusion injury by inhibiting cathepsin mediated NLRP3 inflammasome activation.	Hydroxychloroquine	0-18	NLR family pyrin domain containing 3	Homo sapiens	97-102
29500339-8	2018	Mechanistic studies showed that HCQ could inhibit the priming of the NLRP3 inflammasome by down-regulating I/R or H/R-induced NF-kappaB signaling.	Hydroxychloroquine	32-35	NLR family pyrin domain containing 3	Homo sapiens	69-74
29500339-11	2018	Notably, we found that HCQ attenuated renal injury through downregulation of CTSB and CTSL-mediated NLRP3 inflammasome activation.	Hydroxychloroquine	23-26	NLR family pyrin domain containing 3	Homo sapiens	100-105
29193391-0	2018	Dihydromyricetin inhibits NLRP3 inflammasome-dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells.	dihydromyricetin	0-16	NLR family pyrin domain containing 3	Homo sapiens	26-31
29193391-4	2018	In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1beta and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels.	Palmitic Acid	22-35	NLR family pyrin domain containing 3	Homo sapiens	307-312
29193391-4	2018	In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1beta and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels.	Palmitic Acid	37-39	NLR family pyrin domain containing 3	Homo sapiens	307-312
29516278-6	2018	RECENT FINDINGS: CPP crystals induce inflammation through the NLRP3 inflammasome while BCP crystals mediate both NLRP3 dependent and independent effects.	bcp	87-90	NLR family pyrin domain containing 3	Homo sapiens	113-118
29193391-5	2018	Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis.	Palmitic Acid	87-89	NLR family pyrin domain containing 3	Homo sapiens	10-15
29193391-5	2018	Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis.	Reactive Oxygen Species	138-141	NLR family pyrin domain containing 3	Homo sapiens	193-198
29193391-5	2018	Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis.	Palmitic Acid	182-184	NLR family pyrin domain containing 3	Homo sapiens	10-15
29193391-5	2018	Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis.	Palmitic Acid	182-184	NLR family pyrin domain containing 3	Homo sapiens	193-198
29251661-9	2018	Arhalofenate also acts by blocking URAT-1; however, it also blocks the NALP-3 inflammasome providing gout-specific anti-inflammatory effect.	arhalofenate	0-12	NLR family pyrin domain containing 3	Homo sapiens	71-77
29230505-8	2018	In LPS + ATP-treated monocytes, NLRP3 and NLRC4 expressions were also significantly higher in patients compared with controls.	Adenosine Triphosphate	9-12	NLR family pyrin domain containing 3	Homo sapiens	32-37
29383704-4	2018	We have recently identified platelet TLR4, NLRP3, and Bruton tyrosine kinase (BTK) as critical regulators of platelet aggregation and thrombus formation, suggesting that the BTK inhibitor ibrutinib is a potential therapeutic target.	ibrutinib	188-197	NLR family pyrin domain containing 3	Homo sapiens	43-48
29024030-13	2018	Together, our results suggest that melatonin prevents endothelial cell pyroptosis via MEG3/miR-223/NLRP3 axis in atherosclerosis, and therefore, melatonin replacement might be considered a new strategy for protecting endothelium against pyroptosis, thereby for the treatment of atherosclerosis associated with pyroptosis.	Melatonin	35-44	NLR family pyrin domain containing 3	Homo sapiens	99-104
29318480-0	2018	Rosmarinic Acid Mitigates Lipopolysaccharide-Induced Neuroinflammatory Responses through the Inhibition of TLR4 and CD14 Expression and NF-kappaB and NLRP3 Inflammasome Activation.	rosmarinic acid	0-15	NLR family pyrin domain containing 3	Homo sapiens	150-155
29318480-6	2018	Further study showed that rosmarinic acid suppresses the activation of the NF-kappaB pathway and NLRP3 inflammasome, which may contribute to its anti-inflammatory effects.	rosmarinic acid	26-41	NLR family pyrin domain containing 3	Homo sapiens	97-102
29318480-7	2018	These results suggest that rosmarinic acid significantly reduced TLR4 and CD14 expression and NF-kappaB and NLRP3 inflammasome activation, which is involved in anti-neuroinflammation.	rosmarinic acid	27-42	NLR family pyrin domain containing 3	Homo sapiens	108-113
28345767-4	2018	Modern hypotheses introduce atherosclerosis as an inflammatory/lipid-based disease and NLRP3 inflammasome has been considered as a link between lipid metabolism and inflammation because crystalline cholesterol and oxidized low-density lipoprotein (oxLDL) (two abundant components in atherosclerotic plaques) activate NLRP3 inflammasome.	Cholesterol	198-209	NLR family pyrin domain containing 3	Homo sapiens	87-92
29358279-0	2018	Copper Regulates the Canonical NLRP3 Inflammasome.	Copper	0-6	NLR family pyrin domain containing 3	Homo sapiens	31-36
29358279-3	2018	In this study we show that NLRP3 inflammasome activation requires intracellular copper.	Copper	80-86	NLR family pyrin domain containing 3	Homo sapiens	27-32
29358279-4	2018	A clinically approved copper chelator, tetrathiomolybdate, inhibited the canonical NLRP3 but not the AIM2, NLRC4, and NLRP1 inflammasomes or NF-kappaB-dependent priming.	Copper	22-28	NLR family pyrin domain containing 3	Homo sapiens	83-88
29358279-4	2018	A clinically approved copper chelator, tetrathiomolybdate, inhibited the canonical NLRP3 but not the AIM2, NLRC4, and NLRP1 inflammasomes or NF-kappaB-dependent priming.	tetrathiomolybdate	39-57	NLR family pyrin domain containing 3	Homo sapiens	83-88
29358279-8	2018	Our results indicate that targeting the intracellular copper homeostasis has potential for the treatment of NLRP3-dependent diseases.	Copper	54-60	NLR family pyrin domain containing 3	Homo sapiens	108-113
29024030-0	2018	Melatonin prevents endothelial cell pyroptosis via regulation of long noncoding RNA MEG3/miR-223/NLRP3 axis.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	97-102
29024030-8	2018	Meanwhile, melatonin also attenuated the expression of pyroptosis-related genes, including NLRP3, ASC, cleaved caspase1, NF-kappaB/GSDMD, GSDMD N-termini, IL-1beta, and IL-18 in aortic endothelium of melatonin-treated animals.	Melatonin	11-20	NLR family pyrin domain containing 3	Homo sapiens	91-96
28726161-0	2018	Celastrol specifically inhibits the activation of NLRP3 inflammasome.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	50-55
29331080-0	2018	Design, Synthesis and Evaluation of Oxazaborine Inhibitors of the NLRP3 Inflammasome.	oxazaborine	36-47	NLR family pyrin domain containing 3	Homo sapiens	66-71
29682582-0	2018	Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway.	Cholecalciferol	0-10	NLR family pyrin domain containing 3	Homo sapiens	112-117
29682582-0	2018	Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway.	Glucose	68-75	NLR family pyrin domain containing 3	Homo sapiens	112-117
29682582-0	2018	Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway.	Reactive Oxygen Species	102-105	NLR family pyrin domain containing 3	Homo sapiens	112-117
29682582-7	2018	Results: Vitamin D3 significantly downregulated intracellular ROS and inhibited TRX-interacting protein (TXNIP)/NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathway activation.	Cholecalciferol	9-19	NLR family pyrin domain containing 3	Homo sapiens	165-170
29682582-10	2018	Conclusions: Vitamin D3 decreases diabetes-induced ROS and exerts protective effects against retinal vascular damage and cell apoptosis in association with inhibition of the ROS/TXNIP/NLRP3 inflammasome pathway.	Cholecalciferol	13-23	NLR family pyrin domain containing 3	Homo sapiens	184-189
29331080-3	2018	In this study, we report the design, synthesis and biological evaluation of novel boron compounds (NBCs) as NLRP3 inflammasome inhibitors.	Boron	82-87	NLR family pyrin domain containing 3	Homo sapiens	108-113
29479354-7	2018	To further understand the differential expression of cytokines/chemokines, we showed that WFA alters the nigericin-induced co-localization of NLRP3 and ASC proteins, thereby inhibiting caspase-1 activation, which is responsible for the cleavage and maturation of pro-inflammatory cytokines IL-1beta and IL-18.	Nigericin	105-114	NLR family pyrin domain containing 3	Homo sapiens	142-147
29378952-2	2018	Here, we demonstrate that OLT1177, an orally active beta-sulfonyl nitrile molecule, inhibits activation of the NLRP3 inflammasome.	beta-sulfonyl nitrile	52-73	NLR family pyrin domain containing 3	Homo sapiens	111-116
29415757-0	2018	Soluble uric acid increases PDZK1 and ABCG2 expression in human intestinal cell lines via the TLR4-NLRP3 inflammasome and PI3K/Akt signaling pathway.	Uric Acid	8-17	NLR family pyrin domain containing 3	Homo sapiens	99-104
29415757-12	2018	Moreover, the upregulation of PDZK1 and ABCG2 by soluble uric acid was partially decreased by either TLR4-NLRP3 inflammasome inhibitors or PI3K/Akt signaling inhibitors.	Uric Acid	57-66	NLR family pyrin domain containing 3	Homo sapiens	106-111
29415757-14	2018	CONCLUSIONS: These findings suggest that urate upregulates the expression of PDZK1 and ABCG2 for excretion in intestinal cells via activating the TLR4-NLRP3 inflammasome and PI3K/Akt signaling pathway.	Uric Acid	41-46	NLR family pyrin domain containing 3	Homo sapiens	151-156
29416034-7	2018	Moreover, silencing NLRP3 or ASC by small interfering RNA efficiently suppressed nicotine-induced caspase-1 cleavage, IL-18 and IL-1beta production, and pyroptosis in HAECs.	Nicotine	81-89	NLR family pyrin domain containing 3	Homo sapiens	20-25
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Nicotine	38-46	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Reactive Oxygen Species	93-116	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Reactive Oxygen Species	118-121	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Reactive Oxygen Species	130-133	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Acetylcysteine	145-162	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-0	2018	Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis.	Nicotine	0-8	NLR family pyrin domain containing 3	Homo sapiens	42-47
29416034-0	2018	Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis.	Reactive Oxygen Species	38-41	NLR family pyrin domain containing 3	Homo sapiens	42-47
29416034-6	2018	Treatment of human aortic endothelial cells (HAECs) with nicotine resulted in NLRP3-ASC inflammasome activation and pyroptosis, as evidenced by cleavage of caspase-1, production of downstream interleukin (IL)-1beta and IL-18, and elevation of LDH activity and increase of propidium iodide (PI) positive cells, which were all inhibited by caspase-1 inhibitor.	Nicotine	57-65	NLR family pyrin domain containing 3	Homo sapiens	78-83
29416034-9	2018	We conclude that pyroptosis is likely a cellular mechanism for the pro-atherosclerotic property of nicotine and stimulation of ROS to activate NLRP3 inflammasome is a signaling mechanism for nicotine-induced pyroptosis.	Reactive Oxygen Species	127-130	NLR family pyrin domain containing 3	Homo sapiens	143-148
29063476-0	2018	Fungal beta-Glucan Activates the NLRP3 Inflammasome in Human Bronchial Epithelial Cells Through ROS Production.	beta-Glucans	7-18	NLR family pyrin domain containing 3	Homo sapiens	33-38
29416034-9	2018	We conclude that pyroptosis is likely a cellular mechanism for the pro-atherosclerotic property of nicotine and stimulation of ROS to activate NLRP3 inflammasome is a signaling mechanism for nicotine-induced pyroptosis.	Nicotine	191-199	NLR family pyrin domain containing 3	Homo sapiens	143-148
27133472-0	2018	Poly-gamma-glutamic acid from Bacillus subtilis upregulates pro-inflammatory cytokines while inhibiting NLRP3, NLRC4 and AIM2 inflammasome activation.	poly(gamma-glutamic acid)	0-24	NLR family pyrin domain containing 3	Homo sapiens	104-109
28988346-13	2018	Palmitate or C2 ceramide induced ER stress in macrophages as well as increased expression of TXNIP, NLRP3 and IL-1beta.	Palmitates	0-9	NLR family pyrin domain containing 3	Homo sapiens	100-105
28988346-13	2018	Palmitate or C2 ceramide induced ER stress in macrophages as well as increased expression of TXNIP, NLRP3 and IL-1beta.	Ceramides	16-24	NLR family pyrin domain containing 3	Homo sapiens	100-105
29198726-6	2018	Moreover, a significant inhibition of the inflammasome activation was observed in neopterin pre-conditioned human astrocytes, when challenged with LPS, by reducing IL-1beta, caspase-1 and ASC expression or content, components of the NLRP3 inflammasome.	Neopterin	82-91	NLR family pyrin domain containing 3	Homo sapiens	233-238
29098483-0	2018	Irisin Alleviates Advanced Glycation End Products-Induced Inflammation and Endothelial Dysfunction via Inhibiting ROS-NLRP3 Inflammasome Signaling.	ros	114-117	NLR family pyrin domain containing 3	Homo sapiens	118-123
29098483-9	2018	Taken together, our results reveal that irisin alleviates AGEs-induced inflammation and endothelial dysfunction via inhibiting ROS-NLRP3 inflammasome signaling, suggest a likely mechanism for irisin-induced therapeutic effect in vascular complications of diabetes.	ros	127-130	NLR family pyrin domain containing 3	Homo sapiens	131-136
29266859-0	2018	Cytokine Profiling of Primary Human Macrophages Exposed to Endotoxin-Free Graphene Oxide: Size-Independent NLRP3 Inflammasome Activation.	graphene oxide	74-88	NLR family pyrin domain containing 3	Homo sapiens	107-112
29352570-3	2018	It is now also known that cholesterol crystals are present through all stages of atherosclerosis and can activate the NLRP3 inflammasome within these inflammatory cells to produce interleukin 1beta and interleukin 18 - key mediators in the inflammatory cascade that drive plaque progression and instability.	Cholesterol	26-37	NLR family pyrin domain containing 3	Homo sapiens	118-123
29352570-4	2018	In this review, we describe the role of monocytes/macrophages and neutrophils in atherosclerosis, outline mechanisms of activation of the NLRP3 inflammasome in the setting of atherosclerosis-associated inflammation and discuss potential therapies that specifically target the NLRP3 inflammasome and/or its downstream mediators in atherosclerosis, with a particular focus on the emerging role of colchicine.	Colchicine	395-405	NLR family pyrin domain containing 3	Homo sapiens	138-143
27133472-4	2018	In this study, we observed that gamma-PGA attenuated NLRP3, NLRC4 and AIM2 inflammasome activation, whereas it upregulated pro-inflammatory cytokine expression in human and murine macrophages.	poly(gamma-glutamic acid)	32-41	NLR family pyrin domain containing 3	Homo sapiens	53-58
29063476-0	2018	Fungal beta-Glucan Activates the NLRP3 Inflammasome in Human Bronchial Epithelial Cells Through ROS Production.	ros	96-99	NLR family pyrin domain containing 3	Homo sapiens	33-38
29063476-3	2018	Also, the relationship between fungal beta-glucan and NLRP3 inflammasome is not clear yet.	beta-Glucans	38-49	NLR family pyrin domain containing 3	Homo sapiens	54-59
29063476-4	2018	In this study, we first identified that curdlan, a large particulate beta-glucan, could activate the NLRP3 inflammasome in LPS-primed human bronchial epithelial cells (HBECs).	beta-Glucans	69-80	NLR family pyrin domain containing 3	Homo sapiens	101-106
29063476-6	2018	Further studies demonstrated that the activation of NLRP3 inflammasome could be attenuated by NAC, an inhibitor of ROS.	ros	115-118	NLR family pyrin domain containing 3	Homo sapiens	52-57
29063476-7	2018	Thus, it indicated curdlan activate NLRP3 inflammasome through a pathway requiring ROS production in HBECs.	ros	83-86	NLR family pyrin domain containing 3	Homo sapiens	36-41
29232311-9	2018	Concurrent treatment with lithium and low-dose colchicine could facilitate the responsiveness of bipolar patients to lithium by reducing leukocyte tissue emigration, the release of neutrophil elastase, and the release of leukocyte pro-inflammatory cytokines such as IL-1beta that are regulated by the NLRP3 inflammasome assembly complex.	Lithium	26-33	NLR family pyrin domain containing 3	Homo sapiens	301-306
29232311-9	2018	Concurrent treatment with lithium and low-dose colchicine could facilitate the responsiveness of bipolar patients to lithium by reducing leukocyte tissue emigration, the release of neutrophil elastase, and the release of leukocyte pro-inflammatory cytokines such as IL-1beta that are regulated by the NLRP3 inflammasome assembly complex.	Colchicine	47-57	NLR family pyrin domain containing 3	Homo sapiens	301-306
29232311-9	2018	Concurrent treatment with lithium and low-dose colchicine could facilitate the responsiveness of bipolar patients to lithium by reducing leukocyte tissue emigration, the release of neutrophil elastase, and the release of leukocyte pro-inflammatory cytokines such as IL-1beta that are regulated by the NLRP3 inflammasome assembly complex.	Lithium	117-124	NLR family pyrin domain containing 3	Homo sapiens	301-306
29207123-7	2018	In conclusion, berberine reduced NLRP3 inflammasone expression by suppressing the activation of the TLR4/Myd88/NF-kappaB signaling pathway in PMA-induced macrophages.	Berberine	15-24	NLR family pyrin domain containing 3	Homo sapiens	33-38
29207123-7	2018	In conclusion, berberine reduced NLRP3 inflammasone expression by suppressing the activation of the TLR4/Myd88/NF-kappaB signaling pathway in PMA-induced macrophages.	Tetradecanoylphorbol Acetate	142-145	NLR family pyrin domain containing 3	Homo sapiens	33-38
29207123-0	2018	NACHT, LRR and PYD domains-containing protein 3 inflammasome is activated and inhibited by berberine via toll-like receptor 4/myeloid differentiation primary response gene 88/nuclear factor-kappaB pathway, in phorbol 12-myristate 13-acetate-induced macrophages.	Berberine	91-100	NLR family pyrin domain containing 3	Homo sapiens	0-47
29207123-0	2018	NACHT, LRR and PYD domains-containing protein 3 inflammasome is activated and inhibited by berberine via toll-like receptor 4/myeloid differentiation primary response gene 88/nuclear factor-kappaB pathway, in phorbol 12-myristate 13-acetate-induced macrophages.	Tetradecanoylphorbol Acetate	209-240	NLR family pyrin domain containing 3	Homo sapiens	0-47
29207123-2	2018	The present study investigated the expression of NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages, and aimed to identify the effects of berberine on the inflammasome.	Tetradecanoylphorbol Acetate	71-102	NLR family pyrin domain containing 3	Homo sapiens	49-54
29207123-2	2018	The present study investigated the expression of NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages, and aimed to identify the effects of berberine on the inflammasome.	Tetradecanoylphorbol Acetate	104-107	NLR family pyrin domain containing 3	Homo sapiens	49-54
29207123-5	2018	The present study demonstrated that NLRP3 inflammasome and IL-1beta were activated in PMA-induced macrophages in a time-dependent manner, whereas berberine significantly inhibited their expression in a dose-dependent manner in PMA-induced macrophages.	Tetradecanoylphorbol Acetate	86-89	NLR family pyrin domain containing 3	Homo sapiens	36-41
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Oxygen	73-79	NLR family pyrin domain containing 3	Homo sapiens	183-188
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Reactive Oxygen Species	141-164	NLR family pyrin domain containing 3	Homo sapiens	183-188
29956204-11	2018	In both experimental and human NASH, livers contain cholesterol crystals which are a second signal for NLRP3 activation; this causes interleukin (IL)-1beta and IL18 secretion to attract and activate macrophages and neutrophils.	Cholesterol	52-63	NLR family pyrin domain containing 3	Homo sapiens	103-108
29054699-0	2018	Silymarin attenuated paraquat-induced cytotoxicity in macrophage by regulating Trx/TXNIP complex, inhibiting NLRP3 inflammasome activation and apoptosis.	Silymarin	0-9	NLR family pyrin domain containing 3	Homo sapiens	109-114
29054699-0	2018	Silymarin attenuated paraquat-induced cytotoxicity in macrophage by regulating Trx/TXNIP complex, inhibiting NLRP3 inflammasome activation and apoptosis.	Paraquat	21-29	NLR family pyrin domain containing 3	Homo sapiens	109-114
29054699-7	2018	NLRP3 inflammasome and cytokines secretion in macrophage exposed to paraquat at 24h were measured via immunofluorescence microscopy, western blot or Elisa.	Paraquat	68-76	NLR family pyrin domain containing 3	Homo sapiens	0-5
29054699-8	2018	Our results revealed that paraquat could dramatically cause cytotoxicity and reactive oxygen species generation, enhance TXNIP expression, and induce NLRP3 inflammasome activation and cytokines secretion.	Paraquat	26-34	NLR family pyrin domain containing 3	Homo sapiens	150-155
29054699-9	2018	The pretreatment with silymarin could remarkably reduce the cytotoxicity, promote the expression of Trx and antioxidant enzymes, and suppress the TXNIP and NLRP3 inflammasome activation.	Silymarin	22-31	NLR family pyrin domain containing 3	Homo sapiens	156-161
29054699-10	2018	In conclusion, silymarin attenuated paraquat-induced cytotoxicity in macrophage by inhibiting oxidative stress, NLRP3 inflammasome activation, cytokines secretion and apoptosis.	Silymarin	15-24	NLR family pyrin domain containing 3	Homo sapiens	112-117
29054699-10	2018	In conclusion, silymarin attenuated paraquat-induced cytotoxicity in macrophage by inhibiting oxidative stress, NLRP3 inflammasome activation, cytokines secretion and apoptosis.	Paraquat	36-44	NLR family pyrin domain containing 3	Homo sapiens	112-117
29403480-3	2017	Inhalation of crystalline silica can induce inflammation by stimulating the NLRP3 inflammasome, a cytosolic receptor complex that plays a critical role in driving inflammatory immune responses.	Silicon Dioxide	26-32	NLR family pyrin domain containing 3	Homo sapiens	76-81
29403480-6	2017	In this study, we target the NLRP3 inflammasome as a crystalline silica responsive element to clarify volcanic cristobalite reactivity.	Silicon Dioxide	65-71	NLR family pyrin domain containing 3	Homo sapiens	29-34
29403480-13	2017	Inflammasome activation mediated by inhaled ash and its potential relevance in chronic pulmonary disease was further evidenced in PBMC using the NLRP3 small-molecule inhibitor CP-456,773 (CRID3, MCC950).	cp-456	176-182	NLR family pyrin domain containing 3	Homo sapiens	145-150
29203171-3	2018	This functionality allows the classical NLRP3 pathway to serve as a highly sensitive, but non-specific surveillance mechanism responding to any type of perturbation that breaches plasma membrane integrity and the associated potassium gradient across the membrane.	Potassium	224-233	NLR family pyrin domain containing 3	Homo sapiens	40-45
29203171-4	2018	Here, we review our current knowledge on potassium efflux-dependent NLRP3 activation, with a special focus on how major cell death programs are rendered pro-inflammatory by secondary NLRP3 activation.	Potassium	41-50	NLR family pyrin domain containing 3	Homo sapiens	68-73
29203171-4	2018	Here, we review our current knowledge on potassium efflux-dependent NLRP3 activation, with a special focus on how major cell death programs are rendered pro-inflammatory by secondary NLRP3 activation.	Potassium	41-50	NLR family pyrin domain containing 3	Homo sapiens	183-188
29258746-0	2018	NLRP3 inflammasome inhibition attenuates silica-induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells.	Silicon Dioxide	41-47	NLR family pyrin domain containing 3	Homo sapiens	0-5
29258746-3	2018	NLRP3 inflammasome is a critical mediator of inflammation in response to a wide range of stimuli (including silica particles), and plays an important role in many respiratory diseases.	Silicon Dioxide	108-114	NLR family pyrin domain containing 3	Homo sapiens	0-5
29258746-4	2018	However, whether NLRP3 inflammasome regulates silica-induced EMT remains unknown.	Silicon Dioxide	46-52	NLR family pyrin domain containing 3	Homo sapiens	17-22
29258746-6	2018	Meanwhile, silica persistently activated NLRP3 inflammasome as indicated by continuously elevated extracellular levels of interleukin-1beta (IL-1beta) and IL-18.	Silicon Dioxide	11-17	NLR family pyrin domain containing 3	Homo sapiens	41-46
29258746-7	2018	NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	140-150	NLR family pyrin domain containing 3	Homo sapiens	0-5
29258746-7	2018	NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT.	Silicon Dioxide	162-168	NLR family pyrin domain containing 3	Homo sapiens	0-5
29258746-7	2018	NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT.	Silicon Dioxide	162-168	NLR family pyrin domain containing 3	Homo sapiens	81-86
29258746-9	2018	Moreover, pirfenidone, a commercially and clinically available drug approved for treating idiopathic pulmonary fibrosis (IPF), effectively suppressed silica-induced EMT of 16HBE cells in line with NLRP3 inflammasome inhibition.	pirfenidone	10-21	NLR family pyrin domain containing 3	Homo sapiens	197-202
29258746-9	2018	Moreover, pirfenidone, a commercially and clinically available drug approved for treating idiopathic pulmonary fibrosis (IPF), effectively suppressed silica-induced EMT of 16HBE cells in line with NLRP3 inflammasome inhibition.	Silicon Dioxide	150-156	NLR family pyrin domain containing 3	Homo sapiens	197-202
29127038-0	2018	Lysine-containing cationic liposomes activate the NLRP3 inflammasome: Effect of a spacer between the head group and the hydrophobic moieties of the lipids.	Lysine	0-6	NLR family pyrin domain containing 3	Homo sapiens	50-55
29127038-3	2018	Comparatively, L3C14 and L5C14 liposomes, made from the lipids bearing lysine head groups, ditetradecyl hydrophobic chains and propyl or pentyl spacers, respectively, were the most potent to activate the NLRP3 inflammasome.	Lysine	71-77	NLR family pyrin domain containing 3	Homo sapiens	204-209
29359681-0	2018	Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians.	Sodium	52-58	NLR family pyrin domain containing 3	Homo sapiens	15-20
29122594-0	2018	Inhibition of the NLRP3 inflammasome attenuates foam cell formation of THP-1 macrophages by suppressing ox-LDL uptake and promoting cholesterol efflux.	Cholesterol	132-143	NLR family pyrin domain containing 3	Homo sapiens	18-23
29122594-4	2018	Inhibition of the NLRP3 inflammasome attenuated foam cell formation, diminished ox-LDL uptake, and promoted cholesterol efflux from THP-1 macrophages.	Cholesterol	108-119	NLR family pyrin domain containing 3	Homo sapiens	18-23
29122594-6	2018	Collectively, our findings show that inhibition of the NLRP3 inflammasome decreases foam cell formation of THP-1 macrophages via suppression of ox-LDL uptake and enhancement of cholesterol efflux, which may be due to downregulation of CD36 expression and upregulation of ABCA1 and SR-BI expression, respectively.	Cholesterol	177-188	NLR family pyrin domain containing 3	Homo sapiens	55-60
29359681-0	2018	Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians.	Potassium	63-72	NLR family pyrin domain containing 3	Homo sapiens	15-20
29359681-8	2018	In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.	Acetylcysteine	22-41	NLR family pyrin domain containing 3	Homo sapiens	116-121
29359681-8	2018	In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.	Acetylcysteine	22-41	NLR family pyrin domain containing 3	Homo sapiens	202-207
29247992-3	2018	The NLRP3 inflammasome has been shown to sense metabolites such as palmitate, uric acid, and cholesterol crystals and is inhibited by ketone bodies produced during metabolic flux.	Palmitates	67-76	NLR family pyrin domain containing 3	Homo sapiens	4-9
30468127-5	2018	RESULTS: Exposure of SH-SY5Y cells to free-Mg2+ solutions increased the expression of NLRP3 inflammasome with a concomitant increase in neuronal apoptosis.	magnesium ion	43-47	NLR family pyrin domain containing 3	Homo sapiens	86-91
30138914-0	2018	Short-Chain Fatty Acids Manifest Stimulative and Protective Effects on Intestinal Barrier Function Through the Inhibition of NLRP3 Inflammasome and Autophagy.	Fatty Acids, Volatile	0-23	NLR family pyrin domain containing 3	Homo sapiens	125-130
30138914-6	2018	To activate NLRP3 inflammasome and autophagy, Caco-2 cells were treated with LPS+ATP and rapamycin respectively without or with SCFAs.	Adenosine Triphosphate	81-84	NLR family pyrin domain containing 3	Homo sapiens	12-17
30138914-6	2018	To activate NLRP3 inflammasome and autophagy, Caco-2 cells were treated with LPS+ATP and rapamycin respectively without or with SCFAs.	Sirolimus	89-98	NLR family pyrin domain containing 3	Homo sapiens	12-17
30138914-13	2018	In addition, the activation of autophagy and NLRP3 inflammasome by rapamycin and LPS+ATP resulted in TER reduction, paracellular permeability increase and morphological disruption of both ZO-1 and occludin, which was alleviated by SCFAs.	Adenosine Triphosphate	85-88	NLR family pyrin domain containing 3	Homo sapiens	45-50
30138927-1	2018	BACKGROUND/AIMS: Previously, we demonstrated that blockade of the intracellular clearance systems in human retinal pigment epithelial (RPE) cells by MG-132 and bafilomycin A1 (BafA) induces NLRP3 inflammasome signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-155	NLR family pyrin domain containing 3	Homo sapiens	190-195
30138927-3	2018	NLRP3 is an intracellular receptor detecting factors ranging from the endogenous alarmins and adenosine triphosphate (ATP) to ultraviolet radiation and solid particles.	Adenosine Triphosphate	94-116	NLR family pyrin domain containing 3	Homo sapiens	0-5
30138927-3	2018	NLRP3 is an intracellular receptor detecting factors ranging from the endogenous alarmins and adenosine triphosphate (ATP) to ultraviolet radiation and solid particles.	Adenosine Triphosphate	118-121	NLR family pyrin domain containing 3	Homo sapiens	0-5
30138927-6	2018	METHODS: NLRP3 inflammasomes were activated in human RPE cells by blocking proteasomes and autophagy using MG-132 and bafilomycin A1 (BafA), respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	NLR family pyrin domain containing 3	Homo sapiens	9-14
30138927-6	2018	METHODS: NLRP3 inflammasomes were activated in human RPE cells by blocking proteasomes and autophagy using MG-132 and bafilomycin A1 (BafA), respectively.	bafilomycin	118-129	NLR family pyrin domain containing 3	Homo sapiens	9-14
30138927-6	2018	METHODS: NLRP3 inflammasomes were activated in human RPE cells by blocking proteasomes and autophagy using MG-132 and bafilomycin A1 (BafA), respectively.	bafilomycin A1	134-138	NLR family pyrin domain containing 3	Homo sapiens	9-14
29214547-1	2018	The NLRP3-interleukin1beta (IL1beta) signaling pathway is involved in monosodium urate (MSU)-mediated inflammation.	Uric Acid	70-86	NLR family pyrin domain containing 3	Homo sapiens	4-9
29214547-1	2018	The NLRP3-interleukin1beta (IL1beta) signaling pathway is involved in monosodium urate (MSU)-mediated inflammation.	Uric Acid	88-91	NLR family pyrin domain containing 3	Homo sapiens	4-9
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	98-102	NLR family pyrin domain containing 3	Homo sapiens	76-81
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	98-102	NLR family pyrin domain containing 3	Homo sapiens	138-143
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	98-102	NLR family pyrin domain containing 3	Homo sapiens	138-143
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	76-81
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	138-143
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	138-143
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	76-81
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	138-143
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	NLR family pyrin domain containing 3	Homo sapiens	138-143
29145789-8	2018	Moreover, secreted IL-10 correlated with the down-regulation of nigericin-induced NLRP3 inflammasome activation of LPS-primed THP-1 monocytes and human PBMCs from volunteers.	Nigericin	64-73	NLR family pyrin domain containing 3	Homo sapiens	82-87
29100037-4	2018	Dexmedetomidine (Dex) has been documented to protect the liver against ischemia-reperfusion injury via the suppression of the TLR4/NF-kappaB pathway, which is important for NLRP3 inflammasome activation and liver regeneration.	Dexmedetomidine	0-15	NLR family pyrin domain containing 3	Homo sapiens	173-178
29247992-3	2018	The NLRP3 inflammasome has been shown to sense metabolites such as palmitate, uric acid, and cholesterol crystals and is inhibited by ketone bodies produced during metabolic flux.	Uric Acid	78-87	NLR family pyrin domain containing 3	Homo sapiens	4-9
29100037-4	2018	Dexmedetomidine (Dex) has been documented to protect the liver against ischemia-reperfusion injury via the suppression of the TLR4/NF-kappaB pathway, which is important for NLRP3 inflammasome activation and liver regeneration.	Dexmedetomidine	0-3	NLR family pyrin domain containing 3	Homo sapiens	173-178
29247992-3	2018	The NLRP3 inflammasome has been shown to sense metabolites such as palmitate, uric acid, and cholesterol crystals and is inhibited by ketone bodies produced during metabolic flux.	Cholesterol	93-104	NLR family pyrin domain containing 3	Homo sapiens	4-9
29247992-3	2018	The NLRP3 inflammasome has been shown to sense metabolites such as palmitate, uric acid, and cholesterol crystals and is inhibited by ketone bodies produced during metabolic flux.	Ketones	134-140	NLR family pyrin domain containing 3	Homo sapiens	4-9
29100037-9	2018	In vivo, Dex+PHx exhibited promoted effect on liver regeneration and liver function recovery via inhibiting NLRP3 inflammasome activation.	dex+phx	9-16	NLR family pyrin domain containing 3	Homo sapiens	108-113
29247992-4	2018	The NLRP3 inflammasome has also been shown to be regulated by mitochondrial reactive oxygen species and components of glycolysis, such as Hexokinase.	Reactive Oxygen Species	76-99	NLR family pyrin domain containing 3	Homo sapiens	4-9
30014749-4	2018	Although reactive oxygen species (ROS) were reported to be involved in activation of NLRP3 inflammasome, we were hypothesized that IAPP could directly activate NLRP3 inflammasome, leading to islets beta-cell death.	Reactive Oxygen Species	9-32	NLR family pyrin domain containing 3	Homo sapiens	85-90
29107864-0	2018	TRPM2 dependence of ROS-induced NLRP3 activation in Alzheimer"s disease.	Reactive Oxygen Species	20-23	NLR family pyrin domain containing 3	Homo sapiens	32-37
29107864-6	2018	According to this study, ROS produced from both mitochondria and NADPH oxidase was responsible for NLRP3 activation.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	99-104
29107864-9	2018	Altogether, our findings supported the role of TRPM2 channel in ROS-induced NLRP3 activation in microglial cells through the exposure to Abeta.	Reactive Oxygen Species	64-67	NLR family pyrin domain containing 3	Homo sapiens	76-81
30014749-4	2018	Although reactive oxygen species (ROS) were reported to be involved in activation of NLRP3 inflammasome, we were hypothesized that IAPP could directly activate NLRP3 inflammasome, leading to islets beta-cell death.	Reactive Oxygen Species	34-37	NLR family pyrin domain containing 3	Homo sapiens	85-90
29229137-0	2018	Effects of MgSO4 on inhibiting Nod-like receptor protein 3 inflammasome involve decreasing intracellular calcium.	Calcium	105-112	NLR family pyrin domain containing 3	Homo sapiens	31-58
30123891-6	2018	Excessive ROS can then result in activation of the NLRP3 inflammasome and secretion of IL-1 and IL-18 by caspase-1.	Reactive Oxygen Species	10-13	NLR family pyrin domain containing 3	Homo sapiens	51-56
29229137-3	2018	Of note, calcium signaling is crucial for NLRP3 inflammasome activation.	Calcium	9-16	NLR family pyrin domain containing 3	Homo sapiens	42-47
29229137-0	2018	Effects of MgSO4 on inhibiting Nod-like receptor protein 3 inflammasome involve decreasing intracellular calcium.	Magnesium Sulfate	11-16	NLR family pyrin domain containing 3	Homo sapiens	31-58
29229137-4	2018	This study elucidated the effects of magnesium sulfate (MgSO4), a potent calcium antagonist, on modulating NLRP3 inflammasome.	Magnesium Sulfate	37-54	NLR family pyrin domain containing 3	Homo sapiens	107-112
29229137-4	2018	This study elucidated the effects of magnesium sulfate (MgSO4), a potent calcium antagonist, on modulating NLRP3 inflammasome.	Magnesium Sulfate	56-61	NLR family pyrin domain containing 3	Homo sapiens	107-112
29229137-4	2018	This study elucidated the effects of magnesium sulfate (MgSO4), a potent calcium antagonist, on modulating NLRP3 inflammasome.	Calcium	73-80	NLR family pyrin domain containing 3	Homo sapiens	107-112
29229137-13	2018	CONCLUSIONS: MgSO4 inhibits NLRP3 inflammasome, IL-1beta upregulation, and pyroptosis.	Magnesium Sulfate	13-18	NLR family pyrin domain containing 3	Homo sapiens	28-33
29263464-0	2017	[Effect of high glucose-based peritoneal dialysis fluids on NLRP3-IL-1beta in human peritoneal mesothelial cells].	Glucose	16-23	NLR family pyrin domain containing 3	Homo sapiens	60-65
29031534-13	2017	The expression levels of TXNIP, NLRP3, ASC, and caspase-1 were reduced in the SAL treated cells.	rhodioloside	78-81	NLR family pyrin domain containing 3	Homo sapiens	32-37
29262323-0	2017	Extracellular ATP Activates the NLRP3 Inflammasome and Is an Early Danger Signal of Skin Allograft Rejection.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	32-37
29262323-3	2017	ATP then acts via a feedback mechanism on the P2X7 channel to activate the NLRP3 inflammasome and subsequently process and release interleukin (IL)-18.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	75-80
29263464-12	2017	We also found that downregulation of ATG5 and Beclin1 sensitized cells for the release of IL-1beta induced by MSU (monosodium urate) or nigericin which was the NLRP3 inflammasome activator.	Uric Acid	110-115	NLR family pyrin domain containing 3	Homo sapiens	160-165
29263464-12	2017	We also found that downregulation of ATG5 and Beclin1 sensitized cells for the release of IL-1beta induced by MSU (monosodium urate) or nigericin which was the NLRP3 inflammasome activator.	Uric Acid	115-131	NLR family pyrin domain containing 3	Homo sapiens	160-165
28952191-10	2018	NLRP3, which plays a central role in inflammation and STARD3 that is involved in cholesterol metabolism, were identified as hub genes for the respective modules.	Cholesterol	81-92	NLR family pyrin domain containing 3	Homo sapiens	0-5
29651937-9	2018	To date many promising inhibitors of inflammasome complex activation have been described, such as MCC950, beta-Hydroxybutyrate or Micro RNAs that affect NALP3 expression and activation.	Hydroxybutyrates	111-126	NLR family pyrin domain containing 3	Homo sapiens	153-158
29263464-12	2017	We also found that downregulation of ATG5 and Beclin1 sensitized cells for the release of IL-1beta induced by MSU (monosodium urate) or nigericin which was the NLRP3 inflammasome activator.	Nigericin	136-145	NLR family pyrin domain containing 3	Homo sapiens	160-165
29263464-1	2017	OBJECTIVE: To explore the effect of high glucose-based peritoneal dialysis fluids on NLRP3-IL-1beta in human peritoneal mesothelial cells.	Glucose	41-48	NLR family pyrin domain containing 3	Homo sapiens	85-90
29263464-14	2017	CONCLUSION: Long-term application of high glucose-based peritoneal dialysis fluids can trigger the consistent activation of NLRP3-IL-1beta in peritoneal mesothelial cells.	Glucose	42-49	NLR family pyrin domain containing 3	Homo sapiens	124-129
29255148-4	2017	This mechanism prevents collapse of mitochondrial membrane potential and the subsequent release of mitochondrial DNA and reactive oxygen species, thus preventing hyperactivation of NLRP3 inflammasome.	Reactive Oxygen Species	121-144	NLR family pyrin domain containing 3	Homo sapiens	181-186
28940479-0	2017	Activation of the NLRP3 inflammasome in microglia: the role of ceramide.	Ceramides	63-71	NLR family pyrin domain containing 3	Homo sapiens	18-23
28968864-6	2017	Low doses of silica induced NLRP3 activation, DNA damage accumulation, and ATM phosphorylation.	Silicon Dioxide	13-19	NLR family pyrin domain containing 3	Homo sapiens	28-33
29030458-6	2017	Additionally, when combined with a priming signal, cGAMP activates the inflammasome through an AIM2, NLRP3, ASC, and caspase-1 dependent process.	cyclic guanosine monophosphate-adenosine monophosphate	51-56	NLR family pyrin domain containing 3	Homo sapiens	101-106
28940479-12	2017	Taken together, our findings reveal a critical role for ceramide as a positive modulator of NLRP3 inflammasome assembly and the resulting release of IL-1beta.	Ceramides	56-64	NLR family pyrin domain containing 3	Homo sapiens	92-97
29258239-0	2017	MicroRNA-132 Negatively Regulates Palmitate-Induced NLRP3 Inflammasome Activation through FOXO3 Down-Regulation in THP-1 Cells.	Palmitates	34-43	NLR family pyrin domain containing 3	Homo sapiens	52-57
29258239-1	2017	Saturated fatty acids were proposed to activate the NLRP3 inflammasome, a molecular platform that mediates the processing of interleukin (IL)-1beta and IL-18.	Fatty Acids	0-21	NLR family pyrin domain containing 3	Homo sapiens	52-57
29258239-3	2017	We examined the role of miR-132 in PA-induced NLRP3 inflammasome activation in THP-1 cells.	Palmitates	35-37	NLR family pyrin domain containing 3	Homo sapiens	46-51
29258239-4	2017	To understand the regulatory role of miR-132 in inflammasome activation, we either overexpressed or suppressed miR-132 in THP-1 cells that expressed the NLRP3 inflammasome in response to stimulation by PA.	Palmitates	202-204	NLR family pyrin domain containing 3	Homo sapiens	153-158
29258239-6	2017	The presence of PA activated the NLRP3 inflammasome and increased miR-132 expression.	Palmitates	16-18	NLR family pyrin domain containing 3	Homo sapiens	33-38
29258239-9	2017	FOXO3 suppression by small interfering RNA decreased NLRP3 inflammasome activity stimulated by PA.	Palmitates	95-97	NLR family pyrin domain containing 3	Homo sapiens	53-58
29258239-11	2017	Based on these findings, we conclude that miR-132 negatively regulates PA-induced NLRP3 inflammasome activation through FOXO3 down-regulation in THP-1 cells.	Palmitates	71-73	NLR family pyrin domain containing 3	Homo sapiens	82-87
28836226-4	2017	Recently the ketone body, beta-hydroxy butyrate (BHB), was shown to efficiently inhibit the NLRP3 inflammasome in macrophages, and in vivo models of inflammatory disease.	Ketones	13-19	NLR family pyrin domain containing 3	Homo sapiens	92-97
28836226-4	2017	Recently the ketone body, beta-hydroxy butyrate (BHB), was shown to efficiently inhibit the NLRP3 inflammasome in macrophages, and in vivo models of inflammatory disease.	3-Hydroxybutyric Acid	26-47	NLR family pyrin domain containing 3	Homo sapiens	92-97
28836226-4	2017	Recently the ketone body, beta-hydroxy butyrate (BHB), was shown to efficiently inhibit the NLRP3 inflammasome in macrophages, and in vivo models of inflammatory disease.	3-Hydroxybutyric Acid	49-52	NLR family pyrin domain containing 3	Homo sapiens	92-97
28940479-5	2017	Growing evidence suggests that ceramide plays a critical role in NLRP3 inflammasome assembly, however, the relationship between ceramide and inflammasome activation in microglia remains unknown.	Ceramides	31-39	NLR family pyrin domain containing 3	Homo sapiens	65-70
28940479-6	2017	Here, we investigated potential mechanistic links between ceramide as a modulator of NLRP3 inflammasome assembly and the resulting secretion of IL-1beta using small bioactive enzyme stimulators and inhibitors of ceramide signaling in wild-type and apoptosis-associated speck-like protein containing a CARD knockout (ASC-/- ) primary microglia.	Ceramides	58-66	NLR family pyrin domain containing 3	Homo sapiens	85-90
29187200-2	2017	While plasma HDL level almost exclusively depends on concentration of LpAI having 3 to 4 apoA-I molecules, LpAI:AII appeared with almost constant concentration regardless of plasma HDL levels having stable structure with two apoA-I and one disulfide-dimeric apoA-II molecules (Sci.	lpai	107-111	NLR family pyrin domain containing 3	Homo sapiens	112-115
29187200-7	2017	In contrast, apoA-I in LpAI:AII and apoA-II positively correlated to the apoB-lipoprotein parameters even within their small range of variation.	lpai	23-27	NLR family pyrin domain containing 3	Homo sapiens	28-31
28943355-0	2017	Boron-Based Inhibitors of the NLRP3 Inflammasome.	Boron	0-5	NLR family pyrin domain containing 3	Homo sapiens	30-35
29033128-4	2017	Instead, detection of cytosolic DNA by the cGAS-STING axis induces a cell death program initiating potassium efflux upstream of NLRP3.	Potassium	99-108	NLR family pyrin domain containing 3	Homo sapiens	128-133
29312598-6	2017	In the present study, we demonstrated that IL-22 promoting IL-1beta secretion from keratinocytes via the Reactive oxygen species (ROS)-NOD-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1 pathway.	Reactive Oxygen Species	105-128	NLR family pyrin domain containing 3	Homo sapiens	188-193
29312598-6	2017	In the present study, we demonstrated that IL-22 promoting IL-1beta secretion from keratinocytes via the Reactive oxygen species (ROS)-NOD-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1 pathway.	Reactive Oxygen Species	130-133	NLR family pyrin domain containing 3	Homo sapiens	188-193
28972154-3	2017	We hypothesized that raising glucose above the physiological level of 5.5 mm would stimulate leukocytes to produce MPs and activate the nucleotide-binding domain, leucine-rich repeat pyrin domain-containing 3 (NLRP3) inflammasome.	Glucose	29-36	NLR family pyrin domain containing 3	Homo sapiens	210-215
28942022-0	2017	X-11-5-27, a daidzein derivative, inhibits NLRP3 inflammasome activity via promoting autophagy.	daidzein	13-21	NLR family pyrin domain containing 3	Homo sapiens	43-48
28942022-2	2017	In our study, we investigate the inhibitory effect of X-11-5-27, a daidzein derivative, on the NLRP3 inflammasome.	x-11-5-27	54-63	NLR family pyrin domain containing 3	Homo sapiens	95-100
28942022-2	2017	In our study, we investigate the inhibitory effect of X-11-5-27, a daidzein derivative, on the NLRP3 inflammasome.	daidzein	67-75	NLR family pyrin domain containing 3	Homo sapiens	95-100
28942022-3	2017	The results showed that the activation of NLRP3 inflammasome was inhibited by X-11-5-27 in a dose-dependent manner, followed by a decrease in the cleavage of caspase-1 and maturation of IL-1beta.	x-11	78-82	NLR family pyrin domain containing 3	Homo sapiens	42-47
28942022-10	2017	In conclusion, our results demonstrate that autophagy-mediated ROS reduction is responsible for X-11-5-27-induced NLRP3 flammasome inactivation.	ros	63-66	NLR family pyrin domain containing 3	Homo sapiens	114-119
29170665-14	2017	In conclusion, this study describes a differential response of NLRP3 to beta-glucan and CpG antigens and identifies the NLRP3 inflammasome of human circulating B-lymphocytes as a modulator of the innate and adaptive immune systems.	beta-Glucans	72-83	NLR family pyrin domain containing 3	Homo sapiens	63-68
29021150-3	2017	Here we show that the compound CY-09 specifically blocks NLRP3 inflammasome activation.	CY5.5 cyanine dye	31-36	NLR family pyrin domain containing 3	Homo sapiens	57-62
29021150-4	2017	CY-09 directly binds to the ATP-binding motif of NLRP3 NACHT domain and inhibits NLRP3 ATPase activity, resulting in the suppression of NLRP3 inflammasome assembly and activation.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	49-54
29021150-4	2017	CY-09 directly binds to the ATP-binding motif of NLRP3 NACHT domain and inhibits NLRP3 ATPase activity, resulting in the suppression of NLRP3 inflammasome assembly and activation.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	81-86
29021150-4	2017	CY-09 directly binds to the ATP-binding motif of NLRP3 NACHT domain and inhibits NLRP3 ATPase activity, resulting in the suppression of NLRP3 inflammasome assembly and activation.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	81-86
29021150-4	2017	CY-09 directly binds to the ATP-binding motif of NLRP3 NACHT domain and inhibits NLRP3 ATPase activity, resulting in the suppression of NLRP3 inflammasome assembly and activation.	Adenosine Triphosphate	28-31	NLR family pyrin domain containing 3	Homo sapiens	49-54
29096724-9	2017	RESULTS: Treating HepG2 cells with PA-LPS caused NLRP3 inflammation activation, including overexpression of NLRP3 and caspase-1, and overproduction of IL-1beta and IL-18 as well as TNF-alpha from HepG2 cells.	pa-lps	35-41	NLR family pyrin domain containing 3	Homo sapiens	49-54
29096724-9	2017	RESULTS: Treating HepG2 cells with PA-LPS caused NLRP3 inflammation activation, including overexpression of NLRP3 and caspase-1, and overproduction of IL-1beta and IL-18 as well as TNF-alpha from HepG2 cells.	pa-lps	35-41	NLR family pyrin domain containing 3	Homo sapiens	108-113
29096724-12	2017	Furthermore, knockdown of NLRP3 or IL-1beta partially improved PA and LPS-induced insulin signaling impairments in the presence of UC-MSCs.	Palmitic Acid	63-65	NLR family pyrin domain containing 3	Homo sapiens	26-31
29263046-0	2017	Berberine Attenuates NLRP3 Inflammasome Activation in Macrophages to Reduce the Secretion of Interleukin-1beta.	Berberine	0-9	NLR family pyrin domain containing 3	Homo sapiens	21-26
29263046-4	2017	Human peripheral blood mononuclear cells were then pretreated with different concentrations of berberine after treatment with NLRP3 activator ATP.	Berberine	95-104	NLR family pyrin domain containing 3	Homo sapiens	126-131
29263046-7	2017	RESULTS: In this study we observed that berberine suppressed IL-1beta secretion that was induced by the activation of the NLRP3 inflammasome in macrophages.	Berberine	40-49	NLR family pyrin domain containing 3	Homo sapiens	122-127
29263046-8	2017	In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation.	Berberine	34-43	NLR family pyrin domain containing 3	Homo sapiens	104-109
29263046-8	2017	In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation.	Reactive Oxygen Species	64-87	NLR family pyrin domain containing 3	Homo sapiens	104-109
29263046-8	2017	In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation.	Reactive Oxygen Species	89-92	NLR family pyrin domain containing 3	Homo sapiens	104-109
29263046-10	2017	CONCLUSION: Our results suggest that berberine alleviates NLRP3 inflammation activation by reducing IL-1beta secretion from macrophages, which could be an important therapeutic target in atherosclerosis.	Berberine	37-46	NLR family pyrin domain containing 3	Homo sapiens	58-63
29113588-0	2017	Silica nanoparticles induce NLRP3 inflammasome activation in human primary immune cells.	Silicon Dioxide	0-6	NLR family pyrin domain containing 3	Homo sapiens	28-33
29118033-0	2017	Trimethylamine-N-Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3-SOD2-mtROS Signaling Pathway.	trimethyloxamine	0-22	NLR family pyrin domain containing 3	Homo sapiens	71-76
28729291-2	2017	Here, we show that the NLRP3-activating agonists, ATP and nigericin, prevent STING pathway activation in association with mitochondrial fragmentation; however, the suppression of the STING pathway and mitochondria fission were not dependent on NLRP3 or potassium efflux.	Adenosine Triphosphate	50-53	NLR family pyrin domain containing 3	Homo sapiens	23-28
28729291-2	2017	Here, we show that the NLRP3-activating agonists, ATP and nigericin, prevent STING pathway activation in association with mitochondrial fragmentation; however, the suppression of the STING pathway and mitochondria fission were not dependent on NLRP3 or potassium efflux.	Nigericin	58-67	NLR family pyrin domain containing 3	Homo sapiens	23-28
28729291-2	2017	Here, we show that the NLRP3-activating agonists, ATP and nigericin, prevent STING pathway activation in association with mitochondrial fragmentation; however, the suppression of the STING pathway and mitochondria fission were not dependent on NLRP3 or potassium efflux.	Potassium	253-262	NLR family pyrin domain containing 3	Homo sapiens	23-28
28116820-8	2017	T allele of NLRP3 rs4612666 had a significantly greater negative impact on the ASAS20 improvement than C allele.	asas20	79-85	NLR family pyrin domain containing 3	Homo sapiens	12-17
28116820-9	2017	Whereas the A allele of NLRP3 rs3806268 had a significantly greater positive impact on the ASAS20 improvement than G allele.	asas20	91-97	NLR family pyrin domain containing 3	Homo sapiens	24-29
29078913-11	2017	CONCLUSIONS: Naloxone inhibits NLRP3 inflammasome activation.	Naloxone	13-21	NLR family pyrin domain containing 3	Homo sapiens	31-36
28532674-3	2017	Furthermore, we propose a mechanism by which a known neurotoxin, beta-N-methylamino-l-alanine (BMAA), may trigger this cytokine expression profile through motor neuron protein misfolding and subsequent NLRP3 (nucleotide-binding domain (NOD)-like receptor protein 3) inflammasome activation.	beta-N-methylamino-L-alanine	65-93	NLR family pyrin domain containing 3	Homo sapiens	202-207
29057315-6	2017	Interestingly, exposure of LPS-primed microglial cells to the mitochondrial complex-I inhibitory pesticides rotenone and tebufenpyrad specifically potentiated the NLRP3 induction, ASC speck formation and pro-IL-1beta processing to IL-1beta in a dose-dependent manner, indicating that mitochondrial impairment heightened the NLRP3 inflammasome-mediated proinflammatory response in microglia.	Rotenone	108-116	NLR family pyrin domain containing 3	Homo sapiens	163-168
29057315-6	2017	Interestingly, exposure of LPS-primed microglial cells to the mitochondrial complex-I inhibitory pesticides rotenone and tebufenpyrad specifically potentiated the NLRP3 induction, ASC speck formation and pro-IL-1beta processing to IL-1beta in a dose-dependent manner, indicating that mitochondrial impairment heightened the NLRP3 inflammasome-mediated proinflammatory response in microglia.	Rotenone	108-116	NLR family pyrin domain containing 3	Homo sapiens	324-329
29057315-8	2017	Furthermore, the pesticides enhanced mitochondrial ROS generation in primary microglia, while amelioration of mitochondria-derived ROS by the mitochondria-targeted antioxidant mito-apocynin completely abolished IL-1beta release, indicating mitochondrial ROS drives potentiation of the NLRP3 inflammasome in microglia.	ros	131-134	NLR family pyrin domain containing 3	Homo sapiens	285-290
29057315-8	2017	Furthermore, the pesticides enhanced mitochondrial ROS generation in primary microglia, while amelioration of mitochondria-derived ROS by the mitochondria-targeted antioxidant mito-apocynin completely abolished IL-1beta release, indicating mitochondrial ROS drives potentiation of the NLRP3 inflammasome in microglia.	ros	131-134	NLR family pyrin domain containing 3	Homo sapiens	285-290
29057315-10	2017	Notably, our in vivo results with chronic rotenone rodent models of PD further support the activation of proinflammatory NLRP3 inflammasome signaling due to mitochondrial dysfunction.	Rotenone	42-50	NLR family pyrin domain containing 3	Homo sapiens	121-126
29078913-0	2017	Naloxone inhibits nod-like receptor protein 3 inflammasome.	Naloxone	0-8	NLR family pyrin domain containing 3	Homo sapiens	18-45
29078913-4	2017	We elucidated whether naloxone could inhibit the activation of NLRP3 inflammasome.	Naloxone	22-30	NLR family pyrin domain containing 3	Homo sapiens	63-68
28653829-7	2017	Collectively, these results suggest that JC-171 is a selective NLRP3 inflammasome inhibitor with biological activity in vivo, thus strongly encouraging further development of this lead compound as a potential therapeutic agent for human MS.	CHEMBL4583133	41-47	NLR family pyrin domain containing 3	Homo sapiens	63-68
28904126-5	2017	Treatment of primary monocytes with the NLRP3 inhibitor MCC950 or with extracellular potassium significantly reduced IL-1beta cleavage and release in response to T. gondii infection, without affecting the release of TNF-alpha, and indicated a role for the inflammasome sensor NLRP3 and for potassium efflux in T. gondii-induced IL-1beta production.	Potassium	85-94	NLR family pyrin domain containing 3	Homo sapiens	276-281
28904126-5	2017	Treatment of primary monocytes with the NLRP3 inhibitor MCC950 or with extracellular potassium significantly reduced IL-1beta cleavage and release in response to T. gondii infection, without affecting the release of TNF-alpha, and indicated a role for the inflammasome sensor NLRP3 and for potassium efflux in T. gondii-induced IL-1beta production.	Potassium	290-299	NLR family pyrin domain containing 3	Homo sapiens	40-45
28904126-8	2017	To our knowledge, these findings are the first to identify NLRP3 as an inflammasome sensor for T. gondii in primary human peripheral blood cells and to define an upstream regulator of its activation through the release of intracellular potassium.	Potassium	236-245	NLR family pyrin domain containing 3	Homo sapiens	59-64
28532674-3	2017	Furthermore, we propose a mechanism by which a known neurotoxin, beta-N-methylamino-l-alanine (BMAA), may trigger this cytokine expression profile through motor neuron protein misfolding and subsequent NLRP3 (nucleotide-binding domain (NOD)-like receptor protein 3) inflammasome activation.	beta-N-methylamino-L-alanine	95-99	NLR family pyrin domain containing 3	Homo sapiens	202-207
29067455-0	2017	Hyperbaric oxygen alleviates the activation of NLRP-3-inflammasomes in traumatic brain injury.	Oxygen	11-17	NLR family pyrin domain containing 3	Homo sapiens	47-53
31966371-2	2017	Mutations of SCN2A, the gene encoding the aII subunit of the voltage-gated sodium channel (Nav1.2), have been detected in some EOEE patients.	Sodium	75-81	NLR family pyrin domain containing 3	Homo sapiens	42-45
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	polyinosinic:	15-28	NLR family pyrin domain containing 3	Homo sapiens	331-336
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	48-56	NLR family pyrin domain containing 3	Homo sapiens	331-336
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	196-204	NLR family pyrin domain containing 3	Homo sapiens	331-336
28266737-7	2017	The activation of keratinocyte NLRP3 inflammasome by transfected poly I:C was dependent on dsRNA-induced protein kinase (PKR) activation, and priming with type I interferons upregulated NLRP3 inflammasome activation through promoting PKR activation in poly I:C-transfected keratinocytes.	Iodine	70-71	NLR family pyrin domain containing 3	Homo sapiens	31-36
28266737-7	2017	The activation of keratinocyte NLRP3 inflammasome by transfected poly I:C was dependent on dsRNA-induced protein kinase (PKR) activation, and priming with type I interferons upregulated NLRP3 inflammasome activation through promoting PKR activation in poly I:C-transfected keratinocytes.	Iodine	70-71	NLR family pyrin domain containing 3	Homo sapiens	186-191
28266737-7	2017	The activation of keratinocyte NLRP3 inflammasome by transfected poly I:C was dependent on dsRNA-induced protein kinase (PKR) activation, and priming with type I interferons upregulated NLRP3 inflammasome activation through promoting PKR activation in poly I:C-transfected keratinocytes.	Poly I-C	65-73	NLR family pyrin domain containing 3	Homo sapiens	31-36
28216434-6	2017	RESULTS: Here we show that BTK is a critical regulator of NLRP3 inflammasome activation: pharmacologic (using the US Food and Drug Administration-approved inhibitor ibrutinib) and genetic (in patients with XLA and Btk knockout mice) BTK ablation in primary immune cells led to reduced IL-1beta processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin AB (LukAB).	ibrutinib	165-174	NLR family pyrin domain containing 3	Homo sapiens	58-63
28216434-6	2017	RESULTS: Here we show that BTK is a critical regulator of NLRP3 inflammasome activation: pharmacologic (using the US Food and Drug Administration-approved inhibitor ibrutinib) and genetic (in patients with XLA and Btk knockout mice) BTK ablation in primary immune cells led to reduced IL-1beta processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin AB (LukAB).	Nigericin	334-343	NLR family pyrin domain containing 3	Homo sapiens	58-63
29056256-0	2017	Glibenclamide inhibits NLRP3 inflammasome-mediated IL-1beta secretion in human trophoblasts.	Glyburide	0-13	NLR family pyrin domain containing 3	Homo sapiens	23-28
29056256-7	2017	In addition, dibutyryl-cAMP, which induces trophoblast differentiation, decreased expression of NLRP3, caspase-1, and IL-1beta.	Bucladesine	13-27	NLR family pyrin domain containing 3	Homo sapiens	96-101
29056256-8	2017	These findings suggest that trophoblasts can secrete IL-1beta through the NLRP3/caspase-1 pathway, which is suppressed by glibenclamide, and that the TLR4-mediated NLRP3 inflammasome pathway is more likely to be stimulated in undifferentiated than differentiated trophoblasts.	Glyburide	122-135	NLR family pyrin domain containing 3	Homo sapiens	74-79
29067455-2	2017	In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP-3 inflammasome pathway following TBI.	Oxygen	73-79	NLR family pyrin domain containing 3	Homo sapiens	101-107
28870124-0	2017	Reactive oxygen species trigger NF-kappaB-mediated NLRP3 inflammasome activation induced by zinc oxide nanoparticles in A549 cells.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	51-56
28849014-0	2017	Zinc inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells.	Glucose	19-26	NLR family pyrin domain containing 3	Homo sapiens	35-40
28849014-1	2017	Zinc (Zn) deficiency is important for inducing nucleotide-binding domain and leucine-rich repeat-containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation in macrophages.	Zinc	6-8	NLR family pyrin domain containing 3	Homo sapiens	143-148
28849014-6	2017	It was found that Zn supplementation inhibited HG-induced NLRP3 inflammasome activation in the HPMCs by attenuating ROS production.	Zinc	18-20	NLR family pyrin domain containing 3	Homo sapiens	58-63
28849014-6	2017	It was found that Zn supplementation inhibited HG-induced NLRP3 inflammasome activation in the HPMCs by attenuating ROS production.	Reactive Oxygen Species	116-119	NLR family pyrin domain containing 3	Homo sapiens	58-63
28849014-8	2017	These results indicated that Zn inhibited NLRP3 inflammasome activation in the HG-treated HPMCs by activating the Nrf2 antioxidant pathway and reducing the production of ROS.	Zinc	29-31	NLR family pyrin domain containing 3	Homo sapiens	42-47
28849014-8	2017	These results indicated that Zn inhibited NLRP3 inflammasome activation in the HG-treated HPMCs by activating the Nrf2 antioxidant pathway and reducing the production of ROS.	Hypromellose Derivatives	90-95	NLR family pyrin domain containing 3	Homo sapiens	42-47
28849014-8	2017	These results indicated that Zn inhibited NLRP3 inflammasome activation in the HG-treated HPMCs by activating the Nrf2 antioxidant pathway and reducing the production of ROS.	Reactive Oxygen Species	170-173	NLR family pyrin domain containing 3	Homo sapiens	42-47
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	126-129	NLR family pyrin domain containing 3	Homo sapiens	29-34
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	126-129	NLR family pyrin domain containing 3	Homo sapiens	170-175
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	206-209	NLR family pyrin domain containing 3	Homo sapiens	29-34
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	206-209	NLR family pyrin domain containing 3	Homo sapiens	170-175
28870124-8	2017	Meanwhile, NAC pretreatment inhibited ZnO-NPs-induced activation of NF-kappaB and NLRP3 inflammasome.	Zinc Oxide	38-41	NLR family pyrin domain containing 3	Homo sapiens	82-87
28870124-0	2017	Reactive oxygen species trigger NF-kappaB-mediated NLRP3 inflammasome activation induced by zinc oxide nanoparticles in A549 cells.	Zinc Oxide	92-102	NLR family pyrin domain containing 3	Homo sapiens	51-56
28870124-9	2017	The NF-kappaB inhibitor BAY11-7082 did not affect ROS production but significantly reduced the NLRP3 inflammasome activation induced by ZnO-NPs.	3-(4-methylphenylsulfonyl)-2-propenenitrile	24-34	NLR family pyrin domain containing 3	Homo sapiens	95-100
28870124-11	2017	The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway.	Zinc Oxide	4-7	NLR family pyrin domain containing 3	Homo sapiens	42-47
28870124-11	2017	The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway.	Zinc Oxide	4-7	NLR family pyrin domain containing 3	Homo sapiens	111-116
28870124-11	2017	The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway.	Reactive Oxygen Species	97-100	NLR family pyrin domain containing 3	Homo sapiens	42-47
28870124-11	2017	The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway.	Reactive Oxygen Species	97-100	NLR family pyrin domain containing 3	Homo sapiens	111-116
29312552-6	2017	NLRP3 inflammasome could be activated by ATP plus LPS in lymphoma cells accompanied with the increasing expression of NLRP3-related genes.	Adenosine Triphosphate	41-44	NLR family pyrin domain containing 3	Homo sapiens	0-5
29312552-6	2017	NLRP3 inflammasome could be activated by ATP plus LPS in lymphoma cells accompanied with the increasing expression of NLRP3-related genes.	Adenosine Triphosphate	41-44	NLR family pyrin domain containing 3	Homo sapiens	118-123
29312552-7	2017	NLRP3 inflammasome activation reduced the dexamethasone-induced proliferation-inhibiting effect by promoting cells into S phase.	Dexamethasone	42-55	NLR family pyrin domain containing 3	Homo sapiens	0-5
29312552-8	2017	NLRP3 inflammasome activation promoted lymphoma cells proliferation and inhibited apoptosis through up-regulation of c-myc and bcl-2, and down-regulation of TP53 and bax, and then reduced the anti-tumor effect of dexamethasone.	Dexamethasone	213-226	NLR family pyrin domain containing 3	Homo sapiens	0-5
28778433-3	2017	LPC-induced caspase-1 activation in microglia was found to depend on LPS prestimulation, inflammasome NLRP3 and adaptor molecule ASC.	Lysophosphatidylcholines	0-3	NLR family pyrin domain containing 3	Homo sapiens	102-107
28739604-6	2017	Transcriptome analysis of isolated TAMs from both entities revealed reduced expression of the inflammasome component Nlrp3 in S1PR1-deficient TAMs.	tams	35-39	NLR family pyrin domain containing 3	Homo sapiens	117-122
29259717-3	2017	Recent studies suggest that cholesterol crystals play a pivotal role in activation of NLRP3 inflammasomes, which regulate caspase-1 activation and the subsequent processing of IL-1beta, in atherosclerotic lesions.	Cholesterol	28-39	NLR family pyrin domain containing 3	Homo sapiens	86-91
29245937-0	2017	NLRP3-inflammasome inhibition prevents high fat and high sugar diets-induced heart damage through autophagy induction.	Sugars	57-62	NLR family pyrin domain containing 3	Homo sapiens	0-5
28887507-8	2017	CA inhibited DSS-induced NLRP3 inflammasome activation by reducing caspase 1 activity.	dss	13-16	NLR family pyrin domain containing 3	Homo sapiens	25-30
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	52-62	NLR family pyrin domain containing 3	Homo sapiens	117-122
28787755-0	2017	A rapid administration of GW4064 inhibits the NLRP3 inflammasome activation independent of farnesoid X receptor agonism.	GW 4064	26-32	NLR family pyrin domain containing 3	Homo sapiens	46-51
28787755-2	2017	We found that GW4064 inhibits the NLR family CARD domain containing 3 (NLRP3) inflammasome activation in an FXR-independent manner as evidenced by its similar inhibitory effect on NLRP3 inflammasome activation in FXR-deficient macrophages.	GW 4064	14-20	NLR family pyrin domain containing 3	Homo sapiens	71-76
28787755-2	2017	We found that GW4064 inhibits the NLR family CARD domain containing 3 (NLRP3) inflammasome activation in an FXR-independent manner as evidenced by its similar inhibitory effect on NLRP3 inflammasome activation in FXR-deficient macrophages.	GW 4064	14-20	NLR family pyrin domain containing 3	Homo sapiens	180-185
28787755-3	2017	Interestingly, GW4064 decreases the nigericin-induced oligomerization and ubiquitination of ASC which is critical for the NLRP3 inflammasome activation.	GW 4064	15-21	NLR family pyrin domain containing 3	Homo sapiens	122-127
28787755-3	2017	Interestingly, GW4064 decreases the nigericin-induced oligomerization and ubiquitination of ASC which is critical for the NLRP3 inflammasome activation.	Nigericin	36-45	NLR family pyrin domain containing 3	Homo sapiens	122-127
28787755-4	2017	In vivo results indicate that GW4064 could partially rescue the symptoms of NLRP3-dependent inflammatory disease models.	GW 4064	30-36	NLR family pyrin domain containing 3	Homo sapiens	76-81
28787755-5	2017	These results not only necessitate cautious interpretation of the biological function of GW4064 as an FXR agonist, but also provide a potential therapeutic approach using GW4064 in the treatment of NLRP3-related diseases.	GW 4064	171-177	NLR family pyrin domain containing 3	Homo sapiens	198-203
28651232-0	2017	Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage.	Silymarin	0-9	NLR family pyrin domain containing 3	Homo sapiens	19-24
28547650-8	2017	Leu-Leu-OMe increased the expression of NLRP3, IL-1beta, and IL-18 in HUVECs.	leucyl-leucine-methyl ester	0-11	NLR family pyrin domain containing 3	Homo sapiens	40-45
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	pyrrolidine dithiocarbamic acid	0-4	NLR family pyrin domain containing 3	Homo sapiens	117-122
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	pyrrolidine dithiocarbamic acid	6-36	NLR family pyrin domain containing 3	Homo sapiens	117-122
28668606-9	2017	In contrast, when NLRP3/Caspase-1 pathway was blocked with Z-YVAD-FMK, TNF-alpha, IL-6 and IL-1beta levels, LDH enzyme activity, and Caspase-1 and NLRP3 protein levels were significantly declined (P &lt; 0.05) in HMEC-1 cells except IL-8(P &gt; 0.05).	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	59-69	NLR family pyrin domain containing 3	Homo sapiens	18-23
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	39-47	NLR family pyrin domain containing 3	Homo sapiens	117-122
28878677-0	2017	Teuvincenone F Suppresses LPS-Induced Inflammation and NLRP3 Inflammasome Activation by Attenuating NEMO Ubiquitination.	teuvincenone f	0-14	NLR family pyrin domain containing 3	Homo sapiens	55-60
28546421-6	2017	In addition, PXR agonists (rifampicin and SR12813) or overexpression of a constitutively active PXR markedly suppressed the NLRP3 inflammasome activation.	SR 12813	42-49	NLR family pyrin domain containing 3	Homo sapiens	124-129
28546421-7	2017	Conversely, PXR knockdown abrogated the suppressive effect of rifampicin on NLRP3 inflammasome activation.	Rifampin	62-72	NLR family pyrin domain containing 3	Homo sapiens	76-81
28546421-9	2017	Chromatin immunoprecipitation assays indicated that mevastatin inhibited nuclear factor-kappaB binding to the promoter regions of the human NLRP3 gene.	mevastatin	52-62	NLR family pyrin domain containing 3	Homo sapiens	140-145
28546421-5	2017	Simvastatin or mevastatin significantly suppressed the effects of ox-LDL or TNFalpha Promoter reporter assays and small interfering RNA knockdown revealed that statins inhibit ox-LDL-mediated NLRP3 inflammasome activation via the pregnane X receptor (PXR).	Simvastatin	0-11	NLR family pyrin domain containing 3	Homo sapiens	192-197
28546421-5	2017	Simvastatin or mevastatin significantly suppressed the effects of ox-LDL or TNFalpha Promoter reporter assays and small interfering RNA knockdown revealed that statins inhibit ox-LDL-mediated NLRP3 inflammasome activation via the pregnane X receptor (PXR).	mevastatin	15-25	NLR family pyrin domain containing 3	Homo sapiens	192-197
28546421-6	2017	In addition, PXR agonists (rifampicin and SR12813) or overexpression of a constitutively active PXR markedly suppressed the NLRP3 inflammasome activation.	Rifampin	27-37	NLR family pyrin domain containing 3	Homo sapiens	124-129
32258687-0	2017	NLRP3 inflammasome as a potential target to reduce epileptic-like activity: PS188.	ps188	76-81	NLR family pyrin domain containing 3	Homo sapiens	0-5
28878677-3	2017	Here, we found that the natural compound Teuvincenone F, which was isolated and purified from the stems and leaves of Premna szemaoensis, could significantly inhibit lipopolysaccharide (LPS)-induced pro-inflammatory cytokines production and NLRP3 inflammasome activation.	teuvincenone f	41-55	NLR family pyrin domain containing 3	Homo sapiens	241-246
28878677-4	2017	Our results showed that Teuvincenone F attenuated K63-linked ubiquitination of NF-kappaB-essential modulator (NEMO, also known as IKKgamma) to suppress LPS-induced phosphorylation of NF-kappaB, and inhibited mRNA expression of IL-1beta, IL-6, TNF-alpha, and NLRP3.	teuvincenone	24-36	NLR family pyrin domain containing 3	Homo sapiens	258-263
28878677-5	2017	In addition, we found that decreased NLRP3 expression by Teuvincenone F suppressed NLRP3 inflammasome activation and IL-1beta/IL-18 maturation.	teuvincenone	57-69	NLR family pyrin domain containing 3	Homo sapiens	37-42
28878677-5	2017	In addition, we found that decreased NLRP3 expression by Teuvincenone F suppressed NLRP3 inflammasome activation and IL-1beta/IL-18 maturation.	teuvincenone	57-69	NLR family pyrin domain containing 3	Homo sapiens	83-88
28878677-7	2017	In conclusion, Teuvincenone F is a highly effective natural compound to suppress LPS-induced inflammation by attenuating K63-linked ubiquitination of NEMO, highlighting that Teuvincenone F may be a potential new anti-inflammatory drug for the treatment of inflammatory and NLRP3 inflammasome-driven diseases.	teuvincenone f	15-29	NLR family pyrin domain containing 3	Homo sapiens	273-278
28826373-5	2017	The NLRP3 inflammasome can be influenced by various metabolites, including fatty acids.	Fatty Acids	75-86	NLR family pyrin domain containing 3	Homo sapiens	4-9
28878677-7	2017	In conclusion, Teuvincenone F is a highly effective natural compound to suppress LPS-induced inflammation by attenuating K63-linked ubiquitination of NEMO, highlighting that Teuvincenone F may be a potential new anti-inflammatory drug for the treatment of inflammatory and NLRP3 inflammasome-driven diseases.	teuvincenone f	174-188	NLR family pyrin domain containing 3	Homo sapiens	273-278
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	13-17	NLR family pyrin domain containing 3	Homo sapiens	116-121
28826373-6	2017	Specifically, although saturated fatty acids may promote NLRP3 inflammasome activation, monounsaturated fatty acids and polyunsaturated fatty acids have recently been shown to impede NLRP3 activity.	Fatty Acids, Monounsaturated	88-115	NLR family pyrin domain containing 3	Homo sapiens	183-188
28826373-6	2017	Specifically, although saturated fatty acids may promote NLRP3 inflammasome activation, monounsaturated fatty acids and polyunsaturated fatty acids have recently been shown to impede NLRP3 activity.	Fatty Acids, Unsaturated	120-147	NLR family pyrin domain containing 3	Homo sapiens	183-188
28826373-7	2017	Therefore, the NLRP3 inflammasome and associated metabolic inflammation have key roles in the relationships among fatty acids, metabolites, and metabolic disease.	Fatty Acids	114-125	NLR family pyrin domain containing 3	Homo sapiens	15-20
28629999-0	2017	Trimethylamine N-oxide prime NLRP3 inflammasome via inhibiting ATG16L1-induced autophagy in colonic epithelial cells.	trimethyloxamine	0-22	NLR family pyrin domain containing 3	Homo sapiens	29-34
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	13-17	NLR family pyrin domain containing 3	Homo sapiens	272-277
28629999-4	2017	Whether TMAO prime NLRP3 inflammasome via ATG16L1-induced autophagy remains unclear.	trimethyloxamine	8-12	NLR family pyrin domain containing 3	Homo sapiens	19-24
28629999-5	2017	This study observed the expression of ATG16L1, LC3-II and p62 and activation of NLRP3 inflammasome stimulated by TMAO in fetal human colon cells (FHCs), aiming to elucidate the mechanism by which the TMAO may contribute to colonic epithelial inflammation.	trimethyloxamine	113-117	NLR family pyrin domain containing 3	Homo sapiens	80-85
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	170-174	NLR family pyrin domain containing 3	Homo sapiens	116-121
28629999-6	2017	Our results demonstrated that TMAO significantly inhibited ATG16L1, LC3-II and p62 expression, and triggered the activated NLRP3 inflammasome and production of ROS in a dose- and time-dependent manner.	trimethyloxamine	30-34	NLR family pyrin domain containing 3	Homo sapiens	123-128
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	170-174	NLR family pyrin domain containing 3	Homo sapiens	272-277
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	170-174	NLR family pyrin domain containing 3	Homo sapiens	116-121
28629999-7	2017	Furthermore, TMAO-mediated effects were observably reversed by over-expression ATG16L1 and siRNA-mediated knockdown NLRP3.The present results support the hypothesis that TMAO may be involved in the pathogenesis of IBD by impacting ATG16L1-induced autophagy and activating NLRP3 inflammasome, suggesting a potential therapeutic targets for the treatment of IBD and TMAO-associated complications.	trimethyloxamine	170-174	NLR family pyrin domain containing 3	Homo sapiens	272-277
28821266-6	2017	Administration of S-adenosyl-L-methionine (SAM), a CBS-specific agonist, or sodium hydrosulfide (NaHS), a classical exogenous H2S donor, not only restored brain and plasma H2S content but also attenuated brain oedema, microglial accumulation and neurological deficits at 1 day post-ICH by inhibiting the P2X7R/NLRP3 inflammasome cascade.	S-Adenosylmethionine	18-41	NLR family pyrin domain containing 3	Homo sapiens	310-315
28821266-6	2017	Administration of S-adenosyl-L-methionine (SAM), a CBS-specific agonist, or sodium hydrosulfide (NaHS), a classical exogenous H2S donor, not only restored brain and plasma H2S content but also attenuated brain oedema, microglial accumulation and neurological deficits at 1 day post-ICH by inhibiting the P2X7R/NLRP3 inflammasome cascade.	S-Adenosylmethionine	43-46	NLR family pyrin domain containing 3	Homo sapiens	310-315
28821266-6	2017	Administration of S-adenosyl-L-methionine (SAM), a CBS-specific agonist, or sodium hydrosulfide (NaHS), a classical exogenous H2S donor, not only restored brain and plasma H2S content but also attenuated brain oedema, microglial accumulation and neurological deficits at 1 day post-ICH by inhibiting the P2X7R/NLRP3 inflammasome cascade.	sodium bisulfide	76-95	NLR family pyrin domain containing 3	Homo sapiens	310-315
28821266-6	2017	Administration of S-adenosyl-L-methionine (SAM), a CBS-specific agonist, or sodium hydrosulfide (NaHS), a classical exogenous H2S donor, not only restored brain and plasma H2S content but also attenuated brain oedema, microglial accumulation and neurological deficits at 1 day post-ICH by inhibiting the P2X7R/NLRP3 inflammasome cascade.	sodium bisulfide	97-101	NLR family pyrin domain containing 3	Homo sapiens	310-315
28779175-0	2017	CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation.	Chlorides	16-24	NLR family pyrin domain containing 3	Homo sapiens	80-85
28710289-6	2017	Palmitic acid, in particular, is a well-characterized nutrient that promotes metabolic inflammation via the NLRP3 (the nod-like receptor containing a pyrin domain) inflammasome, which is partly attributable to AMPK inhibition.	Palmitic Acid	0-13	NLR family pyrin domain containing 3	Homo sapiens	108-113
28583762-0	2017	Puerarin inhibits amyloid beta-induced NLRP3 inflammasome activation in retinal pigment epithelial cells via suppressing ROS-dependent oxidative and endoplasmic reticulum stresses.	puerarin	0-8	NLR family pyrin domain containing 3	Homo sapiens	39-44
28583762-0	2017	Puerarin inhibits amyloid beta-induced NLRP3 inflammasome activation in retinal pigment epithelial cells via suppressing ROS-dependent oxidative and endoplasmic reticulum stresses.	ros	121-124	NLR family pyrin domain containing 3	Homo sapiens	39-44
28583762-4	2017	In this study, we investigated the protective effect and underlying mechanism of puerarin against Abeta1-40-induced NLRP3 inflammasome activation in LPS-primed ARPE-19 cells.	puerarin	81-89	NLR family pyrin domain containing 3	Homo sapiens	116-121
28583762-5	2017	The results showed that Abeta1-40 induced NLRP3 inflammasome activation mainly via triggering ROS-dependent oxidative stress, particularly lipid peroxidation, and endoplasmic reticulum stress in LPS-primed ARPE-19 cells; however, such effect could be significantly reversed by puerarin in a dose-dependent manner.	ros	94-97	NLR family pyrin domain containing 3	Homo sapiens	42-47
28583762-5	2017	The results showed that Abeta1-40 induced NLRP3 inflammasome activation mainly via triggering ROS-dependent oxidative stress, particularly lipid peroxidation, and endoplasmic reticulum stress in LPS-primed ARPE-19 cells; however, such effect could be significantly reversed by puerarin in a dose-dependent manner.	puerarin	277-285	NLR family pyrin domain containing 3	Homo sapiens	42-47
28798291-4	2017	RESULTS After six hours, 12 hours, and 24 hours of high glucose stimulation, the secretion of IL-1beta in human glomerular mesangial cells, compared to unstimulated cells, was 1.85-fold, 3.04-fold, and 4.14-fold; the expression of NLRP3 increased by 2.20-fold, 4.62-fold, and 8.32-fold; and the expression of caspase-1 was increased by 1.60-fold, 2.72-fold, and 3.67-fold.	Glucose	56-63	NLR family pyrin domain containing 3	Homo sapiens	231-236
28796264-1	2017	The nucleotide-binding domain and leucine-rich repeat-containing receptor with a pyrin domain 3 (NLRP3) inflammasome is a sensor for different types of infections and alterations of homeostatic parameters, including abnormally high levels of the extracellular nucleotide ATP or crystallization of different metabolites.	Adenosine Triphosphate	271-274	NLR family pyrin domain containing 3	Homo sapiens	97-102
28779175-2	2017	Potassium efflux and mitochondrial damage are both reported to mediate NLRP3 inflammasome activation, but the underlying, orchestrating signaling events are still unclear.	Potassium	0-9	NLR family pyrin domain containing 3	Homo sapiens	71-76
28779175-3	2017	Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation.	Potassium	79-88	NLR family pyrin domain containing 3	Homo sapiens	156-161
28779175-3	2017	Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation.	Reactive Oxygen Species	110-133	NLR family pyrin domain containing 3	Homo sapiens	156-161
28779175-3	2017	Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation.	Reactive Oxygen Species	135-138	NLR family pyrin domain containing 3	Homo sapiens	156-161
28779175-4	2017	NLRP3 agonists induce potassium efflux, which causes mitochondrial damage and ROS production.	Potassium	22-31	NLR family pyrin domain containing 3	Homo sapiens	0-5
28779175-4	2017	NLRP3 agonists induce potassium efflux, which causes mitochondrial damage and ROS production.	Reactive Oxygen Species	78-81	NLR family pyrin domain containing 3	Homo sapiens	0-5
28779175-5	2017	Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1beta secretion.	Reactive Oxygen Species	14-17	NLR family pyrin domain containing 3	Homo sapiens	134-139
28779175-5	2017	Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1beta secretion.	Chlorides	102-110	NLR family pyrin domain containing 3	Homo sapiens	134-139
28779175-6	2017	Thus, our results identify CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.The NLRP3 inflammasome is key to the regulation of innate immunity against pathogens or stress, but the underlying signaling regulation is still unclear.	Chlorides	43-51	NLR family pyrin domain containing 3	Homo sapiens	107-112
28779175-6	2017	Thus, our results identify CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.The NLRP3 inflammasome is key to the regulation of innate immunity against pathogens or stress, but the underlying signaling regulation is still unclear.	Chlorides	43-51	NLR family pyrin domain containing 3	Homo sapiens	128-133
28252317-0	2017	Role for NLRP3 Inflammasome-mediated, IL-1beta-Dependent Responses in Severe, Steroid-Resistant Asthma.	Steroids	78-85	NLR family pyrin domain containing 3	Homo sapiens	9-14
28252317-5	2017	OBJECTIVES: To investigate the roles and therapeutic targeting of the NLRP3 inflammasome and IL-1beta in severe, steroid-resistant asthma.	Steroids	113-120	NLR family pyrin domain containing 3	Homo sapiens	70-75
28252317-10	2017	MEASUREMENTS AND MAIN RESULTS: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1beta responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness.	Steroids	125-132	NLR family pyrin domain containing 3	Homo sapiens	77-82
28252317-11	2017	Neutrophilic airway inflammation, disease severity, and steroid resistance in human asthma correlate with NLRP3 and IL-1beta expression.	Steroids	56-63	NLR family pyrin domain containing 3	Homo sapiens	106-111
28252317-14	2017	CONCLUSIONS: NLRP3 inflammasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic targets in this disease.	Steroids	69-76	NLR family pyrin domain containing 3	Homo sapiens	13-18
28461245-0	2017	LFG-500, a novel synthetic flavonoid, suppresses epithelial-mesenchymal transition in human lung adenocarcinoma cells by inhibiting NLRP3 in inflammatory microenvironment.	LFG-500	0-7	NLR family pyrin domain containing 3	Homo sapiens	132-137
28461245-0	2017	LFG-500, a novel synthetic flavonoid, suppresses epithelial-mesenchymal transition in human lung adenocarcinoma cells by inhibiting NLRP3 in inflammatory microenvironment.	Flavonoids	27-36	NLR family pyrin domain containing 3	Homo sapiens	132-137
28750089-0	2017	A synthetic cationic antimicrobial peptide inhibits inflammatory response and the NLRP3 inflammasome by neutralizing LPS and ATP.	Adenosine Triphosphate	125-128	NLR family pyrin domain containing 3	Homo sapiens	82-87
28356568-3	2017	The NLRP3 inflammasome forms an assembly consisting of the ASC (apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain) adaptor protein and the effector, caspase-1 (cysteine-dependent aspartate-directed protease-1).	Cysteine	201-209	NLR family pyrin domain containing 3	Homo sapiens	4-9
28761045-6	2017	Here, we report that inhibiting NLRP3 with the selective inhibitor MCC950, blocked release of IL-1beta and the related cytokine IL-1alpha from primary human monocytes in response to S. typhimurium.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	67-73	NLR family pyrin domain containing 3	Homo sapiens	32-37
28750089-5	2017	GW-A2 also inhibited NLRP3 inflammasome activation induced by LPS and ATP.	Adenosine Triphosphate	70-73	NLR family pyrin domain containing 3	Homo sapiens	21-26
29744188-0	2017	Hydrogen sulfide exposure induces NLRP3 inflammasome-dependent IL-1beta and IL-18 secretion in human mononuclear leukocytes in vitro.	Hydrogen Sulfide	0-16	NLR family pyrin domain containing 3	Homo sapiens	34-39
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	133-139	NLR family pyrin domain containing 3	Homo sapiens	347-352
28790925-3	2017	ROS may promote the activation of nucleotide-binding oligomerization domain like receptor (NLR) pyrin domain containing 3 (NLRP3) inflammasome, a novel regulator of inflammation and cell death, by nuclear factor-kB (NF-kappaB) and thioredoxin interacting/inhibiting protein (TXNIP).	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	123-128
28726778-2	2017	Mcc950 is a potent and specific inhibitor of the NLRP3 inflammasome but its influence on DR has not been studied.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	0-6	NLR family pyrin domain containing 3	Homo sapiens	49-54
28726778-5	2017	Moreover, in high-glucose-stimulated HRECs, increased production of the NLRP3 inflammasome activation and severe apoptosis were rescued with Mcc950 treatment.	Glucose	18-25	NLR family pyrin domain containing 3	Homo sapiens	72-77
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	39-45	NLR family pyrin domain containing 3	Homo sapiens	180-185
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	39-45	NLR family pyrin domain containing 3	Homo sapiens	347-352
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	Glucose	107-114	NLR family pyrin domain containing 3	Homo sapiens	180-185
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	Glucose	107-114	NLR family pyrin domain containing 3	Homo sapiens	347-352
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	133-139	NLR family pyrin domain containing 3	Homo sapiens	180-185
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	133-139	NLR family pyrin domain containing 3	Homo sapiens	347-352
28726778-6	2017	Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	133-139	NLR family pyrin domain containing 3	Homo sapiens	180-185
28528118-0	2017	Calcium supplementation decreases BCP-induced inflammatory processes in blood cells through the NLRP3 inflammasome down-regulation.	Calcium	0-7	NLR family pyrin domain containing 3	Homo sapiens	96-101
28528118-0	2017	Calcium supplementation decreases BCP-induced inflammatory processes in blood cells through the NLRP3 inflammasome down-regulation.	hydroxyapatite-beta tricalcium phosphate	34-37	NLR family pyrin domain containing 3	Homo sapiens	96-101
28528118-7	2017	Our results strongly suggest that the anti-inflammatory property of calcium supplemented-BCP results from its down-modulating effect on P2X7R gene expression and its capacity to inhibit ATP/P2X7R interactions, decreasing the NLRP3 inflammasome activation.	Calcium	68-75	NLR family pyrin domain containing 3	Homo sapiens	225-230
28528118-7	2017	Our results strongly suggest that the anti-inflammatory property of calcium supplemented-BCP results from its down-modulating effect on P2X7R gene expression and its capacity to inhibit ATP/P2X7R interactions, decreasing the NLRP3 inflammasome activation.	hydroxyapatite-beta tricalcium phosphate	89-92	NLR family pyrin domain containing 3	Homo sapiens	225-230
29744188-10	2017	Further, NaHS triggered the secretion of IL-1ss and IL-18 in human THP1-Null monocytes (p = .0006 and p = .002, respectively), while the NaHS-dependent secretion was reduced in the monocyte cell lines unable to form the NLRP3 inflammasome.	sodium bisulfide	9-13	NLR family pyrin domain containing 3	Homo sapiens	220-225
29744188-11	2017	Hence, the results suggest that NaHS induces the formation of the NLRP3 inflammasome and thus the secretion of IL-1ss and IL-18.	sodium bisulfide	32-36	NLR family pyrin domain containing 3	Homo sapiens	66-71
29744188-12	2017	Enhanced NLRP3 inflammasome-dependent secretion of IL-1beta and IL-18 in human mononuclear leukocytes exposed to NaHS in vitro is reported.	sodium bisulfide	113-117	NLR family pyrin domain containing 3	Homo sapiens	9-14
29744188-1	2017	The aim was to investigate if hydrogen sulfide (H2S) induces the formation of the NLRP3 inflammasome and subsequent IL-1beta and IL-18 secretion in human peripheral blood mononuclear cells (PBMCs) and in the human monocyte cell line THP1.	Hydrogen Sulfide	30-46	NLR family pyrin domain containing 3	Homo sapiens	82-87
29744188-1	2017	The aim was to investigate if hydrogen sulfide (H2S) induces the formation of the NLRP3 inflammasome and subsequent IL-1beta and IL-18 secretion in human peripheral blood mononuclear cells (PBMCs) and in the human monocyte cell line THP1.	Hydrogen Sulfide	48-51	NLR family pyrin domain containing 3	Homo sapiens	82-87
29744188-5	2017	We hypothesize that H2S affects the inflammatory host response by inducing formation of the NLRP3 inflammasome and thereby causes the secretion of IL-1ss and IL-18.	Hydrogen Sulfide	20-23	NLR family pyrin domain containing 3	Homo sapiens	92-97
26848183-8	2017	In vitro, TiO2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1beta and IL-18.	titanium dioxide	10-14	NLR family pyrin domain containing 3	Homo sapiens	145-150
26848183-0	2017	Titanium dioxide nanoparticles exacerbate DSS-induced colitis: role of the NLRP3 inflammasome.	titanium dioxide	0-16	NLR family pyrin domain containing 3	Homo sapiens	75-80
28224704-6	2017	Using NP cells established from healthy tissues, our in vitro study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3-inflammasome-dependent manner related to the receptor for AGEs (RAGE)/NF-kappaB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization.	Reactive Oxygen Species	310-333	NLR family pyrin domain containing 3	Homo sapiens	166-171
26848183-6	2017	RESULTS: Oral administration of TiO2 nanoparticles worsened acute colitis through a mechanism involving the NLRP3 inflammasome.	titanium dioxide	32-36	NLR family pyrin domain containing 3	Homo sapiens	108-113
26848183-8	2017	In vitro, TiO2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1beta and IL-18.	titanium dioxide	10-14	NLR family pyrin domain containing 3	Homo sapiens	77-82
28224704-6	2017	Using NP cells established from healthy tissues, our in vitro study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3-inflammasome-dependent manner related to the receptor for AGEs (RAGE)/NF-kappaB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization.	mtros	335-340	NLR family pyrin domain containing 3	Homo sapiens	166-171
28224704-6	2017	Using NP cells established from healthy tissues, our in vitro study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3-inflammasome-dependent manner related to the receptor for AGEs (RAGE)/NF-kappaB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization.	Calcium	419-426	NLR family pyrin domain containing 3	Homo sapiens	166-171
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Fluoxetine	103-113	NLR family pyrin domain containing 3	Homo sapiens	75-80
28499186-0	2017	Effect of betaine on hepatic insulin resistance through FOXO1-induced NLRP3 inflammasome.	Betaine	10-17	NLR family pyrin domain containing 3	Homo sapiens	70-75
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Paroxetine	115-125	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Mianserin	127-136	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Desvenlafaxine Succinate	164-178	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Amitriptyline	180-193	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Imipramine	195-205	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	agomelatine	210-221	NLR family pyrin domain containing 3	Homo sapiens	75-80
28465217-4	2017	This study evaluates the involvement of nine common antidepressants in the NLRP3-inflammasome complex (fluoxetine, paroxetine, mianserin, mirtazapine, venlafaxine, desvenlafaxine, amitriptyline, imipramine and agomelatine), both in in vitro THP-1 cells stimulated by ATP, and in a stress-induced depressive animal or MDD patients.	Adenosine Triphosphate	267-270	NLR family pyrin domain containing 3	Homo sapiens	75-80
28659178-0	2017	Azithromycin decreases NALP3 mRNA stability in monocytes to limit inflammasome-dependent inflammation.	Azithromycin	0-12	NLR family pyrin domain containing 3	Homo sapiens	23-28
28499186-1	2017	In the present study, we attempted to elucidate whether molecular modulation of inflammation by betaine through the forkhead box O1 (FOXO1)-induced NLRP3 inflammasome improves insulin resistance.	Betaine	96-103	NLR family pyrin domain containing 3	Homo sapiens	148-153
28499186-7	2017	We found that the activation of NLRP3 inflammasome genes was reduced by betaine, which resulted in the suppression of reactive species (RS) production in liver cells.	Betaine	72-79	NLR family pyrin domain containing 3	Homo sapiens	32-37
28499186-10	2017	Our results suggest that betaine inhibits the FOXO1 binding to TXNIP, leading to the suppression of RS-induced NLRP3 inflammasome activation in a diabetic liver.	Betaine	25-32	NLR family pyrin domain containing 3	Homo sapiens	111-116
28499186-10	2017	Our results suggest that betaine inhibits the FOXO1 binding to TXNIP, leading to the suppression of RS-induced NLRP3 inflammasome activation in a diabetic liver.	rs	100-102	NLR family pyrin domain containing 3	Homo sapiens	111-116
28659178-3	2017	Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes.	Azithromycin	37-49	NLR family pyrin domain containing 3	Homo sapiens	57-105
28659178-3	2017	Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes.	Azithromycin	37-49	NLR family pyrin domain containing 3	Homo sapiens	107-112
28659178-3	2017	Here, we investigated the effects of azithromycin on the NACHT, LRR, and PYD domains-containing protein 3 (NALP3) protein, which is the sensing component of the NALP3 inflammasome, in human monocytes.	Azithromycin	37-49	NLR family pyrin domain containing 3	Homo sapiens	161-166
28662085-8	2017	Metabolites such as allantoin, creatinine, proline, and methylamine could be predictive of AII/R injury.	Allantoin	20-29	NLR family pyrin domain containing 3	Homo sapiens	91-94
28662085-8	2017	Metabolites such as allantoin, creatinine, proline, and methylamine could be predictive of AII/R injury.	Creatinine	31-41	NLR family pyrin domain containing 3	Homo sapiens	91-94
28662085-8	2017	Metabolites such as allantoin, creatinine, proline, and methylamine could be predictive of AII/R injury.	Proline	43-50	NLR family pyrin domain containing 3	Homo sapiens	91-94
28662085-8	2017	Metabolites such as allantoin, creatinine, proline, and methylamine could be predictive of AII/R injury.	methylamine	56-67	NLR family pyrin domain containing 3	Homo sapiens	91-94
28659178-9	2017	To confirm azithromycin"s effects on NLRP3 mRNA and promoter activity conclusively, HEK cells were lipofected with luciferase reporter constructs harboring either the 5" untranslated region (UTR) of the NLRP3 gene which included the promoter, the 3" UTR of the gene, or an empty plasmid prior to treatment with azithromycin and/or LPS, and luminescence was measured.	Azithromycin	11-23	NLR family pyrin domain containing 3	Homo sapiens	37-42
28588189-0	2017	Metabolic injury-induced NLRP3 inflammasome activation dampens phospholipid degradation.	Phospholipids	63-75	NLR family pyrin domain containing 3	Homo sapiens	25-30
28659178-10	2017	RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity.	Azithromycin	9-21	NLR family pyrin domain containing 3	Homo sapiens	60-65
28659178-10	2017	RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity.	Azithromycin	9-21	NLR family pyrin domain containing 3	Homo sapiens	177-182
28659178-10	2017	RESULTS: Azithromycin decreased IL-1beta levels and reduced NALP3 protein levels in LPS-stimulated THP-1 monocytes through a mechanism involving decreased mRNA stability of the NALP3 - coding NLRP3 gene transcript as well as by decreasing NF-kappaB activity.	Azithromycin	9-21	NLR family pyrin domain containing 3	Homo sapiens	192-197
28659178-12	2017	CONCLUSIONS: These studies provide a unique mechanism whereby azithromycin exerts immunomodulatory actions in monocytes by destabilizing mRNA levels for a key inflammasome component, NALP3, leading to decreased IL-1beta-mediated inflammation.	Azithromycin	62-74	NLR family pyrin domain containing 3	Homo sapiens	183-188
28978034-0	2017	Celastrol ameliorates inflammation through inhibition of NLRP3 inflammasome activation.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	57-62
28978034-3	2017	Here, we show that celastrol abolishes the NLRP3 inflammasome activation, inhibits subsequent caspase-1 activation and IL-1beta secretion both in vitro and in vivo.	celastrol	19-28	NLR family pyrin domain containing 3	Homo sapiens	43-48
28978034-4	2017	Notably, interruption of ASC oligomerization and autophagy activation are involved in NLRP3 inflammasome inactivation by celastrol.	celastrol	121-130	NLR family pyrin domain containing 3	Homo sapiens	86-91
28978034-5	2017	Importantly, in vivo results indicate that celastrol attenuates NLRP3 inflammasome-dependent inflammation diseases via autophagy-related pathway.	celastrol	43-52	NLR family pyrin domain containing 3	Homo sapiens	64-69
28978034-6	2017	Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases.	celastrol	24-33	NLR family pyrin domain containing 3	Homo sapiens	53-58
28978034-6	2017	Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases.	celastrol	24-33	NLR family pyrin domain containing 3	Homo sapiens	142-147
28978034-6	2017	Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases.	celastrol	116-125	NLR family pyrin domain containing 3	Homo sapiens	142-147
28489580-6	2017	Therefore, our results suggest that rapamycin negatively regulates macrophage activation by restricting a feedback loop of NLRP3 inflammasome-p38 MAPK-NFkappaB pathways in autophagy- and p62/SQSTM1-dependent manners.	Sirolimus	36-45	NLR family pyrin domain containing 3	Homo sapiens	123-128
28592027-0	2017	[Glyburide prevents pulmonary artery smooth muscle cell proliferation and migration via inhibiting NLRP3 activation].	Glyburide	1-10	NLR family pyrin domain containing 3	Homo sapiens	99-104
28592027-1	2017	Objective: To investigate whether glyburide prevents platelet-derived growth factor (PDGF) induced pulmonary artery smooth muscle cells(PASMCs) proliferation and migration via inhibiting nucleotide binding domain leucine-rich repeat-containing receptors protein 3(NLRP3) inflammasome activation.	Glyburide	34-43	NLR family pyrin domain containing 3	Homo sapiens	264-269
28592027-5	2017	Results: Compared with the control group, the protein expressions of NLRP3, caspase-1 and IL-1beta in PASMCs were increased to (1.38+-0.09, t=3.998, P&lt;0.001), (1.32+-0.1, t=3.268, P&lt;0.01)and(1.43+-0.19) (t=2.096, P&lt;0.05) folds in the PDGF group.	pasmcs	102-108	NLR family pyrin domain containing 3	Homo sapiens	69-74
28592027-10	2017	Conclusion: Glyburide could ameliorate PDGF-induced PASMCs proliferation and migration by inhibiting NLRP3 inflammasome activation.	Glyburide	12-21	NLR family pyrin domain containing 3	Homo sapiens	101-106
28637493-11	2017	RESULTS: In the clinical analysis, expression and activation of NLRP3 inflammasome was clearly increased in OSCC tissues of patients who received 5-FU-based chemotherapy.	Fluorouracil	146-150	NLR family pyrin domain containing 3	Homo sapiens	64-69
28588189-6	2017	By inhibiting the sirtuin-1/LKB1/AMPK pathway, NLRP3 inflammasome dampened lipid breakdown, thereby worsening the LDL-induced intratubular phospholipid accumulation.	Phospholipids	139-151	NLR family pyrin domain containing 3	Homo sapiens	47-52
28404639-7	2017	When HepG2 cells were exposed to LDL cholesterol, they developed cholesterol crystals in LD membranes, which caused activation of THP1 cells (macrophages) grown in coculture; upregulation of TNF-alpha, NLRP3, and interleukin 1beta (IL1beta) mRNA; and secretion of IL-1beta.	Cholesterol	37-48	NLR family pyrin domain containing 3	Homo sapiens	202-207
28238526-6	2017	Reactive oxygen species-induced mitochondrial DNA oxidative damage and BRCC36 deubiquitinating activity provide a missing link and mechanism by which innate immunity responds to environmental stress via caspase-8-involved NLRP3/NLRP6 inflammasomes.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	222-227
28326454-0	2017	Quercetin and Ascorbic Acid Suppress Fructose-Induced NLRP3 Inflammasome Activation by Blocking Intracellular Shuttling of TXNIP in Human Macrophage Cell Lines.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	54-59
28326454-0	2017	Quercetin and Ascorbic Acid Suppress Fructose-Induced NLRP3 Inflammasome Activation by Blocking Intracellular Shuttling of TXNIP in Human Macrophage Cell Lines.	Ascorbic Acid	14-27	NLR family pyrin domain containing 3	Homo sapiens	54-59
28326454-0	2017	Quercetin and Ascorbic Acid Suppress Fructose-Induced NLRP3 Inflammasome Activation by Blocking Intracellular Shuttling of TXNIP in Human Macrophage Cell Lines.	Fructose	37-45	NLR family pyrin domain containing 3	Homo sapiens	54-59
28326454-9	2017	Treatment of macrophages with fructose promoted the association between TXNIP and NLRP3 in the cytosol, sequentially resulting in the activation of the NLRP3 inflammasome.	Fructose	30-38	NLR family pyrin domain containing 3	Homo sapiens	82-87
28326454-9	2017	Treatment of macrophages with fructose promoted the association between TXNIP and NLRP3 in the cytosol, sequentially resulting in the activation of the NLRP3 inflammasome.	Fructose	30-38	NLR family pyrin domain containing 3	Homo sapiens	152-157
28326454-10	2017	This study revealed that intracellular TXNIP protein is a critical regulator of activation of the fructose-induced NLRP3 inflammasome, which can be effectively blocked by the antioxidants quercetin and ascorbic acid.	Fructose	98-106	NLR family pyrin domain containing 3	Homo sapiens	115-120
28326454-10	2017	This study revealed that intracellular TXNIP protein is a critical regulator of activation of the fructose-induced NLRP3 inflammasome, which can be effectively blocked by the antioxidants quercetin and ascorbic acid.	Quercetin	188-197	NLR family pyrin domain containing 3	Homo sapiens	115-120
28326454-10	2017	This study revealed that intracellular TXNIP protein is a critical regulator of activation of the fructose-induced NLRP3 inflammasome, which can be effectively blocked by the antioxidants quercetin and ascorbic acid.	Ascorbic Acid	202-215	NLR family pyrin domain containing 3	Homo sapiens	115-120
28004443-0	2017	Amyloid beta induces NLRP3 inflammasome activation in retinal pigment epithelial cells via NADPH oxidase- and mitochondria-dependent ROS production.	Reactive Oxygen Species	133-136	NLR family pyrin domain containing 3	Homo sapiens	21-26
28004443-3	2017	In this study, we investigated the involvement of NADPH oxidase- and mitochondria-derived reactive oxygen species (ROS) in the process of Abeta1-40 -induced NLRP3 inflammasome activation in LPS-primed ARPE-19 cells.	Reactive Oxygen Species	90-113	NLR family pyrin domain containing 3	Homo sapiens	157-162
28004443-3	2017	In this study, we investigated the involvement of NADPH oxidase- and mitochondria-derived reactive oxygen species (ROS) in the process of Abeta1-40 -induced NLRP3 inflammasome activation in LPS-primed ARPE-19 cells.	Reactive Oxygen Species	115-118	NLR family pyrin domain containing 3	Homo sapiens	157-162
28004443-5	2017	Furthermore, the inductive effect of Abeta1-40 on NLRP3 inflammasome activation was mediated in a manner dependent on NADPH oxidase- and mitochondria-derived ROS.	Reactive Oxygen Species	158-161	NLR family pyrin domain containing 3	Homo sapiens	50-55
28569730-5	2017	This is followed by signal two, which involves recognition of PAMPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads to caspase-1-dependent cleavage of pro-IL-1beta to active IL-1beta and pyroptosis.	Uric Acid	125-134	NLR family pyrin domain containing 3	Homo sapiens	147-152
28569730-5	2017	This is followed by signal two, which involves recognition of PAMPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads to caspase-1-dependent cleavage of pro-IL-1beta to active IL-1beta and pyroptosis.	Adenosine Triphosphate	138-141	NLR family pyrin domain containing 3	Homo sapiens	147-152
27726055-9	2017	Treatment with the caspase-1 inhibitor, VX-765, suppressed NLRP3 expression with reduced IL-1beta expression and associated neuroinflammation.	belnacasan	40-46	NLR family pyrin domain containing 3	Homo sapiens	59-64
28404639-7	2017	When HepG2 cells were exposed to LDL cholesterol, they developed cholesterol crystals in LD membranes, which caused activation of THP1 cells (macrophages) grown in coculture; upregulation of TNF-alpha, NLRP3, and interleukin 1beta (IL1beta) mRNA; and secretion of IL-1beta.	Cholesterol	65-76	NLR family pyrin domain containing 3	Homo sapiens	202-207
28596733-6	2017	Melatonin has been shown to preserves BBB integrity and permeability via a variety of pathways: inhibition of matrix metalloproteinase-9 (MMP-9), inhibition of NADPH oxidase-2, and impact on silent information regulator 1 (SIRT1) and nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	324-329
28542146-5	2017	They interact with Toll-like receptors (TLRs), complement and the phospholipids of cell membranes inducing endothelial and epithelial cytotoxicity, TLR2/TLR4/TLR9 activation and pro-inflammatory cytokine/chemokine release via MyD88, NFkappaB and NLRP3 inflammasome-dependent pathways.	Phospholipids	66-79	NLR family pyrin domain containing 3	Homo sapiens	246-251
28579962-5	2017	Furthermore, the gut microbiota and its metabolites, such as short chain fatty acids and secondary bile acids, also contribute to host energy production, ROS modulation and inflammation in the gut by attenuating TNFalpha- mediated immune responses and inflammasomes such as NLRP3.	Fatty Acids, Volatile	61-84	NLR family pyrin domain containing 3	Homo sapiens	274-279
28579962-5	2017	Furthermore, the gut microbiota and its metabolites, such as short chain fatty acids and secondary bile acids, also contribute to host energy production, ROS modulation and inflammation in the gut by attenuating TNFalpha- mediated immune responses and inflammasomes such as NLRP3.	Bile Acids and Salts	99-109	NLR family pyrin domain containing 3	Homo sapiens	274-279
28288918-0	2017	Increased carbon dioxide levels stimulate neutrophils to produce microparticles and activate the nucleotide-binding domain-like receptor 3 inflammasome.	Carbon Dioxide	10-24	NLR family pyrin domain containing 3	Homo sapiens	97-138
28507328-6	2017	In macrophages, ATP-induced K+ efflux plays a key role in activating the NLRP3 inflammasome.	Adenosine Triphosphate	16-19	NLR family pyrin domain containing 3	Homo sapiens	73-78
28232172-0	2017	Activation of NLRP3 inflammasome by cholesterol crystals in alcohol consumption induces atherosclerotic lesions.	Cholesterol	36-47	NLR family pyrin domain containing 3	Homo sapiens	14-19
28232172-0	2017	Activation of NLRP3 inflammasome by cholesterol crystals in alcohol consumption induces atherosclerotic lesions.	Alcohols	60-67	NLR family pyrin domain containing 3	Homo sapiens	14-19
28232172-3	2017	Conversion of cholesterol into sharp edges of cholesterol crystals (CCs) in alcohol intake was key to activation of NLRP3 inflammasome, induction of cerebral atherosclerosis, and development of neuropathy around the atherosclerotic lesions.	Cholesterol	14-25	NLR family pyrin domain containing 3	Homo sapiens	116-121
28232172-3	2017	Conversion of cholesterol into sharp edges of cholesterol crystals (CCs) in alcohol intake was key to activation of NLRP3 inflammasome, induction of cerebral atherosclerosis, and development of neuropathy around the atherosclerotic lesions.	Cholesterol	46-57	NLR family pyrin domain containing 3	Homo sapiens	116-121
28232172-3	2017	Conversion of cholesterol into sharp edges of cholesterol crystals (CCs) in alcohol intake was key to activation of NLRP3 inflammasome, induction of cerebral atherosclerosis, and development of neuropathy around the atherosclerotic lesions.	Alcohols	76-83	NLR family pyrin domain containing 3	Homo sapiens	116-121
28232172-5	2017	Thus, we observed that alcohol consumption elevated the level of plasma cholesterol, deposition and crystallization of cholesterol, as well as activation of NLRP3 inflammasome.	Alcohols	23-30	NLR family pyrin domain containing 3	Homo sapiens	157-162
28232172-8	2017	We demonstrated the molecular mechanisms of NLRP3 activation and downstream signaling cascade event in primary culture of human brain arterial/capillary endothelial cells in the setting of dose-/time-dependent effects of alcohol/CCs using NLRP3 gene silencing technique.	Alcohols	221-228	NLR family pyrin domain containing 3	Homo sapiens	44-49
28232172-8	2017	We demonstrated the molecular mechanisms of NLRP3 activation and downstream signaling cascade event in primary culture of human brain arterial/capillary endothelial cells in the setting of dose-/time-dependent effects of alcohol/CCs using NLRP3 gene silencing technique.	Alcohols	221-228	NLR family pyrin domain containing 3	Homo sapiens	239-244
28232172-10	2017	Finally, combined therapy of acetyl-l-carnitine and Lipitor  prevented deposition of cholesterol, formation of CCs, activation of NLRP3, thickening of vessel walls, and elevation of intracranial blood pressure.	Acetylcarnitine	29-47	NLR family pyrin domain containing 3	Homo sapiens	130-135
28232172-10	2017	Finally, combined therapy of acetyl-l-carnitine and Lipitor  prevented deposition of cholesterol, formation of CCs, activation of NLRP3, thickening of vessel walls, and elevation of intracranial blood pressure.	Atorvastatin	52-59	NLR family pyrin domain containing 3	Homo sapiens	130-135
28232172-11	2017	We conclude that alcohol-induced accumulation and crystallization of cholesterol activates NLRP3/caspase-1 in the cerebral vessel that leads to early development of atherosclerosis.	Alcohols	17-24	NLR family pyrin domain containing 3	Homo sapiens	91-96
28232172-11	2017	We conclude that alcohol-induced accumulation and crystallization of cholesterol activates NLRP3/caspase-1 in the cerebral vessel that leads to early development of atherosclerosis.	Cholesterol	69-80	NLR family pyrin domain containing 3	Homo sapiens	91-96
28013367-5	2017	Here we show the role of actin polymerization in asbestos-induced activation of the nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome.	Asbestos	49-57	NLR family pyrin domain containing 3	Homo sapiens	84-135
28013367-5	2017	Here we show the role of actin polymerization in asbestos-induced activation of the nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome.	Asbestos	49-57	NLR family pyrin domain containing 3	Homo sapiens	137-142
28260724-3	2017	NLRP3 inflammasomes are activated by various danger signals, such as cholesterol crystals, calcium phosphate crystals, and oxidized low-density lipoprotein in macrophages, to initiate inflammatory responses in the atherosclerotic lesion.	Cholesterol	69-80	NLR family pyrin domain containing 3	Homo sapiens	0-5
28260724-3	2017	NLRP3 inflammasomes are activated by various danger signals, such as cholesterol crystals, calcium phosphate crystals, and oxidized low-density lipoprotein in macrophages, to initiate inflammatory responses in the atherosclerotic lesion.	calcium phosphate	91-108	NLR family pyrin domain containing 3	Homo sapiens	0-5
28298525-2	2017	However, recently it has been demonstrated that PGE2 can block the maturation of IL-1beta by inhibiting the NLRP3 inflammasome in macrophages.	Dinoprostone	48-52	NLR family pyrin domain containing 3	Homo sapiens	108-113
28320833-6	2017	Many molecules produced by adipocytes activate the NLRP3 inflammasome, and the NLRP3 inhibitor, glibenclamide, restored B lymphopoiesis and minimized induction of myeloid cells induced by adipocyte-conditioned medium in vitro.	Glyburide	96-109	NLR family pyrin domain containing 3	Homo sapiens	79-84
28288918-1	2017	We hypothesized that elevations of carbon dioxide (CO2) commonly found in modern buildings will stimulate leukocytes to produce microparticles (MPs) and activate the nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome due to mitochondrial oxidative stress.	Carbon Dioxide	35-49	NLR family pyrin domain containing 3	Homo sapiens	166-207
28288918-1	2017	We hypothesized that elevations of carbon dioxide (CO2) commonly found in modern buildings will stimulate leukocytes to produce microparticles (MPs) and activate the nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome due to mitochondrial oxidative stress.	Carbon Dioxide	35-49	NLR family pyrin domain containing 3	Homo sapiens	209-214
28288918-1	2017	We hypothesized that elevations of carbon dioxide (CO2) commonly found in modern buildings will stimulate leukocytes to produce microparticles (MPs) and activate the nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome due to mitochondrial oxidative stress.	Carbon Dioxide	51-54	NLR family pyrin domain containing 3	Homo sapiens	166-207
28288918-1	2017	We hypothesized that elevations of carbon dioxide (CO2) commonly found in modern buildings will stimulate leukocytes to produce microparticles (MPs) and activate the nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome due to mitochondrial oxidative stress.	Carbon Dioxide	51-54	NLR family pyrin domain containing 3	Homo sapiens	209-214
28288918-7	2017	Elevations of CO2 cause oligomerization of the inflammasome components ASC, NLRP3, caspase 1, thioredoxin interacting protein, and calreticulin - a protein from endoplasmic reticulum, leading to IL-1beta synthesis.	Carbon Dioxide	14-17	NLR family pyrin domain containing 3	Homo sapiens	76-81
28302726-5	2017	TTP targets AU-rich elements in the NLRP3 3"-untranslated region (UTR) and represses NLRP3 expression.	Gold	12-14	NLR family pyrin domain containing 3	Homo sapiens	36-41
28322865-6	2017	In addition, expression levels of NOD-like receptor protein 3 (NLRP3) and hedgehog signaling transcription factor Gli-1 were increased in PA-exposed HSCs.	Palmitic Acid	138-140	NLR family pyrin domain containing 3	Homo sapiens	34-61
28322865-6	2017	In addition, expression levels of NOD-like receptor protein 3 (NLRP3) and hedgehog signaling transcription factor Gli-1 were increased in PA-exposed HSCs.	Palmitic Acid	138-140	NLR family pyrin domain containing 3	Homo sapiens	63-68
28052869-0	2017	NLRP3 inflammasome activation contributes to aldosterone-induced podocyte injury.	Aldosterone	45-56	NLR family pyrin domain containing 3	Homo sapiens	0-5
28367997-0	2017	Perfluorodecanoic acid stimulates NLRP3 inflammasome assembly in gastric cells.	perfluorodecanoic acid	0-22	NLR family pyrin domain containing 3	Homo sapiens	34-39
28052869-5	2017	In vitro, exposure of podocytes to Aldo enhanced NLRP3, caspase-1, and IL-18 expressions in dose- and time-dependent manners, indicating an activation of NLRP3 inflammasome, which was significantly blocked by the mineralocorticoid receptor antagonist eplerenone or the antioxidant N-acetylcysteine.	Eplerenone	251-261	NLR family pyrin domain containing 3	Homo sapiens	154-159
28177948-3	2017	Although the importance of the NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome as the initial immune reaction against silica particles has been identified, the mechanisms involved that lead to various autoimmune diseases in patients exposed to silica remain largely unknown.	Silicon Dioxide	265-271	NLR family pyrin domain containing 3	Homo sapiens	80-85
28052869-5	2017	In vitro, exposure of podocytes to Aldo enhanced NLRP3, caspase-1, and IL-18 expressions in dose- and time-dependent manners, indicating an activation of NLRP3 inflammasome, which was significantly blocked by the mineralocorticoid receptor antagonist eplerenone or the antioxidant N-acetylcysteine.	Acetylcysteine	281-297	NLR family pyrin domain containing 3	Homo sapiens	154-159
28052869-7	2017	In vivo, since day 5 of Aldo infusion, NLRP3 inflammasome activation and podocyte injury evidenced by nephrin reduction occurred concurrently.	Aldosterone	24-28	NLR family pyrin domain containing 3	Homo sapiens	39-44
28052869-8	2017	More importantly, immunofluorescence analysis showed a significant induction of NLRP3 in podocytes of glomeruli following Aldo infusion.	Aldosterone	122-126	NLR family pyrin domain containing 3	Homo sapiens	80-85
28177948-3	2017	Although the importance of the NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome as the initial immune reaction against silica particles has been identified, the mechanisms involved that lead to various autoimmune diseases in patients exposed to silica remain largely unknown.	Silicon Dioxide	139-145	NLR family pyrin domain containing 3	Homo sapiens	31-78
28177948-3	2017	Although the importance of the NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome as the initial immune reaction against silica particles has been identified, the mechanisms involved that lead to various autoimmune diseases in patients exposed to silica remain largely unknown.	Silicon Dioxide	139-145	NLR family pyrin domain containing 3	Homo sapiens	80-85
26435068-5	2017	In THP-1 cells, CORM-2 treatment dose-dependently reduced the activation of caspase-1 and the secretion of IL-1beta, and increased the levels of IL-10, in response to LPS and adenosine 5"-triphosphate (ATP), an NLRP3 inflammasome activation model.	Adenosine Triphosphate	175-200	NLR family pyrin domain containing 3	Homo sapiens	211-216
28077335-0	2017	Omega-3 fatty acids regulate NLRP3 inflammasome activation and prevent behavior deficits after traumatic brain injury.	Fatty Acids, Omega-3	0-19	NLR family pyrin domain containing 3	Homo sapiens	29-34
28077335-6	2017	beta-Arrestin-2 (ARRB2), a downstream scaffold protein of GPR40, was activated to inhibit inflammation via directly binding with NLRP3 in the omega-3 FAs treatment group.	ammonium ferrous sulfate	150-153	NLR family pyrin domain containing 3	Homo sapiens	129-134
27913221-8	2017	Formation of the NACHT, leucine-rich repeat (LRR) and pyrin (PYD) domains-containing protein 3 (Nalp3) inflammasome in particular, has directly been attributed to late-stage acetaminophen toxicity.	Acetaminophen	174-187	NLR family pyrin domain containing 3	Homo sapiens	96-101
28167279-6	2017	We activated NLRP3 inflammasome in human MSCs via lipopolysaccharide and palmitic acid (LPS/PA) treatment for self-renewal maintenance, adipogenic differentiation or osteogenic differentiation.	Palmitic Acid	73-86	NLR family pyrin domain containing 3	Homo sapiens	13-18
27692470-8	2017	Another therapeutic candidate can be broad-acting 2-hydroxypropyl-beta-cyclodextrin, a compound that targets several mechanisms such as cholesterol efflux, complement gene expression, and the NLRP3 pathway.	2-Hydroxypropyl-beta-cyclodextrin	50-83	NLR family pyrin domain containing 3	Homo sapiens	192-197
28356505-1	2017	The NLRP3 inflammasome/caspase-1/IL-1beta axis may be a therapeutic target in severe steroid-resistant asthma.	Steroids	85-92	NLR family pyrin domain containing 3	Homo sapiens	4-9
28027970-0	2017	HBV inhibits LPS-induced NLRP3 inflammasome activation and IL-1beta production via suppressing the NF-kappaB pathway and ROS production.	Reactive Oxygen Species	121-124	NLR family pyrin domain containing 3	Homo sapiens	25-30
28027970-10	2017	CONCLUSIONS: HBeAg inhibits LPS-induced NLRP3 inflammasome activation and IL-1beta production via suppressing NF-kappaB pathway and ROS production.	Reactive Oxygen Species	132-135	NLR family pyrin domain containing 3	Homo sapiens	40-45
28027970-12	2017	LAY SUMMARY: HBeAg suppresses LPS-induced NLRP3 inflammasome activation and IL-1beta production in two ways, one is to repress NLRP3 and pro-IL-1beta expression via inhibiting NF-kappaB phosphorylation, and the other is to repress caspase-1 activation and IL-1beta maturation via inhibiting ROS production.	Reactive Oxygen Species	291-294	NLR family pyrin domain containing 3	Homo sapiens	42-47
28129888-11	2017	Recent preclinical studies have reported that beta-hydroxybutyrate (betaOHB) may protect the brain from the adverse effects of both the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome and the deacetylation of histone.	3-Hydroxybutyric Acid	46-66	NLR family pyrin domain containing 3	Homo sapiens	209-214
28129888-11	2017	Recent preclinical studies have reported that beta-hydroxybutyrate (betaOHB) may protect the brain from the adverse effects of both the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome and the deacetylation of histone.	betaohb	68-75	NLR family pyrin domain containing 3	Homo sapiens	209-214
28167279-6	2017	We activated NLRP3 inflammasome in human MSCs via lipopolysaccharide and palmitic acid (LPS/PA) treatment for self-renewal maintenance, adipogenic differentiation or osteogenic differentiation.	Protactinium	92-94	NLR family pyrin domain containing 3	Homo sapiens	13-18
28167279-7	2017	LPS/PA treatment significantly increased NLRP3 expression, decreased SIRT1 expression and promoted caspase-1 activity in MSCs.	Protactinium	4-6	NLR family pyrin domain containing 3	Homo sapiens	41-46
28056339-3	2017	We recently found that asbestos activates the nod-like receptor family member containing a pyrin domain 3 (NLRP3) inflammasome in a protracted manner, leading to an up-regulation of IL-1beta and IL-18 production in human mesothelial cells.	Asbestos	23-31	NLR family pyrin domain containing 3	Homo sapiens	107-112
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Adenosine Triphosphate	16-19	NLR family pyrin domain containing 3	Homo sapiens	52-57
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Reactive Oxygen Species	210-233	NLR family pyrin domain containing 3	Homo sapiens	52-57
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Reactive Oxygen Species	235-238	NLR family pyrin domain containing 3	Homo sapiens	52-57
28064010-0	2017	Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway.	Reactive Oxygen Species	144-167	NLR family pyrin domain containing 3	Homo sapiens	109-114
27908642-5	2017	We found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP)-induced the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs).	Adenosine Triphosphate	43-65	NLR family pyrin domain containing 3	Homo sapiens	98-103
27908642-5	2017	We found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP)-induced the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs).	Adenosine Triphosphate	67-70	NLR family pyrin domain containing 3	Homo sapiens	98-103
27908642-7	2017	Importantly, gene silencing of SIRT1 abrogated the inhibitory effect of SIRT1 activator on NLRP3 inflammasome formation and IL-1beta production in HUVECs stimulated with LPS plus ATP.	Adenosine Triphosphate	179-182	NLR family pyrin domain containing 3	Homo sapiens	91-96
28087670-4	2017	Endoplasmic reticulum-loaded plant lectins then triggered Ca2+ release and mitochondrial damage, and inhibition of Ca2+ release and mitochondrial reactive oxygen species by chemical inhibitors significantly suppressed NLRP3 inflammasome activation.	Reactive Oxygen Species	146-169	NLR family pyrin domain containing 3	Homo sapiens	218-223
28064010-0	2017	Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway.	Reactive Oxygen Species	169-172	NLR family pyrin domain containing 3	Homo sapiens	109-114
28064010-6	2017	NLRP3 inflammasome was found to mediate IL-1beta secretion through the production of ROS (reactive oxygen species) during the senescence of endothelial cells.	Reactive Oxygen Species	85-88	NLR family pyrin domain containing 3	Homo sapiens	0-5
28064010-6	2017	NLRP3 inflammasome was found to mediate IL-1beta secretion through the production of ROS (reactive oxygen species) during the senescence of endothelial cells.	Reactive Oxygen Species	90-113	NLR family pyrin domain containing 3	Homo sapiens	0-5
28064010-7	2017	Furthermore, the association of TXNIP (thioredoxin-interacting protein) with NLRP3 induced by ROS promoted NLRP3 inflammasome activation in senescent endothelial cells.	Reactive Oxygen Species	94-97	NLR family pyrin domain containing 3	Homo sapiens	77-82
28064010-7	2017	Furthermore, the association of TXNIP (thioredoxin-interacting protein) with NLRP3 induced by ROS promoted NLRP3 inflammasome activation in senescent endothelial cells.	Reactive Oxygen Species	94-97	NLR family pyrin domain containing 3	Homo sapiens	107-112
27940204-0	2017	Potentiation of hepatic stellate cell activation by extracellular ATP is dependent on P2X7R-mediated NLRP3 inflammasome activation.	Adenosine Triphosphate	66-69	NLR family pyrin domain containing 3	Homo sapiens	101-106
27940204-11	2017	Additionally LX-2 cells primed with LPS and subsequently stimulated for 30min with ATP greatly increased mRNA and protein expression of caspase-1, NLRP3 and P2x7R, as well as liver fibrosis markers, alpha-SMA and type I collagen.	Adenosine Triphosphate	83-86	NLR family pyrin domain containing 3	Homo sapiens	147-152
28394398-9	2017	Expression of PPARGC1B and NLRP3 was induced in urate crystal-activated THP-1, peripheral blood mononuclear cells and synovial cells from gout patients in acute stage.	Uric Acid	48-53	NLR family pyrin domain containing 3	Homo sapiens	27-32
28394398-10	2017	siRNA knockdown of PPARGC1B upregulated NLRP3 in urate crystal-activated macrophages.	Uric Acid	49-54	NLR family pyrin domain containing 3	Homo sapiens	40-45
27846743-7	2017	RESULTS: We found altered expression of several proteins after enalapril treatment (decreased: NFkappaB, p = .043; NLRP3, p = .050; AMACR, p = .017; and caspase 3, p = .025; increased: p53, p = .050).	Enalapril	63-72	NLR family pyrin domain containing 3	Homo sapiens	115-120
28249154-0	2017	beta-Hydroxybutyrate Deactivates Neutrophil NLRP3 Inflammasome to Relieve Gout Flares.	3-Hydroxybutyric Acid	0-20	NLR family pyrin domain containing 3	Homo sapiens	44-49
28249154-5	2017	BHB inhibited NLRP3 inflammasome in S100A9 fibril-primed and urate crystal-activated macrophages, which serve to recruit inflammatory neutrophils in joints.	3-Hydroxybutyric Acid	0-3	NLR family pyrin domain containing 3	Homo sapiens	14-19
28249154-7	2017	Mechanistically, BHB inhibited the NLRP3 inflammasome in neutrophils by reducing priming and assembly steps.	3-Hydroxybutyric Acid	17-20	NLR family pyrin domain containing 3	Homo sapiens	35-40
28057759-7	2017	However, both NLRP3 depletion and inhibition of K+ efflux mitigated abacavir-induced mitochondrial reactive oxygen species production and cytotoxicity, suggesting that these processes were secondary to NLRP3 activation.	abacavir	68-76	NLR family pyrin domain containing 3	Homo sapiens	14-19
28057759-7	2017	However, both NLRP3 depletion and inhibition of K+ efflux mitigated abacavir-induced mitochondrial reactive oxygen species production and cytotoxicity, suggesting that these processes were secondary to NLRP3 activation.	abacavir	68-76	NLR family pyrin domain containing 3	Homo sapiens	202-207
28057759-0	2017	Potent NLRP3 Inflammasome Activation by the HIV Reverse Transcriptase Inhibitor Abacavir.	abacavir	80-88	NLR family pyrin domain containing 3	Homo sapiens	7-12
28057759-7	2017	However, both NLRP3 depletion and inhibition of K+ efflux mitigated abacavir-induced mitochondrial reactive oxygen species production and cytotoxicity, suggesting that these processes were secondary to NLRP3 activation.	Reactive Oxygen Species	99-122	NLR family pyrin domain containing 3	Homo sapiens	14-19
28208613-5	2017	In addition, purpurin could down-regulate NLRP3 inflammasome assembly and activation, suggesting that it might protect foods against oxidative damage and prevent in vivo oxidative stress and inflammation.	purpurin	13-21	NLR family pyrin domain containing 3	Homo sapiens	42-47
28261091-5	2017	Succinate promoted IL-1beta production through NLRP3 inflammasome activation and then increased cAMP accumulation by impairing PDE3B expression, leading to increased lipolysis.	Succinic Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	47-52
28261091-6	2017	Ginsenoside Rg5 treatment suppressed NLRP3 inflammasome activation, preserved PDE3B expression and then reduced cAMP accumulation, contributing to inhibition of lipolysis.	Ginsenosides	0-11	NLR family pyrin domain containing 3	Homo sapiens	37-42
28261091-10	2017	These findings establish a previously unrecognized role of ginsenosides in the regulation of lipid and glucose homeostasis and suggest that adipose succinate-associated NLRP3 inflammasome activation might be targeted therapeutically to prevent lipolysis and insulin resistance.	Ginsenosides	59-71	NLR family pyrin domain containing 3	Homo sapiens	169-174
28261091-10	2017	These findings establish a previously unrecognized role of ginsenosides in the regulation of lipid and glucose homeostasis and suggest that adipose succinate-associated NLRP3 inflammasome activation might be targeted therapeutically to prevent lipolysis and insulin resistance.	Succinic Acid	148-157	NLR family pyrin domain containing 3	Homo sapiens	169-174
28096356-4	2017	Here, we provide evidence that MLKL-induced activation of NLRP3 requires (i) the death effector four-helical bundle of MLKL, (ii) oligomerization and association of MLKL with cellular membranes, and (iii) a reduction in intracellular potassium concentration.	Potassium	234-243	NLR family pyrin domain containing 3	Homo sapiens	58-63
27845246-2	2017	The aims of the study were to (1) assess the potential of palmitate to promote inflammatory signaling in cardiac fibroblasts through TLR4 and the NLRP3 inflammasome and (2) characterize the cellular phenotype of cardiac fibroblasts exposed to palmitate.	Palmitates	58-67	NLR family pyrin domain containing 3	Homo sapiens	146-151
27845246-6	2017	Whereas palmitate did not prime the NLRP3 inflammasome, it induced activation in LPS-primed cardiac fibroblasts as indicated by IL-1beta, IL-18 production and NLRP3-ASC co-localization.	Palmitates	8-17	NLR family pyrin domain containing 3	Homo sapiens	159-164
27845246-7	2017	Palmitate-induced NLRP3 inflammasome activation in LPS-primed cardiac fibroblasts was associated with reduced AMPK activity, mitochondrial reactive oxygen species production and mitochondrial dysfunction.	Palmitates	0-9	NLR family pyrin domain containing 3	Homo sapiens	18-23
27845246-7	2017	Palmitate-induced NLRP3 inflammasome activation in LPS-primed cardiac fibroblasts was associated with reduced AMPK activity, mitochondrial reactive oxygen species production and mitochondrial dysfunction.	Reactive Oxygen Species	139-162	NLR family pyrin domain containing 3	Homo sapiens	18-23
27845246-8	2017	The cardiac fibroblast phenotype caused by palmitate, in an LPS and NLRP3 independent manner, was characterized by decreased cellular proliferation, contractility, collagen and MMP-2 expression, as well as increased senescence-associated beta-galactosidase activity, and consistent with a state of cellular senescence.	Palmitates	43-52	NLR family pyrin domain containing 3	Homo sapiens	68-73
27845246-9	2017	This study establishes that in vitro palmitate exposure of cardiac fibroblasts provides inflammatory responses via TLR4 and NLRP3 inflammasome activation.	Palmitates	37-46	NLR family pyrin domain containing 3	Homo sapiens	124-129
27845246-10	2017	Palmitate also modulates cardiac fibroblast functionality, in a NLRP3 independent manner, resulting in a phenotype related to cellular senescence.	Palmitates	0-9	NLR family pyrin domain containing 3	Homo sapiens	64-69
28110709-5	2017	Mitochondrial reactive oxygen species in turn activate the NLRP3 inflammasome, allowing increased IL-1beta processing and secretion, which likely underlies both chromium(VI)-induced cutaneous toxicity and sensitization.	Reactive Oxygen Species	14-37	NLR family pyrin domain containing 3	Homo sapiens	59-64
28084571-16	2017	Uric acid formed from xanthine-xanthine oxidase interaction stimulates CD36 expression and triggers foam cell formation independent of NLRP3 activation.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	135-140
27842238-1	2017	Classical modes of NLRP3 activation entail a priming step that enables its activation (signal 1) and a potassium efflux-dependent activation signal (signal 2) that triggers pyroptosome formation and pyroptosis, a lytic cell death necessary for IL-1beta release.	Potassium	103-112	NLR family pyrin domain containing 3	Homo sapiens	19-24
28371616-2	2017	The present study was performed to investigate the underlying mechanism of the anti-inflammation effect of Sal A, especially focusing on mTOR-KEAP1-Nrf2 and P2X7R-PKR-NLRP3 signaling pathways.	salvianolic acid A	107-112	NLR family pyrin domain containing 3	Homo sapiens	167-172
28371616-9	2017	Sal A also inhibited RPE inflammation by inactivating the P2x7r-Pkr-Nlrp3 signaling pathway.	salvianolic acid A	0-5	NLR family pyrin domain containing 3	Homo sapiens	68-73
28084571-4	2017	This study was designed to study the role of various scavenger receptors and NLRP3 inflammasome in xanthine oxidase and uric acid-induced foam cell formation.	Uric Acid	120-129	NLR family pyrin domain containing 3	Homo sapiens	77-82
28084571-9	2017	Blockade of LOX-1 or NLRP3 inflammasome with specific siRNAs reduced xanthine oxidase-induced foam cell formation, ROS generation and activation of NLRP3 and downstream signals.	Reactive Oxygen Species	115-118	NLR family pyrin domain containing 3	Homo sapiens	21-26
28084571-13	2017	Xanthine oxidase stimulates LOX-1 expression on the cell membrane of macrophages and vascular smooth muscle cells (VSMCs) and increases generation of ROS, which activate NLRP3 inflammasome and downstream pro-inflammatory mediators such as Caspase-1, IL-1beta and IL-18.	Reactive Oxygen Species	150-153	NLR family pyrin domain containing 3	Homo sapiens	170-175
27751866-6	2017	Inflammasome activation was initiated by mitochondrial reactive oxygen species production triggered by chromium (VI), as indicated by sensitivity to treatment with the ROS scavenger N-acetyl cysteine and a coinciding failure of K+ efflux, caspase-1, or NLRP3 inhibition to prevent mitochondrial reactive oxygen species accumulation.	Reactive Oxygen Species	55-78	NLR family pyrin domain containing 3	Homo sapiens	253-258
28110709-6	2017	Interrupting this mechanism, perhaps with reducing agents or inhibitors of the NLRP3/IL-1 axis, may be a new option to prevent occupational chromium toxicity and allergy.	Chromium	140-148	NLR family pyrin domain containing 3	Homo sapiens	79-84
28808190-5	2017	In fact, animal studies have demonstrated that cholesterol crystals can trigger an inflammatory response via NLRP3 inflammasome similar to that seen with gout.	Cholesterol	47-58	NLR family pyrin domain containing 3	Homo sapiens	109-114
28146092-0	2017	Synthesis and Biological Evaluation of Novel Benzimidazole Derivatives and Analogs Targeting the NLRP3 Inflammasome.	benzimidazole	45-58	NLR family pyrin domain containing 3	Homo sapiens	97-102
28146092-1	2017	A series of benzo[d]imidazole analogues of thiabenzole were synthesized and their antiinflammatory activities toward NLRP3 (nucleotide-binding domain leucine-rich repeat containing protein family,pyrin domain-containing 3,also known as cryopyrin or NALP3) inflammasome were evaluated in vitro.	benzo[d]imidazole	12-29	NLR family pyrin domain containing 3	Homo sapiens	117-122
28146092-1	2017	A series of benzo[d]imidazole analogues of thiabenzole were synthesized and their antiinflammatory activities toward NLRP3 (nucleotide-binding domain leucine-rich repeat containing protein family,pyrin domain-containing 3,also known as cryopyrin or NALP3) inflammasome were evaluated in vitro.	Thiabendazole	43-54	NLR family pyrin domain containing 3	Homo sapiens	117-122
28146092-1	2017	A series of benzo[d]imidazole analogues of thiabenzole were synthesized and their antiinflammatory activities toward NLRP3 (nucleotide-binding domain leucine-rich repeat containing protein family,pyrin domain-containing 3,also known as cryopyrin or NALP3) inflammasome were evaluated in vitro.	Thiabendazole	43-54	NLR family pyrin domain containing 3	Homo sapiens	236-245
28146092-1	2017	A series of benzo[d]imidazole analogues of thiabenzole were synthesized and their antiinflammatory activities toward NLRP3 (nucleotide-binding domain leucine-rich repeat containing protein family,pyrin domain-containing 3,also known as cryopyrin or NALP3) inflammasome were evaluated in vitro.	Thiabendazole	43-54	NLR family pyrin domain containing 3	Homo sapiens	249-254
28334721-6	2017	RESULTS: MiR-9 inhibited while anti-miR-9 antisense oligonucleotides induced interleukin-1 beta (IL-1beta) and NLRP3 inflammasome activation in all in vitro models.	Oligonucleotides	52-68	NLR family pyrin domain containing 3	Homo sapiens	111-116
28135700-2	2017	As a response to cholesterol crystal accumulation, the NLRP3 inflammasome is activated to produce IL-1beta which eventually leads to atherosclerotic lesions.	Cholesterol	17-28	NLR family pyrin domain containing 3	Homo sapiens	55-60
27784694-9	2017	Moreover, CAY10598 prevented the activation of NLRP3 inflammasomes induced by angiotensin II in human proximal tubule cells (HK2).	CAY10598	10-18	NLR family pyrin domain containing 3	Homo sapiens	47-52
28854426-0	2017	Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages.	Reactive Oxygen Species	36-39	NLR family pyrin domain containing 3	Homo sapiens	50-55
28738323-1	2017	BACKGROUND: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by free fatty acids (FFA) by blunting NLRP3 inflammasome activation via a specific TLR4/NF-kappaB pathway.	Hydrogen Sulfide	62-78	NLR family pyrin domain containing 3	Homo sapiens	193-198
28738323-1	2017	BACKGROUND: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by free fatty acids (FFA) by blunting NLRP3 inflammasome activation via a specific TLR4/NF-kappaB pathway.	Hydrogen Sulfide	80-83	NLR family pyrin domain containing 3	Homo sapiens	193-198
28738323-1	2017	BACKGROUND: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by free fatty acids (FFA) by blunting NLRP3 inflammasome activation via a specific TLR4/NF-kappaB pathway.	Fatty Acids, Nonesterified	176-179	NLR family pyrin domain containing 3	Homo sapiens	193-198
28738323-5	2017	RESULTS: H2S attenuated FFA-induced cell apoptosis, and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL- 1beta, IL-18 and caspase-3.	Hydrogen Sulfide	9-12	NLR family pyrin domain containing 3	Homo sapiens	82-87
28738323-8	2017	CONCLUSION: The present study demonstrated for the first time that H2S appears to suppress FFA-induced macrophage inflammation and apoptosis by inhibiting the TLR4/ NF-kappaB pathway and its downstream NLRP3 inflammasome activation.	Hydrogen Sulfide	67-70	NLR family pyrin domain containing 3	Homo sapiens	202-207
28628921-0	2017	Activation of COX-2/mPGES-1/PGE2 Cascade via NLRP3 Inflammasome Contributes to Albumin-Induced Proximal Tubule Cell Injury.	Dinoprostone	28-32	NLR family pyrin domain containing 3	Homo sapiens	45-50
28628921-9	2017	CONCLUSIONS: The findings suggest that COX-2/mPGES-1/PGE2 axis could be activated by albumin in the proximal tubular cells via a NLRP3 inflammasome-mediated mechanism and could thus contribute to proteinuria-related renal tubular cell injury.	Dinoprostone	53-57	NLR family pyrin domain containing 3	Homo sapiens	129-134
28854426-0	2017	Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages.	Glucose	121-128	NLR family pyrin domain containing 3	Homo sapiens	50-55
28977782-0	2017	Edaravone Attenuates the Proinflammatory Response in Amyloid-beta-Treated Microglia by Inhibiting NLRP3 Inflammasome-Mediated IL-1beta Secretion.	Edaravone	0-9	NLR family pyrin domain containing 3	Homo sapiens	98-103
28854426-2	2017	We hypothesized that stimulation with high glucose following a pro-inflammatory signal would lead to autophagy inhibition, reactive oxygen species (ROS) production and eventually to the activation of the Nod-like receptor protein (NLRP) -3.	Glucose	43-50	NLR family pyrin domain containing 3	Homo sapiens	204-239
28977782-10	2017	Moreover, EDA obviously attenuated the depolarization of  psim, reduced mitochondria-derived ROS production and increased SOD-2 activity, resulting in the suppression of NLRP3 inflammasome-mediated IL-1beta secretion in Abeta-treated microglia.	Edaravone	10-13	NLR family pyrin domain containing 3	Homo sapiens	170-175
28854426-9	2017	Our data showed that high glucose inhibited autophagy, induced ROS production, and activated NLRP3 inflammasome and cytokine secretion in THP-1-derived macrophages.	Glucose	26-33	NLR family pyrin domain containing 3	Homo sapiens	93-98
28854426-10	2017	To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion.	Glucose	14-21	NLR family pyrin domain containing 3	Homo sapiens	30-35
28854426-10	2017	To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion.	Glucose	14-21	NLR family pyrin domain containing 3	Homo sapiens	132-137
28854426-10	2017	To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion.	Glucose	14-21	NLR family pyrin domain containing 3	Homo sapiens	132-137
28854426-12	2017	Autophagy inhibition and ROS generation play an essential role in high glucose-induced NLRP3 inflammasome activation and cytokine secretion in macrophages.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	87-92
28854426-12	2017	Autophagy inhibition and ROS generation play an essential role in high glucose-induced NLRP3 inflammasome activation and cytokine secretion in macrophages.	Glucose	71-78	NLR family pyrin domain containing 3	Homo sapiens	87-92
27538510-5	2017	Several molecular signaling pathways are shown to mediate the activation of the NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production.	Reactive Oxygen Species	225-248	NLR family pyrin domain containing 3	Homo sapiens	80-85
27538510-5	2017	Several molecular signaling pathways are shown to mediate the activation of the NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production.	Reactive Oxygen Species	250-253	NLR family pyrin domain containing 3	Homo sapiens	80-85
28164132-0	2017	NLRP3 Inflammasome Expression and Signaling in Human Diabetic Wounds and in High Glucose Induced Macrophages.	Glucose	81-88	NLR family pyrin domain containing 3	Homo sapiens	0-5
28928791-8	2017	These results suggested that WMW could alleviate palmitate-induced insulin resistance in HepG2 cells via inhibition of NLRP3 inflammasome and reduction of proinflammatory cytokine production.	Palmitates	49-58	NLR family pyrin domain containing 3	Homo sapiens	119-124
29104591-7	2017	This review, first, gives an overview concerning the growing importance of melatonin in the inflammatory-mediated pathological conditions and, then, focuses on its roles and its protective effects against the activation of the inflammasomes and, in particular, of the NLRP3 inflammasome.	Melatonin	75-84	NLR family pyrin domain containing 3	Homo sapiens	268-273
28164132-2	2017	To investigate the contribution and mechanism of NLRP3 inflammasome expression in human wounds in diabetes mellitus and in high glucose induced macrophages.	Glucose	128-135	NLR family pyrin domain containing 3	Homo sapiens	49-54
28164132-5	2017	We also examined whether high glucose induces NLRP3 inflammasome expression in cultures THP-1-derived macrophages and the influence on IL-1beta expression.	Glucose	30-37	NLR family pyrin domain containing 3	Homo sapiens	46-51
28164132-8	2017	High glucose induced a significant increase in NLRP3 inflammasome and IL-1beta expression in THP-1-derived macrophages.	Glucose	5-12	NLR family pyrin domain containing 3	Homo sapiens	47-52
28164132-12	2017	The higher expression of NLRP3, caspase1, and secretion of IL-1beta, signaling, and activation might contribute to the hyperinflammation in the human diabetic wound and in high glucose induced macrophages.	Glucose	177-184	NLR family pyrin domain containing 3	Homo sapiens	25-30
28740332-4	2017	Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells.	Glyburide	0-13	NLR family pyrin domain containing 3	Homo sapiens	109-114
27903743-4	2017	One of these damage-associated molecular patterns, uric acid, is increased in the maternal circulation in pathological pregnancies and is a known agonist of the Nlrp3 inflammasome and inducer of inflammation.	Uric Acid	51-60	NLR family pyrin domain containing 3	Homo sapiens	161-166
27655219-0	2017	Hemin and Cobalt Protoporphyrin Inhibit NLRP3 Inflammasome Activation by Enhancing Autophagy: A Novel Mechanism of Inflammasome Regulation.	Hemin	0-5	NLR family pyrin domain containing 3	Homo sapiens	40-45
27655219-0	2017	Hemin and Cobalt Protoporphyrin Inhibit NLRP3 Inflammasome Activation by Enhancing Autophagy: A Novel Mechanism of Inflammasome Regulation.	cobaltiprotoporphyrin	10-31	NLR family pyrin domain containing 3	Homo sapiens	40-45
27655219-6	2017	In cultured macrophages, hemin and CoPP inhibited NLRP3 inflammasome assembly by reducing the amount of intracellular apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC).	cobaltiprotoporphyrin	35-39	NLR family pyrin domain containing 3	Homo sapiens	50-55
29911779-0	2017	[Inhibitory effect and mechanism of deoxyschizandrin on NLRP3 inflammasome].	schizandrin A	36-52	NLR family pyrin domain containing 3	Homo sapiens	56-61
29911779-7	2017	Deoxyschizandrin (25, 50, 100, and 200 mumol L(-1)) could inhibit the activation of NLRP3 inflammasome caused by nigericin and ATP, and inhibit the secretion of IL-1beta, which was associated with inhibiting the cleavage of pro-caspase-1.	schizandrin A	0-16	NLR family pyrin domain containing 3	Homo sapiens	84-89
29911779-7	2017	Deoxyschizandrin (25, 50, 100, and 200 mumol L(-1)) could inhibit the activation of NLRP3 inflammasome caused by nigericin and ATP, and inhibit the secretion of IL-1beta, which was associated with inhibiting the cleavage of pro-caspase-1.	Nigericin	113-122	NLR family pyrin domain containing 3	Homo sapiens	84-89
29911779-7	2017	Deoxyschizandrin (25, 50, 100, and 200 mumol L(-1)) could inhibit the activation of NLRP3 inflammasome caused by nigericin and ATP, and inhibit the secretion of IL-1beta, which was associated with inhibiting the cleavage of pro-caspase-1.	Adenosine Triphosphate	127-130	NLR family pyrin domain containing 3	Homo sapiens	84-89
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	schizandrin A	27-43	NLR family pyrin domain containing 3	Homo sapiens	117-122
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	schizandrin A	27-43	NLR family pyrin domain containing 3	Homo sapiens	321-326
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	schizandrin A	285-301	NLR family pyrin domain containing 3	Homo sapiens	117-122
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	Adenosine Triphosphate	532-535	NLR family pyrin domain containing 3	Homo sapiens	117-122
29911779-1	2017	This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome.	schizandrin A	93-109	NLR family pyrin domain containing 3	Homo sapiens	129-134
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	Nigericin	540-549	NLR family pyrin domain containing 3	Homo sapiens	117-122
27737891-6	2016	Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in MDSs and are sufficient to restore effective hematopoiesis.	Reactive Oxygen Species	134-137	NLR family pyrin domain containing 3	Homo sapiens	22-27
28083517-4	2016	Methods:P. gingivalis strain CCUG25226 was used to study the mechanisms underlying the regulation of HGF NLRP3 expression by the infection of high-glucose-treated P. gingivalis (HGPg).	Glucose	147-154	NLR family pyrin domain containing 3	Homo sapiens	105-110
27737891-6	2016	Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in MDSs and are sufficient to restore effective hematopoiesis.	Reactive Oxygen Species	134-137	NLR family pyrin domain containing 3	Homo sapiens	100-105
27447246-9	2016	These results demonstrate the importance of the NLRP3 inflammasome in mediating BS- and CS-induced HBE cell damage and proapoptosis.	Cesium	88-90	NLR family pyrin domain containing 3	Homo sapiens	48-53
28031693-9	2016	Salt-induced osmotic stress also induces priming of the NLRP3 inflammasome and activates inflammatory enzymes in RPE cells.	Salts	0-4	NLR family pyrin domain containing 3	Homo sapiens	56-61
27929137-6	2016	We also revealed that inhibition of PKR suppressed H2O2 induced NFkappaB pathway and NLRP3 activation.	Hydrogen Peroxide	51-55	NLR family pyrin domain containing 3	Homo sapiens	85-90
27803035-9	2016	In addition, aldosterone increased the expression of NLRP3, active caspase-1, and mature interleukin-1beta in human peripheral blood mononuclear cells.	Aldosterone	13-24	NLR family pyrin domain containing 3	Homo sapiens	53-58
27803035-10	2016	Hypertensive patients with hyperaldosteronism or normal levels of aldosterone exhibited increased activity of NLRP3 inflammasome, suggesting that the effect of hyperaldosteronism on the inflammasome may be mediated through high blood pressure.	Aldosterone	66-77	NLR family pyrin domain containing 3	Homo sapiens	110-115
27929086-7	2016	Furthermore, TRIM31 deficiency attenuates the severity of dextran sodium sulfate (DSS)-induced colitis, an inflammatory bowel diseases model in which NLRP3 possesses protective roles.	dss	82-85	NLR family pyrin domain containing 3	Homo sapiens	150-155
27833015-0	2016	Trimethylamine N-oxide induces inflammation and endothelial dysfunction in human umbilical vein endothelial cells via activating ROS-TXNIP-NLRP3 inflammasome.	trimethyloxamine	0-22	NLR family pyrin domain containing 3	Homo sapiens	139-144
27833015-0	2016	Trimethylamine N-oxide induces inflammation and endothelial dysfunction in human umbilical vein endothelial cells via activating ROS-TXNIP-NLRP3 inflammasome.	Reactive Oxygen Species	129-132	NLR family pyrin domain containing 3	Homo sapiens	139-144
27833015-3	2016	Moreover, thioredoxin-interactive protein (TXNIP) activation is a key event linked to NLRP3 inflammasome via reactive oxygen species (ROS).	Reactive Oxygen Species	109-132	NLR family pyrin domain containing 3	Homo sapiens	86-91
27833015-3	2016	Moreover, thioredoxin-interactive protein (TXNIP) activation is a key event linked to NLRP3 inflammasome via reactive oxygen species (ROS).	Reactive Oxygen Species	134-137	NLR family pyrin domain containing 3	Homo sapiens	86-91
27833015-4	2016	Whether TMAO prime NLRP3 inflammasome via ROS-TXNIP pathway remains unclear.	trimethyloxamine	8-12	NLR family pyrin domain containing 3	Homo sapiens	19-24
27833015-5	2016	This study observed the expression of TXNIP-NLRP3 inflammasome stimulated by TMAO in human umbilical vein endothelial cells (HUVECs), aiming to elucidate the mechanism by which the TMAO may contribute to inflammation and endothelial dysfunction.	trimethyloxamine	77-81	NLR family pyrin domain containing 3	Homo sapiens	44-49
27833015-5	2016	This study observed the expression of TXNIP-NLRP3 inflammasome stimulated by TMAO in human umbilical vein endothelial cells (HUVECs), aiming to elucidate the mechanism by which the TMAO may contribute to inflammation and endothelial dysfunction.	trimethyloxamine	181-185	NLR family pyrin domain containing 3	Homo sapiens	44-49
27833015-6	2016	Our data showed that TMAO significantly triggered oxidative stress and activated TXNIP-NLRP3 inflammasome whereat inflammatory cytokines interleukin (IL)-1beta and IL-18 were released in a dose- and time-dependent manner, but endothelial nitric oxide synthase (eNOS) and production of nitric oxide (NO) were inhibited.	trimethyloxamine	21-25	NLR family pyrin domain containing 3	Homo sapiens	87-92
27833015-6	2016	Our data showed that TMAO significantly triggered oxidative stress and activated TXNIP-NLRP3 inflammasome whereat inflammatory cytokines interleukin (IL)-1beta and IL-18 were released in a dose- and time-dependent manner, but endothelial nitric oxide synthase (eNOS) and production of nitric oxide (NO) were inhibited.	Nitric Oxide	238-250	NLR family pyrin domain containing 3	Homo sapiens	87-92
27833015-7	2016	Moreover, TMAO-mediated effects were observably reversed by ROS inhibitor N-acetylcysteine (NAC) treatment or siRNA-mediated knockdown TXPIN and NLRP3.	trimethyloxamine	10-14	NLR family pyrin domain containing 3	Homo sapiens	145-150
27833015-8	2016	Taken together, our results firstly reveal that TMAO induces inflammation and endothelial dysfunction via activating ROS-TXNIP-NLRP3 inflammasome, suggest a likely mechanism for TMAO-dependent enhancement in atherosclerosis and cardiovascular risks.	trimethyloxamine	48-52	NLR family pyrin domain containing 3	Homo sapiens	127-132
27833015-8	2016	Taken together, our results firstly reveal that TMAO induces inflammation and endothelial dysfunction via activating ROS-TXNIP-NLRP3 inflammasome, suggest a likely mechanism for TMAO-dependent enhancement in atherosclerosis and cardiovascular risks.	Reactive Oxygen Species	117-120	NLR family pyrin domain containing 3	Homo sapiens	127-132
27833015-8	2016	Taken together, our results firstly reveal that TMAO induces inflammation and endothelial dysfunction via activating ROS-TXNIP-NLRP3 inflammasome, suggest a likely mechanism for TMAO-dependent enhancement in atherosclerosis and cardiovascular risks.	trimethyloxamine	178-182	NLR family pyrin domain containing 3	Homo sapiens	127-132
27650785-7	2016	Elimination of TLR4 and NLRP3 abolishes many neuroimmune effects of EtOH.	Ethanol	68-72	NLR family pyrin domain containing 3	Homo sapiens	24-29
27614764-5	2016	Moreover, human nasal epithelial cells (HNECs) were used to evaluate the effects of lipopolysaccharide (LPS) and glyburide on NLRP3 inflammasome signaling pathway.	Glyburide	113-122	NLR family pyrin domain containing 3	Homo sapiens	126-131
27614764-9	2016	NLRP3 inflammasome signaling pathway was augmented by LPS but suppressed by glyburide.	Glyburide	76-85	NLR family pyrin domain containing 3	Homo sapiens	0-5
27614764-11	2016	NLRP3 inflammasome signaling pathway was augmented by LPS, but suppressed by glyburide.	Glyburide	77-86	NLR family pyrin domain containing 3	Homo sapiens	0-5
27826011-5	2016	Hyperglycaemia, hyperlipidaemia and hyperuricaemia can activate the NLRP3 inflammasome, which then mediates the occurrence and development of DN through the K+ channel model, the lysosomal damage model and the active oxygen cluster model.	Oxygen	217-223	NLR family pyrin domain containing 3	Homo sapiens	68-73
27883019-0	2016	17-oxo-DHA displays additive anti-inflammatory effects with fluticasone propionate and inhibits the NLRP3 inflammasome.	(4Z,7Z,10Z,13Z,15E,19Z)-17-Oxodocosahexaenoic acid	0-10	NLR family pyrin domain containing 3	Homo sapiens	100-105
27883019-8	2016	17-oxo-DHA, but not FP, was able to suppress the release of mature IL-1beta through inhibition of the NLRP3 inflammasome.	(4Z,7Z,10Z,13Z,15E,19Z)-17-Oxodocosahexaenoic acid	0-10	NLR family pyrin domain containing 3	Homo sapiens	102-107
27821769-2	2016	Heme has been described as a potent proinflammatory molecule that is able to induce multiple innate immune responses, such as those triggered by TLR4 and the NLRP3 inflammasome, as well as necroptosis in macrophages.	Heme	0-4	NLR family pyrin domain containing 3	Homo sapiens	158-163
28516117-4	2016	Here, we describe how to co-transfect the NLRP3 inflammasome components into HEK293T cells, which enables inflammasome activation and the production of IL-1beta upon stimulation with nigericin.	Nigericin	183-192	NLR family pyrin domain containing 3	Homo sapiens	42-47
27600432-5	2016	Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3.	Reactive Oxygen Species	73-96	NLR family pyrin domain containing 3	Homo sapiens	43-48
27600432-5	2016	Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3.	Reactive Oxygen Species	98-101	NLR family pyrin domain containing 3	Homo sapiens	43-48
27600432-5	2016	Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3.	Reactive Oxygen Species	98-101	NLR family pyrin domain containing 3	Homo sapiens	114-119
27600432-5	2016	Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3.	Reactive Oxygen Species	98-101	NLR family pyrin domain containing 3	Homo sapiens	114-119
27614220-0	2016	Nicotinic acid inhibits NLRP3 inflammasome activation via SIRT1 in vascular endothelial cells.	Niacin	0-14	NLR family pyrin domain containing 3	Homo sapiens	24-29
27614220-4	2016	It was found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs).	Adenosine Triphosphate	47-69	NLR family pyrin domain containing 3	Homo sapiens	104-109
27614220-4	2016	It was found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs).	Adenosine Triphosphate	71-74	NLR family pyrin domain containing 3	Homo sapiens	104-109
27614220-9	2016	In addition, NA inhibited NLRP3 inflammasome activation partly through suppression of ROS.	Reactive Oxygen Species	86-89	NLR family pyrin domain containing 3	Homo sapiens	26-31
27614220-10	2016	Taken together, these findings indicate that NA is able to regulate the activation of NLRP3 inflammasome in HUVECs, which may be partly mediated by SIRT1 and ROS.	Reactive Oxygen Species	158-161	NLR family pyrin domain containing 3	Homo sapiens	86-91
27801679-0	2016	NLRP3 tyrosine phosphorylation is controlled by protein tyrosine phosphatase PTPN22.	Tyrosine	6-14	NLR family pyrin domain containing 3	Homo sapiens	0-5
27694492-4	2016	We show that the KD-associated genetic polymorphism in inositol-triphosphate 3-kinase C (ITPKC) (rs28493229) has important functional consequences, governing ITPKC protein levels and thereby intracellular calcium, which in turn regulates NLRP3 expression and production of IL-1beta and IL-18.	Calcium	205-212	NLR family pyrin domain containing 3	Homo sapiens	238-243
27760332-3	2016	(2016) reveal bile acids as negative regulators of the NLRP3 inflammasome.	Bile Acids and Salts	14-24	NLR family pyrin domain containing 3	Homo sapiens	55-60
27788256-0	2016	P2Y1 Receptor Signaling Contributes to High Salt-Induced Priming of the NLRP3 Inflammasome in Retinal Pigment Epithelial Cells.	Salts	44-48	NLR family pyrin domain containing 3	Homo sapiens	72-77
27788256-8	2016	High extracellular NaCl induced NLRP3 and pro-IL-1beta gene expression, while the gene expression of further inflammasome-associated proteins (NLRP1, NLRP2, NLRP6, NLRP7, NLRP12, NLRC4, AIM2, ASC, procaspase-1, pro-IL-18) was not altered or below the detection threshold.	Sodium Chloride	19-23	NLR family pyrin domain containing 3	Homo sapiens	32-37
27788256-9	2016	The NaCl-induced NLRP3 gene expression was partially dependent on the activities of phospholipase C, IP3 receptors, protein kinase C, the serum and glucocorticoid-regulated kinase, p38 MAPK, ERK1/2, JNK, PI3K, and the transcription factors HIF-1 and NFAT5.	Sodium Chloride	4-8	NLR family pyrin domain containing 3	Homo sapiens	17-22
27788256-10	2016	Pannexin-dependent ATP release and P2Y1 receptor activation is required for the full induction of NLRP3 gene expression.	Adenosine Triphosphate	19-22	NLR family pyrin domain containing 3	Homo sapiens	98-103
27788256-11	2016	High NaCl induced a transient increase of the NLRP3 protein level and a moderate NLRP3 inflammasome activation, as indicated by the transient increase of the cytosolic level of mature IL-1beta.	Sodium Chloride	5-9	NLR family pyrin domain containing 3	Homo sapiens	46-51
27788256-11	2016	High NaCl induced a transient increase of the NLRP3 protein level and a moderate NLRP3 inflammasome activation, as indicated by the transient increase of the cytosolic level of mature IL-1beta.	Sodium Chloride	5-9	NLR family pyrin domain containing 3	Homo sapiens	81-86
27788256-13	2016	CONCLUSION: High extracellular NaCl induces priming of the NLRP3 inflammasome in RPE cells, in part via P2Y1 receptor signaling.	Sodium Chloride	31-35	NLR family pyrin domain containing 3	Homo sapiens	59-64
27760108-0	2016	Bile acids block NLRP3.	Bile Acids and Salts	0-10	NLR family pyrin domain containing 3	Homo sapiens	17-22
27692610-3	2016	Here, we demonstrated that bile acids inhibited NLRP3 inflammasome activation via the TGR5-cAMP-PKA axis.	Cyclic AMP	91-95	NLR family pyrin domain containing 3	Homo sapiens	48-53
27692610-4	2016	TGR5 bile acid receptor-induced PKA kinase activation led to the ubiquitination of NLRP3, which was associated with the PKA-induced phosphorylation of NLRP3 on a single residue, Ser 291.	Serine	178-181	NLR family pyrin domain containing 3	Homo sapiens	83-88
27692610-4	2016	TGR5 bile acid receptor-induced PKA kinase activation led to the ubiquitination of NLRP3, which was associated with the PKA-induced phosphorylation of NLRP3 on a single residue, Ser 291.	Serine	178-181	NLR family pyrin domain containing 3	Homo sapiens	151-156
27692610-6	2016	In addition, in vivo results indicated that bile acids and TGR5 activation blocked NLRP3 inflammasome-dependent inflammation, including lipopolysaccharide-induced systemic inflammation, alum-induced peritoneal inflammation, and type-2 diabetes-related inflammation.	Bile Acids and Salts	44-54	NLR family pyrin domain containing 3	Homo sapiens	83-88
27796369-6	2016	Moreover, the clinical-trial-tested Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model used for studying the consequences of NLRP3 activation.	PF-562271	60-69	NLR family pyrin domain containing 3	Homo sapiens	171-176
27779191-0	2016	25-hydroxycholesterol contributes to cerebral inflammation of X-linked adrenoleukodystrophy through activation of the NLRP3 inflammasome.	25-hydroxycholesterol	0-21	NLR family pyrin domain containing 3	Homo sapiens	118-123
27779191-4	2016	Intriguingly, 25-HC, but not VLCFA, promotes robust NLRP3 inflammasome assembly and activation via potassium efflux-, mitochondrial reactive oxygen species (ROS)- and liver X receptor (LXR)-mediated pathways.	Potassium	99-108	NLR family pyrin domain containing 3	Homo sapiens	52-57
27779191-4	2016	Intriguingly, 25-HC, but not VLCFA, promotes robust NLRP3 inflammasome assembly and activation via potassium efflux-, mitochondrial reactive oxygen species (ROS)- and liver X receptor (LXR)-mediated pathways.	Reactive Oxygen Species	132-155	NLR family pyrin domain containing 3	Homo sapiens	52-57
27779191-4	2016	Intriguingly, 25-HC, but not VLCFA, promotes robust NLRP3 inflammasome assembly and activation via potassium efflux-, mitochondrial reactive oxygen species (ROS)- and liver X receptor (LXR)-mediated pathways.	Reactive Oxygen Species	157-160	NLR family pyrin domain containing 3	Homo sapiens	52-57
27692610-0	2016	Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome.	Bile Acids and Salts	0-10	NLR family pyrin domain containing 3	Homo sapiens	77-82
27692610-3	2016	Here, we demonstrated that bile acids inhibited NLRP3 inflammasome activation via the TGR5-cAMP-PKA axis.	Bile Acids and Salts	27-37	NLR family pyrin domain containing 3	Homo sapiens	48-53
27760343-0	2016	Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome.	Bile Acids and Salts	0-10	NLR family pyrin domain containing 3	Homo sapiens	77-82
27731349-0	2016	TRPM2 regulates TXNIP-mediated NLRP3 inflammasome activation via interaction with p47 phox under high glucose in human monocytic cells.	Glucose	102-109	NLR family pyrin domain containing 3	Homo sapiens	31-36
27638862-9	2016	Furthermore, ATP-driven NLRP3 inflammasome activation was also dependent on calpain activity.	Adenosine Triphosphate	13-16	NLR family pyrin domain containing 3	Homo sapiens	24-29
27731349-3	2016	Here, we identified that HG (30 mM glucose for 48 h) induced the activation of the NLRP3-ASC inflammasome, leading to caspase-1 activation, and IL-1beta and IL-18 secretion in human monocytic cell lines.	Glucose	35-42	NLR family pyrin domain containing 3	Homo sapiens	83-88
27731349-7	2016	These results provided a mechanistic linking between TRPM2-mediated Ca2+ influx and p47 phox signaling to induce excess ROS production and TXNIP-mediated NLRP3 inflammasome activation under HG, and suggested that TRPM2 represented a potential target for alleviating NLRP3 inflammasome activation related to hyperglycemia-induced oxidative stress in Type 2 diabetes Mellitus (T2DM).	Reactive Oxygen Species	120-123	NLR family pyrin domain containing 3	Homo sapiens	266-271
27777559-0	2016	Curcumin Represses NLRP3 Inflammasome Activation via TLR4/MyD88/NF-kappaB and P2X7R Signaling in PMA-Induced Macrophages.	Curcumin	0-8	NLR family pyrin domain containing 3	Homo sapiens	19-24
27777559-2	2016	This study aimed to assess the effects of curcumin on NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages and explore its underlying mechanism.	Curcumin	42-50	NLR family pyrin domain containing 3	Homo sapiens	54-59
27777559-0	2016	Curcumin Represses NLRP3 Inflammasome Activation via TLR4/MyD88/NF-kappaB and P2X7R Signaling in PMA-Induced Macrophages.	Tetradecanoylphorbol Acetate	97-100	NLR family pyrin domain containing 3	Homo sapiens	19-24
27777559-2	2016	This study aimed to assess the effects of curcumin on NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages and explore its underlying mechanism.	Tetradecanoylphorbol Acetate	76-107	NLR family pyrin domain containing 3	Homo sapiens	54-59
27777559-2	2016	This study aimed to assess the effects of curcumin on NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages and explore its underlying mechanism.	Tetradecanoylphorbol Acetate	109-112	NLR family pyrin domain containing 3	Homo sapiens	54-59
27548431-3	2016	We found that rapid NLRP3 inflammasome activation was directly inhibited by protein kinase A (PKA), which was induced by prostaglandin E2 (PGE2) signaling via the PGE2 receptor E-prostanoid 4 (EP4).	Dinoprostone	121-137	NLR family pyrin domain containing 3	Homo sapiens	20-25
27777559-5	2016	Results: Curcumin significantly reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion in PMA-induced macrophages.	Curcumin	9-17	NLR family pyrin domain containing 3	Homo sapiens	58-63
27777559-9	2016	Furthermore, curcumin reversed PMA-stimulated P2X7R activation, which further reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion.	Curcumin	13-21	NLR family pyrin domain containing 3	Homo sapiens	104-109
27777559-9	2016	Furthermore, curcumin reversed PMA-stimulated P2X7R activation, which further reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion.	Tetradecanoylphorbol Acetate	31-34	NLR family pyrin domain containing 3	Homo sapiens	104-109
27777559-11	2016	Conclusion: Curcumin inhibited NLRP3 inflammasome through suppressing TLR4/MyD88/NF-kappaB and P2X7R pathways in PMA-induced macrophages.	Curcumin	12-20	NLR family pyrin domain containing 3	Homo sapiens	31-36
27777559-11	2016	Conclusion: Curcumin inhibited NLRP3 inflammasome through suppressing TLR4/MyD88/NF-kappaB and P2X7R pathways in PMA-induced macrophages.	Tetradecanoylphorbol Acetate	113-116	NLR family pyrin domain containing 3	Homo sapiens	31-36
27614934-0	2016	Corrigendum to "Angiotensin(1-7) attenuated angiotensin II-induced hepatocyte EMT by inhibiting NOX-derived H2O2-activated NLRP3 inflammasome/IL-1beta/Smad circuit": [Free Radic.	nicotine 1-N-oxide	96-99	NLR family pyrin domain containing 3	Homo sapiens	123-128
27614934-0	2016	Corrigendum to "Angiotensin(1-7) attenuated angiotensin II-induced hepatocyte EMT by inhibiting NOX-derived H2O2-activated NLRP3 inflammasome/IL-1beta/Smad circuit": [Free Radic.	Hydrogen Peroxide	108-112	NLR family pyrin domain containing 3	Homo sapiens	123-128
27548431-3	2016	We found that rapid NLRP3 inflammasome activation was directly inhibited by protein kinase A (PKA), which was induced by prostaglandin E2 (PGE2) signaling via the PGE2 receptor E-prostanoid 4 (EP4).	Dinoprostone	139-143	NLR family pyrin domain containing 3	Homo sapiens	20-25
27548431-3	2016	We found that rapid NLRP3 inflammasome activation was directly inhibited by protein kinase A (PKA), which was induced by prostaglandin E2 (PGE2) signaling via the PGE2 receptor E-prostanoid 4 (EP4).	e-prostanoid 4	177-191	NLR family pyrin domain containing 3	Homo sapiens	20-25
27994733-0	2016	Identification, Synthesis, and Biological Evaluation of the Major Human Metabolite of NLRP3 Inflammasome Inhibitor MCC950.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	115-121	NLR family pyrin domain containing 3	Homo sapiens	86-91
29924571-4	2016	In this review, we focused on the studies in the latest five years on the mechanisms of NLRP3 inflammasome regulation which mainly including NLRP3 priming, three protein complex assembly and regulation of NLRP3 inflammasome activation by endogenous metabolic compounds, iron flux, subcellular structure, other types of cells and small molecular compounds.	Iron	270-274	NLR family pyrin domain containing 3	Homo sapiens	88-93
28356883-4	2016	METHODS: A group of 128 RA patients treated with methotrexate and 122 healthy controls were genotyped for NLRP3 rs35829419 (p. Q705K) and CARD8 rs2043211 (p. C10X) polymorphisms.	Methotrexate	49-61	NLR family pyrin domain containing 3	Homo sapiens	106-111
27550992-3	2016	Trimethoprim/sulfamethoxazole given 2-3 times weekly is the drug of choice for the primary prophylaxis of PCP in adults ( A-II: ) and children ( A-I: ) and should be given during the entire period at risk.	Trimethoprim, Sulfamethoxazole Drug Combination	0-29	NLR family pyrin domain containing 3	Homo sapiens	122-126
27417584-2	2016	Atherosclerotic lesions are characterized by the presence of various endogenous activators of the NLR family pyrin domain containing 3 (NLRP3) inflammasome, including cholesterol crystals and extracellular ATP.	Cholesterol	167-178	NLR family pyrin domain containing 3	Homo sapiens	136-141
27417584-2	2016	Atherosclerotic lesions are characterized by the presence of various endogenous activators of the NLR family pyrin domain containing 3 (NLRP3) inflammasome, including cholesterol crystals and extracellular ATP.	Adenosine Triphosphate	206-209	NLR family pyrin domain containing 3	Homo sapiens	136-141
27417584-8	2016	In cultured human monocyte-derived macrophages, the p38delta mitogen-activated protein kinase was activated by intracellular stress signals triggered during ATP- and cholesterol crystal-induced NLRP3 inflammasome activation and was required for NLRP3-mediated IL-1beta secretion.	Adenosine Triphosphate	157-160	NLR family pyrin domain containing 3	Homo sapiens	194-199
27417584-8	2016	In cultured human monocyte-derived macrophages, the p38delta mitogen-activated protein kinase was activated by intracellular stress signals triggered during ATP- and cholesterol crystal-induced NLRP3 inflammasome activation and was required for NLRP3-mediated IL-1beta secretion.	Adenosine Triphosphate	157-160	NLR family pyrin domain containing 3	Homo sapiens	245-250
27417584-8	2016	In cultured human monocyte-derived macrophages, the p38delta mitogen-activated protein kinase was activated by intracellular stress signals triggered during ATP- and cholesterol crystal-induced NLRP3 inflammasome activation and was required for NLRP3-mediated IL-1beta secretion.	Cholesterol	166-177	NLR family pyrin domain containing 3	Homo sapiens	194-199
27417584-8	2016	In cultured human monocyte-derived macrophages, the p38delta mitogen-activated protein kinase was activated by intracellular stress signals triggered during ATP- and cholesterol crystal-induced NLRP3 inflammasome activation and was required for NLRP3-mediated IL-1beta secretion.	Cholesterol	166-177	NLR family pyrin domain containing 3	Homo sapiens	245-250
27607416-14	2016	Inhibition of NLRP3 activation using 10 muM isoliquiritigenin significantly (P &lt; 0.001) inhibited ox-LDL induced cytotoxicity.	isoliquiritigenin	44-61	NLR family pyrin domain containing 3	Homo sapiens	14-19
27505710-5	2016	In this study, we observed that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein ECs (HUVECs).	Adenosine Triphosphate	61-83	NLR family pyrin domain containing 3	Homo sapiens	118-123
27505710-5	2016	In this study, we observed that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein ECs (HUVECs).	Adenosine Triphosphate	85-88	NLR family pyrin domain containing 3	Homo sapiens	118-123
27505710-9	2016	On the other hand, NLRP3 siRNA blocked the activation of the NLRP3 inflammasome in HUVECs stimulated with LPS plus ATP.	Adenosine Triphosphate	115-118	NLR family pyrin domain containing 3	Homo sapiens	19-24
27505710-9	2016	On the other hand, NLRP3 siRNA blocked the activation of the NLRP3 inflammasome in HUVECs stimulated with LPS plus ATP.	Adenosine Triphosphate	115-118	NLR family pyrin domain containing 3	Homo sapiens	61-66
27512900-3	2016	(2016) report that detection of the N-acetylglucosamine component of peptidoglycan by the glycolytic enzyme hexokinase activates the NLRP3 inflammasome, revealing an intriguing interplay between pathogen detection and metabolism.	Acetylglucosamine	36-55	NLR family pyrin domain containing 3	Homo sapiens	133-138
28598074-0	2016	[Sodium Ferulate Attenuates Oxidative Stressvia Suppressing NALP3 Inflammasome and ERK Signal Pathway].	ferulic acid	1-16	NLR family pyrin domain containing 3	Homo sapiens	60-65
28598074-1	2016	OBJECTIVES: Study the gene and protein expression of NACHT-PYD-containing protein 3 (NALP3) inflammasome and extracellular regulated protein kinase (ERK), the intervention effects of sodium ferulate (SF) in human lung epithelial cells A549 under oxidative stress, and to investigate the possible mechanism.	ferulic acid	183-198	NLR family pyrin domain containing 3	Homo sapiens	85-90
28598074-5	2016	RESULTS: Compared with the control group,H2O2 not only increased the mRNA and protein expression levels of caspase-1 and NALP3 and the protein expression levels of p-ERK/ERK, but also enhanced the secretion of IL-1beta in human lung epithelial cells A549 (P&lt;0.05),while SF group showed no statistic significance of those indicators above (P&gt;0.05).	Hydrogen Peroxide	41-45	NLR family pyrin domain containing 3	Homo sapiens	121-126
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	z-vad	4-9	NLR family pyrin domain containing 3	Homo sapiens	164-169
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	46-50	NLR family pyrin domain containing 3	Homo sapiens	164-169
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	dehydroacetic acid	88-91	NLR family pyrin domain containing 3	Homo sapiens	48-53
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	dehydroacetic acid	88-91	NLR family pyrin domain containing 3	Homo sapiens	102-107
27011059-6	2016	Both IL-1 blockade and two recently identified specific NLRP3 inflammasome blockers, MCC950 and beta-hydroxybutyrate, have shown promise in the treatment of inflammasome-mediated conditions.	3-Hydroxybutyric Acid	96-116	NLR family pyrin domain containing 3	Homo sapiens	56-61
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	81-85	NLR family pyrin domain containing 3	Homo sapiens	164-169
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	81-85	NLR family pyrin domain containing 3	Homo sapiens	164-169
26990578-0	2016	Design, Synthesis, and Evaluation of Acrylamide Derivatives as Direct NLRP3 Inflammasome Inhibitors.	Acrylamide	37-47	NLR family pyrin domain containing 3	Homo sapiens	70-75
26990578-3	2016	In this study, the synthesis of acrylamide derivatives and their pharmaco-toxicological evaluation as potential inhibitors of NLRP3-dependent events was undertaken.	Acrylamide	32-42	NLR family pyrin domain containing 3	Homo sapiens	126-131
26990578-6	2016	This screening allowed the identification of 14, 2-(2-chlorobenzyl)-N-(4-sulfamoylphenethyl)acrylamide, which was able to concentration-dependently inhibit NLRP3 ATPase with an IC50 value of 74 mum.	14, 2-(2-chlorobenzyl)-n-(4-sulfamoylphenethyl)acrylamide	45-102	NLR family pyrin domain containing 3	Homo sapiens	156-161
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	dietary fatty acid	0-18	NLR family pyrin domain containing 3	Homo sapiens	48-53
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	dietary fatty acid	0-18	NLR family pyrin domain containing 3	Homo sapiens	102-107
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	Fatty Acids, Omega-3	68-86	NLR family pyrin domain containing 3	Homo sapiens	48-53
27405925-0	2016	Dietary fatty acid composition is sensed by the NLRP3 inflammasome: omega-3 fatty acid (DHA) prevents NLRP3 activation in human macrophages.	Fatty Acids, Omega-3	68-86	NLR family pyrin domain containing 3	Homo sapiens	102-107
27405925-3	2016	We report that dietary fatty acid (FA) composition is sensed by the NLRP3 inflammasome in human macrophages.	dietary fatty acid	15-33	NLR family pyrin domain containing 3	Homo sapiens	68-73
27470352-2	2016	The purpose of the present study was to evaluate the effects of atorvastatin on NLRP3 inflammasome in PMA-stimulated THP-1 cells and explore its underlying mechanism.	Atorvastatin	64-76	NLR family pyrin domain containing 3	Homo sapiens	80-85
27470352-0	2016	Atorvastatin suppresses NLRP3 inflammasome activation via TLR4/MyD88/NF-kappaB signaling in PMA-stimulated THP-1 monocytes.	Atorvastatin	0-12	NLR family pyrin domain containing 3	Homo sapiens	24-29
27470352-7	2016	RESULTS: It was shown that atorvastatin significantly reduced the expression of NLRP3, the cleavage of caspase-1 and IL-1beta in PMA-induced THP-1 cells.	Atorvastatin	27-39	NLR family pyrin domain containing 3	Homo sapiens	80-85
27470352-10	2016	CONCLUSIONS: Atorvastatin exerts an anti-inflammatory effect by inhibiting NLRP3 inflammasome through suppressing TLR4/MyD88/NF-kappaB pathway in PMA-induced THP-1 monocytes.	Atorvastatin	13-25	NLR family pyrin domain containing 3	Homo sapiens	75-80
27300134-13	2016	In conclusion, palmitic acid caused activation of NLRP3 inflammasomes and inflammatory responses, inducing IL-1beta, IL-6, and IL-8 secretion, which is associated with ROS generation, in human Sw.71 placental cells.	Palmitic Acid	15-28	NLR family pyrin domain containing 3	Homo sapiens	50-55
27096899-2	2016	Upon lipopolysaccharide (LPS) triggering of toll-like receptor (TLR)-4 and subsequent ATP signaling, the NOD-like receptor containing-pyrin domain 3 (NLRP3) inflammasome is activated to cleave pro-caspase-1 into caspase-1, allowing the secretion of IL-1beta.	Adenosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	105-148
27096899-2	2016	Upon lipopolysaccharide (LPS) triggering of toll-like receptor (TLR)-4 and subsequent ATP signaling, the NOD-like receptor containing-pyrin domain 3 (NLRP3) inflammasome is activated to cleave pro-caspase-1 into caspase-1, allowing the secretion of IL-1beta.	Adenosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	150-155
27300134-13	2016	In conclusion, palmitic acid caused activation of NLRP3 inflammasomes and inflammatory responses, inducing IL-1beta, IL-6, and IL-8 secretion, which is associated with ROS generation, in human Sw.71 placental cells.	Reactive Oxygen Species	168-171	NLR family pyrin domain containing 3	Homo sapiens	50-55
27300134-0	2016	Palmitic acid induces interleukin-1beta secretion via NLRP3 inflammasomes and inflammatory responses through ROS production in human placental cells.	Palmitic Acid	0-13	NLR family pyrin domain containing 3	Homo sapiens	54-59
27300134-6	2016	To test this hypothesis, we investigated the effect of palmitic acid on the activation of NLRP3 inflammasomes and inflammatory responses in a human Sw.71 trophoblast cell line.	Palmitic Acid	55-68	NLR family pyrin domain containing 3	Homo sapiens	90-95
27374331-2	2016	While many inflammatory responses to peptidoglycan are mediated by detection of its muramyl dipeptide component in the cytosol by NOD2, we report here that NLRP3 inflammasome activation is caused by release of N-acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase.	Acetylglucosamine	210-229	NLR family pyrin domain containing 3	Homo sapiens	156-161
27300134-9	2016	In addition, NLRP3 and caspase-1 genome editing using a CRISPR/Cas9 system in Sw.71 cells suppressed IL-1beta secretion, which was stimulated by palmitic acid.	Palmitic Acid	145-158	NLR family pyrin domain containing 3	Homo sapiens	13-18
27374331-3	2016	Inhibition of hexokinase by N-acetylglucosamine causes its dissociation from mitochondria outer membranes, and we found that this is sufficient to activate the NLRP3 inflammasome.	Acetylglucosamine	28-47	NLR family pyrin domain containing 3	Homo sapiens	160-165
27431477-6	2016	In ATP- or nigericin-activated macrophages, our data further indicate that Flightless-I (FliI) and leucine-rich repeat FliI-interaction protein 2 (LRRFIP2) are required for the co-localization of NLRP3, ASC and F-actin.	Nigericin	11-20	NLR family pyrin domain containing 3	Homo sapiens	196-201
26959386-0	2016	Trichomonas vaginalis induces IL-1beta production in a human prostate epithelial cell line by activating the NLRP3 inflammasome via reactive oxygen species and potassium ion efflux.	Reactive Oxygen Species	132-155	NLR family pyrin domain containing 3	Homo sapiens	109-114
27431477-6	2016	In ATP- or nigericin-activated macrophages, our data further indicate that Flightless-I (FliI) and leucine-rich repeat FliI-interaction protein 2 (LRRFIP2) are required for the co-localization of NLRP3, ASC and F-actin.	Adenosine Triphosphate	3-6	NLR family pyrin domain containing 3	Homo sapiens	196-201
27154322-9	2016	The expression levels of NLRP3, caspase-1, and AQP4 increased after 6h of OGD, but probenecid treatment attenuated this increase.	Probenecid	83-93	NLR family pyrin domain containing 3	Homo sapiens	25-30
26546554-9	2016	It was observed that aluminum potentially enhanced protein levels of PERK, EIF2alpha, caspase 9, caspase 3, and inflammatory markers like NF-kappaB, NLRP3, HMGB1, and nitric oxide (NO).	Aluminum	21-29	NLR family pyrin domain containing 3	Homo sapiens	149-154
27129183-0	2016	Colchicine therapy in acute coronary syndrome patients acts on caspase-1 to suppress NLRP3 inflammasome monocyte activation.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	85-90
27241260-0	2016	Colchicine to decrease NLRP3-activated inflammation and improve obesity-related metabolic dysregulation.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	23-28
27241260-7	2016	Colchicine, a medication classically used for gout, mediates its anti-inflammatory effect by inhibiting tubulin polymerization, and has been shown to attenuate macrophage NLRP3 inflammasome arrangement and activation in vitro and in vivo.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	171-176
26705388-7	2016	Cholesterol crystals initiate inflammation via NLRP3 inflammasome leading to interleukin-1beta (IL-1beta) production inducing C-reactive protein.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	47-52
26959386-0	2016	Trichomonas vaginalis induces IL-1beta production in a human prostate epithelial cell line by activating the NLRP3 inflammasome via reactive oxygen species and potassium ion efflux.	Potassium	160-169	NLR family pyrin domain containing 3	Homo sapiens	109-114
26959386-12	2016	The NADPH oxidase inhibitor DPI and high extracellular potassium ion suppressed the production of IL-1beta, caspase-1, and the expression of NLRP3 and ASC proteins.	3-aminodiphenyleneiodium	28-31	NLR family pyrin domain containing 3	Homo sapiens	141-146
26959386-12	2016	The NADPH oxidase inhibitor DPI and high extracellular potassium ion suppressed the production of IL-1beta, caspase-1, and the expression of NLRP3 and ASC proteins.	Potassium	55-64	NLR family pyrin domain containing 3	Homo sapiens	141-146
26959386-13	2016	The specific NF-kappaB inhibitor, Bay 11-7082, inhibited IL-1beta production, and also inhibited the production of caspase-1, ASC and NLRP3 proteins.	3-(4-methylphenylsulfonyl)-2-propenenitrile	34-45	NLR family pyrin domain containing 3	Homo sapiens	134-139
26959386-14	2016	CONCLUSIONS: T. vaginalis induces the formation of the NLRP3 inflammasome in human prostate epithelial cells via ROS and potassium ion efflux, and this results in IL-1beta production.	Reactive Oxygen Species	113-116	NLR family pyrin domain containing 3	Homo sapiens	55-60
26959386-14	2016	CONCLUSIONS: T. vaginalis induces the formation of the NLRP3 inflammasome in human prostate epithelial cells via ROS and potassium ion efflux, and this results in IL-1beta production.	Potassium	121-130	NLR family pyrin domain containing 3	Homo sapiens	55-60
27287410-5	2016	Indeed, macrophage depletion or the absence of the NLRP3 inflammasome, the adaptor protein ASC or interleukin-18 (IL-18) abolished monobenzone CHS, thereby establishing a non-redundant role for the NLRP3 inflammasome as a critical proinflammatory checkpoint in the induction of hapten-dependent memory NK cells.	monobenzone	131-142	NLR family pyrin domain containing 3	Homo sapiens	51-56
27379212-5	2016	Specifically, the alarmin S100A9 and/or founder gene mutations trigger pyroptosis through the generation of reactive oxygen species leading to assembly and activation of the redox-sensitive NLRP3 inflammasome and beta-catenin, assuring propagation of the MDS clone.	Reactive Oxygen Species	108-131	NLR family pyrin domain containing 3	Homo sapiens	190-195
27321752-2	2016	In human inflammasome PCR array, among different involved in inflammasome formation, in HIV infected macrophages in the presence of cocaine, we have observed significant upregulation of NLRP3, AIM2 genes and downstream genes IL-1beta and PTGS2.	Cocaine	132-139	NLR family pyrin domain containing 3	Homo sapiens	186-191
27321752-8	2016	These results indicate that in case of HIV infected macrophages exposed to cocaine, increased ROS production and IL-1beta transcription serve as an activators for the formation of NLRP3 and AIM2 mediated inflammasomes that leads to caspase 1 mediated apoptosis.	Cocaine	75-82	NLR family pyrin domain containing 3	Homo sapiens	180-185
27321752-8	2016	These results indicate that in case of HIV infected macrophages exposed to cocaine, increased ROS production and IL-1beta transcription serve as an activators for the formation of NLRP3 and AIM2 mediated inflammasomes that leads to caspase 1 mediated apoptosis.	ros	94-97	NLR family pyrin domain containing 3	Homo sapiens	180-185
27210890-9	2016	Furthermore, RA markedly inhibited poly(I:C)-induced NLRP3 and ASC expression.	Poly I-C	35-44	NLR family pyrin domain containing 3	Homo sapiens	53-58
27314526-4	2016	Best characterized in microbial pathogenesis is the nucleotide-binding domain and leucine-rich repeat (NLR)-protein 3 (NLRP3) inflammasome.	Leucine	82-89	NLR family pyrin domain containing 3	Homo sapiens	119-124
27250627-16	2016	CONCLUSIONS: Anti-dsDNA Abs activated NLRP3 inflammasome in monocytes/macrophages from SLE patients by binding to TLR4 and inducing the production of mitochondrial ROS.	ros	164-167	NLR family pyrin domain containing 3	Homo sapiens	38-43
27155490-5	2016	Aluminum hydroxyphosphate nanoparticles also have a more potent adjuvant activity than microparticles in helping a model antigen lysozyme to stimulate specific antibody response, again likely related to their stronger ability to activate the NLRP3 inflammasome.	aluminum hydroxyphosphate	0-25	NLR family pyrin domain containing 3	Homo sapiens	242-247
27103438-0	2016	A translocator protein 18 kDa ligand, Ro5-4864, inhibits ATP-induced NLRP3 inflammasome activation.	4'-chlorodiazepam	38-46	NLR family pyrin domain containing 3	Homo sapiens	69-74
27103438-0	2016	A translocator protein 18 kDa ligand, Ro5-4864, inhibits ATP-induced NLRP3 inflammasome activation.	Adenosine Triphosphate	57-60	NLR family pyrin domain containing 3	Homo sapiens	69-74
27103438-3	2016	Here, we demonstrate for the first time that TSPO ligands, especially Ro5-4864, potently suppressed ATP-induced NLRP3 inflammasome activation in THP-1 and BMDM cells.	4'-chlorodiazepam	70-78	NLR family pyrin domain containing 3	Homo sapiens	112-117
26986854-0	2016	CdSe/ZnS quantum dots induce hepatocyte pyroptosis and liver inflammation via NLRP3 inflammasome activation.	cdse	0-4	NLR family pyrin domain containing 3	Homo sapiens	78-83
27210890-9	2016	Furthermore, RA markedly inhibited poly(I:C)-induced NLRP3 and ASC expression.	rosmarinic acid	13-15	NLR family pyrin domain containing 3	Homo sapiens	53-58
27155490-4	2016	In human THP-1 myeloid cells, wild-type and NLRP3-deficient, both aluminum oxyhydroxide nanoparticles and microparticles stimulate the secretion of proinflammatory cytokine IL-1beta by activating NLRP3 inflammasome, although aluminum oxyhydroxide nanoparticles are more potent than microparticles, likely related to the higher uptake of the nanoparticles by the THP-1 cells than the microparticles.	Boehmite	66-87	NLR family pyrin domain containing 3	Homo sapiens	44-49
27103438-3	2016	Here, we demonstrate for the first time that TSPO ligands, especially Ro5-4864, potently suppressed ATP-induced NLRP3 inflammasome activation in THP-1 and BMDM cells.	Adenosine Triphosphate	100-103	NLR family pyrin domain containing 3	Homo sapiens	112-117
27103438-5	2016	Ro5-4864 efficiently attenuated NLRP3 translocation to mitochondria, inflammasome assembly/oligomerization, activation of caspase-1, and subsequent secretion of the mature forms of interleukin-1beta and -18.	4'-chlorodiazepam	0-8	NLR family pyrin domain containing 3	Homo sapiens	32-37
27103438-6	2016	Ro5-4864 also reduced the production of mitochondrial superoxide and preserved the mitochondrial membrane potential in ATP-treated cells, suggesting that Ro5-4864 may act on mitochondria or more upstream targets in NLRP3 inflammasome signaling.	4'-chlorodiazepam	0-8	NLR family pyrin domain containing 3	Homo sapiens	215-220
27103438-6	2016	Ro5-4864 also reduced the production of mitochondrial superoxide and preserved the mitochondrial membrane potential in ATP-treated cells, suggesting that Ro5-4864 may act on mitochondria or more upstream targets in NLRP3 inflammasome signaling.	Adenosine Triphosphate	119-122	NLR family pyrin domain containing 3	Homo sapiens	215-220
27103438-6	2016	Ro5-4864 also reduced the production of mitochondrial superoxide and preserved the mitochondrial membrane potential in ATP-treated cells, suggesting that Ro5-4864 may act on mitochondria or more upstream targets in NLRP3 inflammasome signaling.	4'-chlorodiazepam	154-162	NLR family pyrin domain containing 3	Homo sapiens	215-220
27103438-8	2016	Collectively, our novel findings demonstrate that Ro5-4864 effectively inhibited ATP-induced NLRP3 inflammasome activation through the prevention of mitochondrial perturbation.	4'-chlorodiazepam	50-58	NLR family pyrin domain containing 3	Homo sapiens	93-98
27103438-8	2016	Collectively, our novel findings demonstrate that Ro5-4864 effectively inhibited ATP-induced NLRP3 inflammasome activation through the prevention of mitochondrial perturbation.	Adenosine Triphosphate	81-84	NLR family pyrin domain containing 3	Homo sapiens	93-98
27103438-9	2016	Our results indicate Ro5-4864 as a promising candidate for the treatment of NLRP3 inflammasome-related diseases.	4'-chlorodiazepam	21-29	NLR family pyrin domain containing 3	Homo sapiens	76-81
25829326-3	2016	Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	215-220
25829326-3	2016	Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome.	Reactive Oxygen Species	178-181	NLR family pyrin domain containing 3	Homo sapiens	215-220
25829326-3	2016	Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome.	Uric Acid	51-56	NLR family pyrin domain containing 3	Homo sapiens	215-220
25829326-3	2016	Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome.	Reactive Oxygen Species	153-176	NLR family pyrin domain containing 3	Homo sapiens	215-220
27105502-8	2016	The in vitro study showed that MALT1 inhibitors decreased production of IL-1beta/IL-18 in phorbol myristate acetate-differentiated THP-1 cells and bone marrow derived macrophage via suppressing the activation of NF-kappaB and NLRP3 inflammasome.	Tetradecanoylphorbol Acetate	90-115	NLR family pyrin domain containing 3	Homo sapiens	226-231
27194621-0	2016	Endocytosis of indium-tin-oxide nanoparticles by macrophages provokes pyroptosis requiring NLRP3-ASC-Caspase1 axis that can be prevented by mesenchymal stem cells.	indium tin oxide	15-31	NLR family pyrin domain containing 3	Homo sapiens	91-96
27160314-0	2016	Ethanol-mediated activation of the NLRP3 inflammasome in iPS cells and iPS cells-derived neural progenitor cells.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	35-40
26728324-3	2016	The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of liver fibrosis.	Reactive Oxygen Species	96-119	NLR family pyrin domain containing 3	Homo sapiens	56-61
26728324-3	2016	The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of liver fibrosis.	Reactive Oxygen Species	121-124	NLR family pyrin domain containing 3	Homo sapiens	56-61
26728324-12	2016	INNOVATION AND CONCLUSIONS: Ang-(1-7) improved liver fibrosis by regulating NLRP3 inflammasome activation induced by Ang II-mediated ROS via redox balance modulation.	Reactive Oxygen Species	133-136	NLR family pyrin domain containing 3	Homo sapiens	76-81
27058421-3	2016	Here we report that hypoxia (1% O2) treatment of PrECs, prostate cell lines, and a macrophage cell line (THP-1) increased the levels of NLRP3, AIM2, and pro-IL-1beta.	Oxygen	32-34	NLR family pyrin domain containing 3	Homo sapiens	136-141
27160314-0	2016	Ethanol-mediated activation of the NLRP3 inflammasome in iPS cells and iPS cells-derived neural progenitor cells.	IPS	57-60	NLR family pyrin domain containing 3	Homo sapiens	35-40
27160314-5	2016	Ethanol exposure for 24 hours or 7 days does not affect the proliferation of iPS cells and NPCs, but primes an innate immune-like response by activating the NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	195-200
27062120-5	2016	In keeping with this, alum did not trigger IL-1beta production from human PMN, and the lysosomotropic peptide Leu-Leu-OMe stimulated only weak NLRP3-dependent IL-1beta production from murine neutrophils, suggesting that lysosomal rupture is not a strong stimulus for NLRP3 activation in neutrophils.	leucyl-leucine-methyl ester	110-121	NLR family pyrin domain containing 3	Homo sapiens	143-148
26998763-4	2016	Activation of T cell antigen receptors induced expression of pro-IL-1beta, whereas ATP stimulation triggered T cell production of IL-1beta via ASC-NLRP3-dependent caspase-8 activation.	Adenosine Triphosphate	83-86	NLR family pyrin domain containing 3	Homo sapiens	147-152
27093923-7	2016	Consistent with the in vitro data, low NLRP3 mRNA expression in kidney biopsies was associated with a linear trend of higher risk of composite endpoint of doubling serum creatinine and end stage renal disease in patients with IgAN.	Creatinine	170-180	NLR family pyrin domain containing 3	Homo sapiens	39-44
27043286-0	2016	NLRP3 tyrosine phosphorylation is controlled by protein tyrosine phosphatase PTPN22.	Tyrosine	6-14	NLR family pyrin domain containing 3	Homo sapiens	0-5
27043286-3	2016	Here, we have described a mechanism of NLRP3 inflammasome regulation by tyrosine phosphorylation of NLRP3 at Tyr861.	Tyrosine	72-80	NLR family pyrin domain containing 3	Homo sapiens	39-44
27043286-3	2016	Here, we have described a mechanism of NLRP3 inflammasome regulation by tyrosine phosphorylation of NLRP3 at Tyr861.	Tyrosine	72-80	NLR family pyrin domain containing 3	Homo sapiens	100-105
27043286-7	2016	Together, our results identify tyrosine phosphorylation as an important regulatory mechanism for NLRP3 that prevents aberrant inflammasome activation.	Tyrosine	31-39	NLR family pyrin domain containing 3	Homo sapiens	97-102
27077881-3	2016	In the setting of excess nutrients, particularly dietary saturated fatty acids (SFAs), activated macrophages develop lysosome dysfunction, which triggers activation of the NLRP3 inflammasome and cell death.	Fatty Acids	57-78	NLR family pyrin domain containing 3	Homo sapiens	172-177
26586371-7	2016	By using Ca-074-Me, N-acetylcysteine and KN-62, we observed that the P2X7 receptor participated in the DBP-induced activation of NLRP3 inflammasome.	CA 074 methyl ester	9-18	NLR family pyrin domain containing 3	Homo sapiens	129-134
26865578-3	2016	Baicalin at 50 microg/ml and 100 microg/ml could inhibit the production of ROS, TNF-alpha, IL-1beta and IL-18, and down-regulate mRNA expression of IL-1beta, IL-18, TNF-alpha and NLRP3, as well as expression of cleaved caspase-1 p20.	baicalin	0-8	NLR family pyrin domain containing 3	Homo sapiens	179-184
26946964-7	2016	Altogether, these results suggest that delirium rats induced by scopolamine may be correlated with an increased cerebral concentration of 5-HT and dopamine neurotransmitters system; the selective 5-HT(1A) antagoniszts can reverse the delirium symptoms at some extent through tendering PI3K/Akt/mammalian target of rapamycin complex 1 (mTOR) activation-induced NLRP3 activity and then reducing IL-1beta release.	Scopolamine	64-75	NLR family pyrin domain containing 3	Homo sapiens	360-365
26586371-7	2016	By using Ca-074-Me, N-acetylcysteine and KN-62, we observed that the P2X7 receptor participated in the DBP-induced activation of NLRP3 inflammasome.	Acetylcysteine	20-36	NLR family pyrin domain containing 3	Homo sapiens	129-134
26782741-4	2016	Using 5-ethynyl-2"-deoxyuridine (EdU) incorporation assay, scratch assay, and Transwell migration assay, we showed that activation of the NLRP3 inflammasome by LPS+ATP enhanced the proliferation and migration of A549 cells.	5-ethynyl-2'-deoxyuridine	6-31	NLR family pyrin domain containing 3	Homo sapiens	138-143
26639394-0	2016	Uric acid regulates hepatic steatosis and insulin resistance through the NLRP3 inflammasome-dependent mechanism.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	73-78
26639394-5	2016	Subsequently, we studied the role of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in uric acid-induced fat accumulation and insulin signaling impairment.	Uric Acid	116-125	NLR family pyrin domain containing 3	Homo sapiens	93-98
26639394-8	2016	Moreover, knocking down NLRP3 expression significantly attenuated uric acid-induced fat accumulation both in HepG2 cells and L02 cells.	Uric Acid	66-75	NLR family pyrin domain containing 3	Homo sapiens	24-29
26782741-4	2016	Using 5-ethynyl-2"-deoxyuridine (EdU) incorporation assay, scratch assay, and Transwell migration assay, we showed that activation of the NLRP3 inflammasome by LPS+ATP enhanced the proliferation and migration of A549 cells.	5-ethynyl-2'-deoxyuridine	33-36	NLR family pyrin domain containing 3	Homo sapiens	138-143
26639394-9	2016	Knocking down NLRP3 expression also rescued uric acid-induced insulin signaling impairment in both cell types.	Uric Acid	44-53	NLR family pyrin domain containing 3	Homo sapiens	14-19
26782741-4	2016	Using 5-ethynyl-2"-deoxyuridine (EdU) incorporation assay, scratch assay, and Transwell migration assay, we showed that activation of the NLRP3 inflammasome by LPS+ATP enhanced the proliferation and migration of A549 cells.	Adenosine Triphosphate	164-167	NLR family pyrin domain containing 3	Homo sapiens	138-143
26639394-10	2016	CONCLUSIONS: Uric acid regulates hepatic steatosis and insulin resistance through the NLRP3 inflammasome.	Uric Acid	13-22	NLR family pyrin domain containing 3	Homo sapiens	86-91
26809137-0	2016	Cadmium induces NLRP3 inflammasome-dependent pyroptosis in vascular endothelial cells.	Cadmium	0-7	NLR family pyrin domain containing 3	Homo sapiens	16-21
27150992-4	2016	RESULTS: The expression levels of NLRP3, ASC and AIM2 in plasma of control and AL complete remission groups were significantly higher than those in newly diagnosed and relapsed groups, and were with statistical significance (P &lt; 0.05), but there were no statistical signifirance between ALL and ANLL groups (P &gt; 0.05).	Aluminum	79-81	NLR family pyrin domain containing 3	Homo sapiens	34-39
26809137-5	2016	In addition, exposure of HUVECs to Cd resulted in NLRP3 inflammasome activation as evidenced by cleavage of caspase-1 and downstream interleukin (IL)-1beta production.	Cadmium	35-37	NLR family pyrin domain containing 3	Homo sapiens	50-55
26809137-6	2016	Moreover, knockdown of NLRP3 by small interfering RNA efficiently suppressed Cd-induced caspase-1 cleavage, IL-1beta production and pyroptosis in HUVECs.	Cadmium	77-79	NLR family pyrin domain containing 3	Homo sapiens	23-28
26809137-8	2016	Accordingly, pre-treatment with mtROS scavenger or total ROS scavenger reduced Cd-induced activation of NLRP3 inflammasome and pyroptotic cell death.	Reactive Oxygen Species	34-37	NLR family pyrin domain containing 3	Homo sapiens	104-109
26809137-8	2016	Accordingly, pre-treatment with mtROS scavenger or total ROS scavenger reduced Cd-induced activation of NLRP3 inflammasome and pyroptotic cell death.	Cadmium	79-81	NLR family pyrin domain containing 3	Homo sapiens	104-109
26809137-9	2016	Taken together, our data suggest that NLRP3 inflammasome, activated by the generation of mtROS, mediates Cd-induced pyroptosis in HUVECs.	Cadmium	105-107	NLR family pyrin domain containing 3	Homo sapiens	38-43
26928328-0	2016	Coordinated Activation of Toll-Like Receptor8 (TLR8) and NLRP3 by the TLR8 Agonist, VTX-2337, Ignites Tumoricidal Natural Killer Cell Activity.	VTX-2337	84-92	NLR family pyrin domain containing 3	Homo sapiens	57-62
26971994-0	2016	Saturated Fatty Acids Engage an IRE1alpha-Dependent Pathway to Activate the NLRP3 Inflammasome in Myeloid Cells.	Fatty Acids	0-21	NLR family pyrin domain containing 3	Homo sapiens	76-81
26968633-7	2016	Further studies demonstrated that NLRP3 protein expression was regulated by NF-kappaB signaling in TNF-alpha or TGF-beta1-induced EMT, as verified by the NF-kappaB inhibitor Bay 11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	174-185	NLR family pyrin domain containing 3	Homo sapiens	34-39
26978350-3	2016	The blocking of the mevalonate pathway in a neuronal cell line (Daoy), using statins or mevalonate, induced an increase in the expression of the inflammasome gene (NLRP3) and programmed cell death related to mitochondrial dysfunction.	Mevalonic Acid	20-30	NLR family pyrin domain containing 3	Homo sapiens	164-169
26978350-3	2016	The blocking of the mevalonate pathway in a neuronal cell line (Daoy), using statins or mevalonate, induced an increase in the expression of the inflammasome gene (NLRP3) and programmed cell death related to mitochondrial dysfunction.	Mevalonic Acid	88-98	NLR family pyrin domain containing 3	Homo sapiens	164-169
25589513-1	2016	OBJECTIVES: Acute gouty arthritis is caused by endogenously formed monosodium urate (MSU) crystals, which are potent activators of the NLRP3 inflammasome.	Uric Acid	67-83	NLR family pyrin domain containing 3	Homo sapiens	135-140
25589513-1	2016	OBJECTIVES: Acute gouty arthritis is caused by endogenously formed monosodium urate (MSU) crystals, which are potent activators of the NLRP3 inflammasome.	Uric Acid	85-88	NLR family pyrin domain containing 3	Homo sapiens	135-140
26901245-0	2016	Tetrachlorobenzoquinone Stimulates NLRP3 Inflammasome-Mediated Post-Translational Activation and Secretion of IL-1beta in the HUVEC Endothelial Cell Line.	tetrachlorobenzoquinone	0-23	NLR family pyrin domain containing 3	Homo sapiens	35-40
26901245-3	2016	Using human umbilical vein endothelial cells, we discovered that TCBQ not only promotes the expression of NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) components [composed of NLRP3, adaptor molecule apoptosis-associated speck like protein containing a caspase activation and recruitment domain (ASC), and pro-caspase 1] but also participates in priming the NLRP3 inflammasome.	tetrachlorobenzoquinone	65-69	NLR family pyrin domain containing 3	Homo sapiens	106-165
26901245-3	2016	Using human umbilical vein endothelial cells, we discovered that TCBQ not only promotes the expression of NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) components [composed of NLRP3, adaptor molecule apoptosis-associated speck like protein containing a caspase activation and recruitment domain (ASC), and pro-caspase 1] but also participates in priming the NLRP3 inflammasome.	tetrachlorobenzoquinone	65-69	NLR family pyrin domain containing 3	Homo sapiens	167-172
26901245-3	2016	Using human umbilical vein endothelial cells, we discovered that TCBQ not only promotes the expression of NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) components [composed of NLRP3, adaptor molecule apoptosis-associated speck like protein containing a caspase activation and recruitment domain (ASC), and pro-caspase 1] but also participates in priming the NLRP3 inflammasome.	tetrachlorobenzoquinone	65-69	NLR family pyrin domain containing 3	Homo sapiens	198-203
26901245-3	2016	Using human umbilical vein endothelial cells, we discovered that TCBQ not only promotes the expression of NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) components [composed of NLRP3, adaptor molecule apoptosis-associated speck like protein containing a caspase activation and recruitment domain (ASC), and pro-caspase 1] but also participates in priming the NLRP3 inflammasome.	tetrachlorobenzoquinone	65-69	NLR family pyrin domain containing 3	Homo sapiens	198-203
26901245-5	2016	Further experiments showed that K(+) efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage may be involved in NLRP3 inflammasome activation mediated by TCBQ.	Reactive Oxygen Species	45-68	NLR family pyrin domain containing 3	Homo sapiens	135-140
26901245-5	2016	Further experiments showed that K(+) efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage may be involved in NLRP3 inflammasome activation mediated by TCBQ.	Reactive Oxygen Species	70-73	NLR family pyrin domain containing 3	Homo sapiens	135-140
26901245-5	2016	Further experiments showed that K(+) efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage may be involved in NLRP3 inflammasome activation mediated by TCBQ.	tetrachlorobenzoquinone	177-181	NLR family pyrin domain containing 3	Homo sapiens	135-140
26901245-6	2016	Moreover, TCBQ downregulates the ubiquitination of NLRP3, further facilitating the activation of the NLRP3 inflammasome.	tetrachlorobenzoquinone	10-14	NLR family pyrin domain containing 3	Homo sapiens	51-56
26901245-6	2016	Moreover, TCBQ downregulates the ubiquitination of NLRP3, further facilitating the activation of the NLRP3 inflammasome.	tetrachlorobenzoquinone	10-14	NLR family pyrin domain containing 3	Homo sapiens	101-106
26901245-7	2016	These results suggest that the NLRP3/IL-1beta signaling pathway plays an important role in TCBQ-induced endothelial cell pro-inflammatory responses, which may point to potential therapeutic approaches against TCBQ-mediated toxicity.	tetrachlorobenzoquinone	91-95	NLR family pyrin domain containing 3	Homo sapiens	31-36
26901245-7	2016	These results suggest that the NLRP3/IL-1beta signaling pathway plays an important role in TCBQ-induced endothelial cell pro-inflammatory responses, which may point to potential therapeutic approaches against TCBQ-mediated toxicity.	tetrachlorobenzoquinone	209-213	NLR family pyrin domain containing 3	Homo sapiens	31-36
26898443-0	2016	Ligustrazine disrupts lipopolysaccharide-activated NLRP3 inflammasome pathway associated with inhibition of Toll-like receptor 4 in hepatocytes.	tetramethylpyrazine	0-12	NLR family pyrin domain containing 3	Homo sapiens	51-56
26898443-3	2016	The present study was aimed to investigate the effects of ligustrazine, a natural alkaloid compound, on the NLRP3 inflammasome pathway activation and interleukin-1beta (IL-1beta) generation in hepatocytes.	tetramethylpyrazine	58-70	NLR family pyrin domain containing 3	Homo sapiens	108-113
26898443-6	2016	Ligustrazine was found to reduce NLRP3 and cleaved-caspase-1, prevented IL-1beta cleavage, and decreased IL-1beta secretion into extracellular environment.	tetramethylpyrazine	0-12	NLR family pyrin domain containing 3	Homo sapiens	33-38
26898443-8	2016	Moreover, pharmacological inhibition of TLR4 by its specific inhibitor TAK-242 downregulated NLRP3 and cleaved-caspase-1, and combination treatment with TAK-242 and ligustrazine led to more significant inhibitory effects on the NLRP3 pathway.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	71-78	NLR family pyrin domain containing 3	Homo sapiens	93-98
26898443-8	2016	Moreover, pharmacological inhibition of TLR4 by its specific inhibitor TAK-242 downregulated NLRP3 and cleaved-caspase-1, and combination treatment with TAK-242 and ligustrazine led to more significant inhibitory effects on the NLRP3 pathway.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	71-78	NLR family pyrin domain containing 3	Homo sapiens	228-233
26898443-8	2016	Moreover, pharmacological inhibition of TLR4 by its specific inhibitor TAK-242 downregulated NLRP3 and cleaved-caspase-1, and combination treatment with TAK-242 and ligustrazine led to more significant inhibitory effects on the NLRP3 pathway.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	153-160	NLR family pyrin domain containing 3	Homo sapiens	228-233
26898443-8	2016	Moreover, pharmacological inhibition of TLR4 by its specific inhibitor TAK-242 downregulated NLRP3 and cleaved-caspase-1, and combination treatment with TAK-242 and ligustrazine led to more significant inhibitory effects on the NLRP3 pathway.	tetramethylpyrazine	165-177	NLR family pyrin domain containing 3	Homo sapiens	93-98
26898443-8	2016	Moreover, pharmacological inhibition of TLR4 by its specific inhibitor TAK-242 downregulated NLRP3 and cleaved-caspase-1, and combination treatment with TAK-242 and ligustrazine led to more significant inhibitory effects on the NLRP3 pathway.	tetramethylpyrazine	165-177	NLR family pyrin domain containing 3	Homo sapiens	228-233
26898443-10	2016	Collectively, the current results revealed that ligustrazine interrupted LPS-activated NLRP3 inflammasome signaling and reduced generation of IL-1beta in hepatocytes, which was associated with inhibition of TLR4.	tetramethylpyrazine	48-60	NLR family pyrin domain containing 3	Homo sapiens	87-92
26743485-1	2016	In this study we investigated the implication of NLRP3 inflammasomes in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and rheumatoid arthritis-usual interstitial pneumonia (RA-UIP).NLRP3 inflammasome activation at baseline and following stimulation with lipopolysaccharide/ATP was evaluated by measuring interleukin (IL)-1beta and IL-18 levels released in the bronchoalveolar lavage fluid (BALF) fluid and by cultures of BALF cells.	Adenosine Triphosphate	283-286	NLR family pyrin domain containing 3	Homo sapiens	49-54
26743485-5	2016	Interestingly, RA-UIP BALF cell cultures treated with lipopolysaccharide/ATP showed a potent stimulation of IL-18 secretion but not IL-1beta, the latter being already elevated in the unstimulated cultures, while examination of the intracellular IL-1beta levels in RA-UIP BALF cells upon NLRP3 inflammasome stimulation showed a significant upregulation of IL-1beta suggesting the NLRP3 pathway could be further activated.Taken together, our results suggest distinct inflammasome activation profiles between autoimmune and idiopathic lung fibrosis.	Adenosine Triphosphate	73-76	NLR family pyrin domain containing 3	Homo sapiens	287-292
26743485-5	2016	Interestingly, RA-UIP BALF cell cultures treated with lipopolysaccharide/ATP showed a potent stimulation of IL-18 secretion but not IL-1beta, the latter being already elevated in the unstimulated cultures, while examination of the intracellular IL-1beta levels in RA-UIP BALF cells upon NLRP3 inflammasome stimulation showed a significant upregulation of IL-1beta suggesting the NLRP3 pathway could be further activated.Taken together, our results suggest distinct inflammasome activation profiles between autoimmune and idiopathic lung fibrosis.	Adenosine Triphosphate	73-76	NLR family pyrin domain containing 3	Homo sapiens	379-384
26928328-3	2016	Here, we show that VTX-2337 stimulates the release of mature IL-1beta and IL-18 from monocytic cells through coordinated actions on both TLR8 and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome complex.	VTX-2337	19-27	NLR family pyrin domain containing 3	Homo sapiens	195-200
26928328-5	2016	Inhibition of caspase-1 blocked VTX-2337-mediated NLRP3 inflammasome activation, but had little impact on production of other TLR8-induced mediators such as TNFalpha.	VTX-2337	32-40	NLR family pyrin domain containing 3	Homo sapiens	50-55
26877061-0	2016	Neutrophil P2X7 receptors mediate NLRP3 inflammasome-dependent IL-1beta secretion in response to ATP.	Adenosine Triphosphate	97-100	NLR family pyrin domain containing 3	Homo sapiens	34-39
26814970-0	2016	NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux.	Potassium	64-73	NLR family pyrin domain containing 3	Homo sapiens	33-38
26814970-4	2016	Potassium efflux is a common step that is essential for NLRP3 inflammasome activation induced by many stimuli.	Potassium	0-9	NLR family pyrin domain containing 3	Homo sapiens	56-61
26814970-5	2016	Despite extensive investigation, the molecular mechanism leading to NLRP3 activation in response to potassium efflux remains unknown.	Potassium	100-109	NLR family pyrin domain containing 3	Homo sapiens	68-73
26814970-6	2016	Here we report the identification of NEK7, a member of the family of mammalian NIMA-related kinases (NEK proteins), as an NLRP3-binding protein that acts downstream of potassium efflux to regulate NLRP3 oligomerization and activation.	Potassium	168-177	NLR family pyrin domain containing 3	Homo sapiens	122-127
26814970-6	2016	Here we report the identification of NEK7, a member of the family of mammalian NIMA-related kinases (NEK proteins), as an NLRP3-binding protein that acts downstream of potassium efflux to regulate NLRP3 oligomerization and activation.	Potassium	168-177	NLR family pyrin domain containing 3	Homo sapiens	197-202
26814970-8	2016	NLRP3-activating stimuli promoted the NLRP3-NEK7 interaction in a process that was dependent on potassium efflux.	Potassium	96-105	NLR family pyrin domain containing 3	Homo sapiens	0-5
26814970-8	2016	NLRP3-activating stimuli promoted the NLRP3-NEK7 interaction in a process that was dependent on potassium efflux.	Potassium	96-105	NLR family pyrin domain containing 3	Homo sapiens	38-43
26814970-13	2016	These studies demonstrate that NEK7 is an essential protein that acts downstream of potassium efflux to mediate NLRP3 inflammasome assembly and activation.	Potassium	84-93	NLR family pyrin domain containing 3	Homo sapiens	112-117
26577567-0	2016	Activation of the NLRP3 inflammasome by cellular labile iron.	Iron	56-60	NLR family pyrin domain containing 3	Homo sapiens	18-23
26866373-9	2016	To determine further the role of HO-1 on the EGCG-mediated inhibition of inflammation, we studied the effect of EGCG on the NLRP3 inflammasome, an upstream signaling of IL-1beta.	epigallocatechin gallate	112-116	NLR family pyrin domain containing 3	Homo sapiens	124-129
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	epigallocatechin gallate	0-4	NLR family pyrin domain containing 3	Homo sapiens	20-25
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	epigallocatechin gallate	0-4	NLR family pyrin domain containing 3	Homo sapiens	102-107
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	zinc protoporphyrin	59-63	NLR family pyrin domain containing 3	Homo sapiens	20-25
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	zinc protoporphyrin	59-63	NLR family pyrin domain containing 3	Homo sapiens	102-107
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	epigallocatechin gallate	92-96	NLR family pyrin domain containing 3	Homo sapiens	20-25
26866373-10	2016	EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3.	epigallocatechin gallate	92-96	NLR family pyrin domain containing 3	Homo sapiens	102-107
26418144-3	2016	In particular, the NLRP3 inflammasome is activated in response to cellular stresses through a two-component pathway, involving Toll-like receptor 4-ligand interaction (priming) followed by a second signal, such as ATP-dependent P2X purinoreceptor 7 receptor activation.	Adenosine Triphosphate	214-217	NLR family pyrin domain containing 3	Homo sapiens	19-24
26577567-5	2016	Here we describe how cellular labile iron activates the NLRP3 inflammasome in human monocytes.	Iron	37-41	NLR family pyrin domain containing 3	Homo sapiens	56-61
26825654-6	2016	Furthermore, we observed that ATG5 and Beclin1 downregulation sensitised cells to IL-1beta release induced by MSU or nigericin, which is an NLRP3 inflammasome activator.	Nigericin	117-126	NLR family pyrin domain containing 3	Homo sapiens	140-145
26825654-0	2016	The role of Resveratrol-induced mitophagy/autophagy in peritoneal mesothelial cells inflammatory injury via NLRP3 inflammasome activation triggered by mitochondrial ROS.	Resveratrol	12-23	NLR family pyrin domain containing 3	Homo sapiens	108-113
26577567-8	2016	Ferric ammonium citrate consistently induced interleukin-1beta secretion in THP1 cells, but not in NLRP3-deficient THP1 cells, indicating a requirement for the NLRP3 inflammasome.	ferric ammonium citrate	0-23	NLR family pyrin domain containing 3	Homo sapiens	160-165
26825654-0	2016	The role of Resveratrol-induced mitophagy/autophagy in peritoneal mesothelial cells inflammatory injury via NLRP3 inflammasome activation triggered by mitochondrial ROS.	Reactive Oxygen Species	165-168	NLR family pyrin domain containing 3	Homo sapiens	108-113
26825654-8	2016	Taken together, this study may provide a potential therapeutic strategy for peritoneal inflammatory injury via NLRP3 inflammasome activation triggered by mitochondrial ROS.	Reactive Oxygen Species	168-171	NLR family pyrin domain containing 3	Homo sapiens	111-116
26825654-2	2016	Here, we investigated the effect of glucose-based PD solutions on mitochondrial reactive oxygen species (ROS) and nod-like receptor 3 (NLRP3) inflammasome activation in human PMCs (HPMCs).	Glucose	36-43	NLR family pyrin domain containing 3	Homo sapiens	114-133
26454448-1	2016	This study investigated the effect of rebamipide on activation of the NLRP3 inflammasome and generation of reactive oxygen species (ROS) in monosodium urate (MSU) crystal-induced interleukin-1beta (IL-1beta) production.	rebamipide	38-48	NLR family pyrin domain containing 3	Homo sapiens	70-75
26825654-3	2016	Exposure of HPMCs to high glucose-based PD solutions resulted in ROS production, which can trigger NLRP3 activation, leading to IL-1beta secretion.	hpmcs	12-17	NLR family pyrin domain containing 3	Homo sapiens	99-104
26825654-3	2016	Exposure of HPMCs to high glucose-based PD solutions resulted in ROS production, which can trigger NLRP3 activation, leading to IL-1beta secretion.	Glucose	26-33	NLR family pyrin domain containing 3	Homo sapiens	99-104
26825654-3	2016	Exposure of HPMCs to high glucose-based PD solutions resulted in ROS production, which can trigger NLRP3 activation, leading to IL-1beta secretion.	Reactive Oxygen Species	65-68	NLR family pyrin domain containing 3	Homo sapiens	99-104
26616294-0	2016	Atrial natriuretic peptide down-regulates LPS/ATP-mediated IL-1beta release by inhibiting NF-kB, NLRP3 inflammasome and caspase-1 activation in THP-1 cells.	Adenosine Triphosphate	46-49	NLR family pyrin domain containing 3	Homo sapiens	97-102
26616294-9	2016	The aim of our study was to evaluate the effect of ANP on IL-1beta/NALP3/caspase-1 expression in LPS/ATP-stimulated human THP1 monocytes.	Adenosine Triphosphate	101-104	NLR family pyrin domain containing 3	Homo sapiens	67-72
26616294-10	2016	We provided new evidence of the direct involvement of ANP/NPR-1/cGMP axis on NF-kB/NALP3/caspase-1-mediated IL-1beta release and NF-kB-mediated pro-IL-1beta production.	Cyclic GMP	64-68	NLR family pyrin domain containing 3	Homo sapiens	83-88
26830368-13	2016	The mechanism of IL-17A-triggered NLRP3 activation and subsequent IL-1beta secretion was found to involve the generation of reactive oxygen species.	Reactive Oxygen Species	124-147	NLR family pyrin domain containing 3	Homo sapiens	34-39
26827637-3	2016	The results showed that sulforaphane preferentially inhibited cathepsin B- and caspase-1-dependent NLRP3 inflammasome activation induced by mostly Abeta1-42 monomers, an effect that potently reduced excessive secretion of the proinflammatory cytokine interleukin-1beta (IL-1beta).	sulforaphane	24-36	NLR family pyrin domain containing 3	Homo sapiens	99-104
26555265-5	2016	Furthermore, our data suggest that the ASC-NLRP3 inflammasome is responsible for QS-21-induced IL-1beta/IL-18 release.	saponin QA-21V1	81-86	NLR family pyrin domain containing 3	Homo sapiens	43-48
26555265-6	2016	At higher concentrations, QS-21 induced macrophage and dendritic cell death in a caspase-1-, ASC-, and NLRP3-independent manner, whereas the presence of cholesterol rescued cell viability.	saponin QA-21V1	26-31	NLR family pyrin domain containing 3	Homo sapiens	103-108
26555265-9	2016	Thus, we have identified QS-21 as a nonparticulate single molecular saponin that activates the NLRP3 inflammasome, but this signaling pathway may contribute to decreased antigen-specific responses in vivo.	Saponins	68-75	NLR family pyrin domain containing 3	Homo sapiens	95-100
26561610-5	2016	Pressure application of NMDA did not evoke a response in rod bipolar cells, but for both AII and A17 amacrines, NMDA evoked responses that were blocked by a competitive antagonist (CPP) applied extracellularly and an open channel blocker (MK-801) applied intracellularly.	N-Methylaspartate	112-116	NLR family pyrin domain containing 3	Homo sapiens	89-92
27689075-11	2016	Meanwhile, there was significant reduction in the expressions of NLRP3 and IL-1beta mRNA in groups 6.25 muM berberine and 25 muM berberine when compared with model group (P &lt; 0.05).	Berberine	108-117	NLR family pyrin domain containing 3	Homo sapiens	65-70
27689075-11	2016	Meanwhile, there was significant reduction in the expressions of NLRP3 and IL-1beta mRNA in groups 6.25 muM berberine and 25 muM berberine when compared with model group (P &lt; 0.05).	Berberine	129-138	NLR family pyrin domain containing 3	Homo sapiens	65-70
27689075-13	2016	Therefore, berberine alleviates monosodium urate crystals-induced inflammation by downregulating NLRP3 and IL-1beta expressions.	Berberine	11-20	NLR family pyrin domain containing 3	Homo sapiens	97-102
27689075-13	2016	Therefore, berberine alleviates monosodium urate crystals-induced inflammation by downregulating NLRP3 and IL-1beta expressions.	Uric Acid	32-48	NLR family pyrin domain containing 3	Homo sapiens	97-102
27689075-14	2016	The regulatory effects of berberine may be related to the inactivation of NLRP3 inflammasome.	Berberine	26-35	NLR family pyrin domain containing 3	Homo sapiens	74-79
26355761-0	2016	Homoplantaginin Inhibits Palmitic Acid-induced Endothelial Cells Inflammation by Suppressing TLR4 and NLRP3 Inflammasome.	Palmitic Acid	25-38	NLR family pyrin domain containing 3	Homo sapiens	102-107
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Palmitic Acid	55-57	NLR family pyrin domain containing 3	Homo sapiens	101-142
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Palmitic Acid	55-57	NLR family pyrin domain containing 3	Homo sapiens	144-149
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Palmitic Acid	55-57	NLR family pyrin domain containing 3	Homo sapiens	257-262
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	66-89	NLR family pyrin domain containing 3	Homo sapiens	101-142
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	66-89	NLR family pyrin domain containing 3	Homo sapiens	144-149
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	66-89	NLR family pyrin domain containing 3	Homo sapiens	257-262
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	190-213	NLR family pyrin domain containing 3	Homo sapiens	101-142
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	190-213	NLR family pyrin domain containing 3	Homo sapiens	144-149
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	190-213	NLR family pyrin domain containing 3	Homo sapiens	257-262
26831644-3	2016	Metaflammation is initiated by the activation of the NOD-like receptor (NLR), leucine-rich repeat, pyrin domaincontaining 3 (NLRP3) gene by mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	154-177	NLR family pyrin domain containing 3	Homo sapiens	125-130
26831644-3	2016	Metaflammation is initiated by the activation of the NOD-like receptor (NLR), leucine-rich repeat, pyrin domaincontaining 3 (NLRP3) gene by mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	179-182	NLR family pyrin domain containing 3	Homo sapiens	125-130
26881256-0	2016	High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells.	Glucose	5-12	NLR family pyrin domain containing 3	Homo sapiens	42-47
26881256-0	2016	High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells.	Reactive Oxygen Species	65-68	NLR family pyrin domain containing 3	Homo sapiens	42-47
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Glucose	86-93	NLR family pyrin domain containing 3	Homo sapiens	38-43
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Glucose	86-93	NLR family pyrin domain containing 3	Homo sapiens	257-262
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Reactive Oxygen Species	119-142	NLR family pyrin domain containing 3	Homo sapiens	38-43
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Reactive Oxygen Species	119-142	NLR family pyrin domain containing 3	Homo sapiens	257-262
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Reactive Oxygen Species	144-147	NLR family pyrin domain containing 3	Homo sapiens	38-43
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Reactive Oxygen Species	144-147	NLR family pyrin domain containing 3	Homo sapiens	257-262
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Acetylcysteine	159-178	NLR family pyrin domain containing 3	Homo sapiens	38-43
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Acetylcysteine	159-178	NLR family pyrin domain containing 3	Homo sapiens	257-262
26881256-6	2016	Simultaneously, the mRNA and protein levels of TXNIP, NLRP3, procaspase-1, and IL-1beta were significantly induced by high glucose concentration and lipopolysaccharide in a dose-dependent and time-dependent manner in vitro.	Glucose	123-130	NLR family pyrin domain containing 3	Homo sapiens	54-59
26881256-8	2016	Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1beta inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy.	Glucose	37-44	NLR family pyrin domain containing 3	Homo sapiens	88-93
26881256-8	2016	Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1beta inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy.	Reactive Oxygen Species	77-80	NLR family pyrin domain containing 3	Homo sapiens	88-93
26540403-2	2016	Mitochondrial production of reactive oxygen species was recently linked to activation of an inflammatory redox sensor, the nod-like receptor family pyrin domain-containing 3 (NLRP3).	Reactive Oxygen Species	28-51	NLR family pyrin domain containing 3	Homo sapiens	175-180
26565031-2	2015	Following priming of RPE cells, the NLRP3 inflammasome can be activated by various stimuli such as lipofuscin-mediated photooxidative damage to lysosomal membranes.	Lipofuscin	99-109	NLR family pyrin domain containing 3	Homo sapiens	36-41
27221485-4	2016	The development of reliable techniques to measure extracellular ATP in vivo has become an urgent need in inflammation studies after the discovery that the most potent plasma membrane receptor responsible for NLRP3 inflammasome activation is an ATP-activated receptor, P2RX7.	Adenosine Triphosphate	64-67	NLR family pyrin domain containing 3	Homo sapiens	208-213
27127546-0	2016	ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	13-18
27127546-5	2016	In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation.	Reactive Oxygen Species	27-30	NLR family pyrin domain containing 3	Homo sapiens	72-77
27127546-7	2016	It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3.	Reactive Oxygen Species	70-73	NLR family pyrin domain containing 3	Homo sapiens	27-32
27127546-7	2016	It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3.	Reactive Oxygen Species	70-73	NLR family pyrin domain containing 3	Homo sapiens	161-166
26719270-6	2015	Interestingly, two of the isolates, named AII and BV2, have a pair of cysteines located within the randomized region of 11 amino acids similar to that identified within the CP Env, an isolate identified in a previous Env library screen on the human renal carcinoma Caki-1 cell line.	Cysteine	70-79	NLR family pyrin domain containing 3	Homo sapiens	42-45
26719270-7	2015	The amino acids within the randomized region of AII and BV2 envelopes that are essential for viral infection have been identified in this study and include these cysteine residues.	Cysteine	162-170	NLR family pyrin domain containing 3	Homo sapiens	48-51
26719270-10	2015	The results indicate that this pair of cysteines creates the structural context to position key hydrophobic (F and W) and basic (K and H) residues critical for viral titer and suggest that AII, BV2, and CP internal cysteines bond together in distinct ways.	Cysteine	39-48	NLR family pyrin domain containing 3	Homo sapiens	189-192
26546608-0	2015	Intracellular ATP Decrease Mediates NLRP3 Inflammasome Activation upon Nigericin and Crystal Stimulation.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	36-41
26689911-5	2015	Based on our preliminary findings we hypothesized that treatment of MMs with chemotherapeutic drugs may elevate the levels of NLRP3 and caspase-1 resulting in increased cell death by pyroptosis while increasing the levels of IL-1beta and other pro-inflammatory molecules.	Methyl Methanesulfonate	68-71	NLR family pyrin domain containing 3	Homo sapiens	126-131
26546608-2	2015	The NLRP3 inflammasome mediates caspase-1 activation and subsequent IL-1beta processing in response to various stimuli, including extracellular ATP, although the roles of intracellular ATP (iATP) in NLRP3 activation remain unclear.	Adenosine Triphosphate	185-188	NLR family pyrin domain containing 3	Homo sapiens	4-9
26546608-3	2015	In this study, we found that in activated macrophages artificial reduction of iATP by 2-deoxyglucose, a glycolysis inhibitor, caused mitochondrial membrane depolarization, leading to IL-1beta secretion via NLRP3 and caspase-1 activation.	Deoxyglucose	86-100	NLR family pyrin domain containing 3	Homo sapiens	206-211
26546608-0	2015	Intracellular ATP Decrease Mediates NLRP3 Inflammasome Activation upon Nigericin and Crystal Stimulation.	Nigericin	71-80	NLR family pyrin domain containing 3	Homo sapiens	36-41
26546608-4	2015	Additionally, the NLRP3 activators nigericin and monosodium urate crystals lowered iATP through K(+)- and Ca(2+)-mediated mitochondrial dysfunction, suggesting a feedback loop between iATP loss and lowering of mitochondrial membrane potential.	Nigericin	35-44	NLR family pyrin domain containing 3	Homo sapiens	18-23
26546608-4	2015	Additionally, the NLRP3 activators nigericin and monosodium urate crystals lowered iATP through K(+)- and Ca(2+)-mediated mitochondrial dysfunction, suggesting a feedback loop between iATP loss and lowering of mitochondrial membrane potential.	Uric Acid	49-65	NLR family pyrin domain containing 3	Homo sapiens	18-23
26546608-4	2015	Additionally, the NLRP3 activators nigericin and monosodium urate crystals lowered iATP through K(+)- and Ca(2+)-mediated mitochondrial dysfunction, suggesting a feedback loop between iATP loss and lowering of mitochondrial membrane potential.	iatp	83-87	NLR family pyrin domain containing 3	Homo sapiens	18-23
26546608-4	2015	Additionally, the NLRP3 activators nigericin and monosodium urate crystals lowered iATP through K(+)- and Ca(2+)-mediated mitochondrial dysfunction, suggesting a feedback loop between iATP loss and lowering of mitochondrial membrane potential.	iatp	184-188	NLR family pyrin domain containing 3	Homo sapiens	18-23
26546608-2	2015	The NLRP3 inflammasome mediates caspase-1 activation and subsequent IL-1beta processing in response to various stimuli, including extracellular ATP, although the roles of intracellular ATP (iATP) in NLRP3 activation remain unclear.	Adenosine Triphosphate	144-147	NLR family pyrin domain containing 3	Homo sapiens	4-9
26668503-7	2015	In HepG2 cells, PA and LPS treatment markedly increased mRNA of several nucleotide-binding and oligomerization domain-like receptor family members (NLRP3, NLRP6, and NLRP10), caspase-1 and IL-1beta.	Palmitic Acid	16-18	NLR family pyrin domain containing 3	Homo sapiens	148-153
26435000-0	2015	Chlorpyrifos induces NLRP3 inflammasome and pyroptosis/apoptosis via mitochondrial oxidative stress in human keratinocyte HaCaT cells.	Chlorpyrifos	0-12	NLR family pyrin domain containing 3	Homo sapiens	21-26
26435000-6	2015	We used mitochondrial ROS (mROS) scavenger mitoTEMPO to demonstrate a role for mROS in NLRP3 inflammasome and programmed cell death induced by CPF.	Reactive Oxygen Species	22-25	NLR family pyrin domain containing 3	Homo sapiens	87-92
26431797-0	2015	CPT-11 activates NLRP3 inflammasome through JNK and NF-kappaB signalings.	Irinotecan	0-6	NLR family pyrin domain containing 3	Homo sapiens	17-22
26611636-5	2015	We discovered the presence of GSDMD protein in nigericin-induced NLRP3 inflammasomes by a quantitative mass spectrometry-based analysis.	Nigericin	47-56	NLR family pyrin domain containing 3	Homo sapiens	65-70
26324406-2	2015	In vitro studies indicate that PA can activate both cell membrane toll-like receptor-4 and the intracellular nucleotide oligomerization domain-like receptor protein (NLRP3).	Palmitic Acid	31-33	NLR family pyrin domain containing 3	Homo sapiens	166-171
26324406-7	2015	Lowering the habitually high PA intake by feeding the HOA diet resulted in lower secretion of interleukin (IL)-1beta, IL-18, IL-10, and tumor necrosis factor-alpha by PBMCs, as well as lower relative mRNA expression of cJun and NLRP3 in muscle.	Palmitic Acid	29-31	NLR family pyrin domain containing 3	Homo sapiens	228-233
26431797-5	2015	In this study, we have discovered that CPT-11 promotes macrophage infiltration into intestinal tissues and activates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, resulting in a robust IL-1beta response and colonic inflammation similar to DSS (dextran sodium sulfate) induced experimental colitis.	Irinotecan	39-45	NLR family pyrin domain containing 3	Homo sapiens	174-179
26431797-5	2015	In this study, we have discovered that CPT-11 promotes macrophage infiltration into intestinal tissues and activates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, resulting in a robust IL-1beta response and colonic inflammation similar to DSS (dextran sodium sulfate) induced experimental colitis.	dss	271-274	NLR family pyrin domain containing 3	Homo sapiens	174-179
26431797-5	2015	In this study, we have discovered that CPT-11 promotes macrophage infiltration into intestinal tissues and activates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, resulting in a robust IL-1beta response and colonic inflammation similar to DSS (dextran sodium sulfate) induced experimental colitis.	dextran sodium sulfate	276-298	NLR family pyrin domain containing 3	Homo sapiens	174-179
26529255-6	2015	We enrolled an additional group of 8 healthy volunteers to assess the effects of the sirtuin activator, nicotinamide riboside, on NLRP3 inflammasome activation.	nicotinamide-beta-riboside	104-125	NLR family pyrin domain containing 3	Homo sapiens	130-135
26416893-0	2015	Rotenone-induced Impairment of Mitochondrial Electron Transport Chain Confers a Selective Priming Signal for NLRP3 Inflammasome Activation.	Rotenone	0-8	NLR family pyrin domain containing 3	Homo sapiens	109-114
26416893-1	2015	Mitochondrial dysfunction is considered crucial for NLRP3 inflammasome activation partly through its release of mitochondrial toxic products, such as mitochondrial reactive oxygen species (mROS)(2) and mitochondrial DNA (mtDNA).	Reactive Oxygen Species	164-187	NLR family pyrin domain containing 3	Homo sapiens	52-57
26416893-3	2015	Here, we demonstrate that impairment of the mitochondrial electron transport chain by rotenone primes NLRP3 inflammasome activation only upon costimulation with ATP and not with nigericin or alum.	Rotenone	86-94	NLR family pyrin domain containing 3	Homo sapiens	102-107
26416893-3	2015	Here, we demonstrate that impairment of the mitochondrial electron transport chain by rotenone primes NLRP3 inflammasome activation only upon costimulation with ATP and not with nigericin or alum.	Adenosine Triphosphate	161-164	NLR family pyrin domain containing 3	Homo sapiens	102-107
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Rotenone	0-8	NLR family pyrin domain containing 3	Homo sapiens	28-33
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Rotenone	0-8	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Rotenone	0-8	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Rotenone	0-8	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	28-33
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Adenosine Triphosphate	53-56	NLR family pyrin domain containing 3	Homo sapiens	94-99
26416893-5	2015	Mechanistically, rotenone confers a priming signal for NLRP3 inflammasome activation only in the context of aberrant high-grade, but not low-grade, mROS production and mitochondrial hyperpolarization.	Rotenone	17-25	NLR family pyrin domain containing 3	Homo sapiens	55-60
26416893-6	2015	By contrast, rotenone/ATP-mediated mtDNA release and mitochondrial depolarization are likely to be merely an indication of mitochondrial damage rather than triggering factors for NLRP3 inflammasome activation.	Adenosine Triphosphate	22-25	NLR family pyrin domain containing 3	Homo sapiens	179-184
26381780-8	2015	The NLRP3 inflammasome was localized in the cytoplasm of macrophages and foam cells and was associated with cholesterol crystal clefts inside and outside of cells.	Cholesterol	108-119	NLR family pyrin domain containing 3	Homo sapiens	4-9
26512962-1	2015	P2X7 purinergic receptor engagement with extracellular ATP induces transmembrane potassium and calcium flux resulting in assembly of the NLRP3 inflammasome in LPS-primed macrophages.	Adenosine Triphosphate	55-58	NLR family pyrin domain containing 3	Homo sapiens	137-142
26512962-1	2015	P2X7 purinergic receptor engagement with extracellular ATP induces transmembrane potassium and calcium flux resulting in assembly of the NLRP3 inflammasome in LPS-primed macrophages.	Potassium	81-90	NLR family pyrin domain containing 3	Homo sapiens	137-142
26512962-1	2015	P2X7 purinergic receptor engagement with extracellular ATP induces transmembrane potassium and calcium flux resulting in assembly of the NLRP3 inflammasome in LPS-primed macrophages.	Calcium	95-102	NLR family pyrin domain containing 3	Homo sapiens	137-142
26512962-7	2015	This evidence suggests that both potassium efflux and calcium influx are necessary for mitochondrial reactive oxygen generation upstream of NLRP3 inflammasome assembly and pyroptotic cell death.	Potassium	33-42	NLR family pyrin domain containing 3	Homo sapiens	140-145
26512962-7	2015	This evidence suggests that both potassium efflux and calcium influx are necessary for mitochondrial reactive oxygen generation upstream of NLRP3 inflammasome assembly and pyroptotic cell death.	Calcium	54-61	NLR family pyrin domain containing 3	Homo sapiens	140-145
26512962-7	2015	This evidence suggests that both potassium efflux and calcium influx are necessary for mitochondrial reactive oxygen generation upstream of NLRP3 inflammasome assembly and pyroptotic cell death.	Oxygen	110-116	NLR family pyrin domain containing 3	Homo sapiens	140-145
26512962-8	2015	We propose a model wherein potassium efflux is necessary for calcium influx, resulting in mitochondrial reactive oxygen generation to trigger the NLRP3 inflammasome.	Potassium	27-36	NLR family pyrin domain containing 3	Homo sapiens	146-151
26512962-8	2015	We propose a model wherein potassium efflux is necessary for calcium influx, resulting in mitochondrial reactive oxygen generation to trigger the NLRP3 inflammasome.	Calcium	61-68	NLR family pyrin domain containing 3	Homo sapiens	146-151
26512962-8	2015	We propose a model wherein potassium efflux is necessary for calcium influx, resulting in mitochondrial reactive oxygen generation to trigger the NLRP3 inflammasome.	Oxygen	113-119	NLR family pyrin domain containing 3	Homo sapiens	146-151
26502906-4	2016	The treatment of cells with a chemical inhibitor of glycosphingolipid biosynthesis, which suppresses the expression of the Stx receptor globotriaosylceramide and subsequent endocytosis of the toxin, substantially blocked activation of the NLRP3 inflammasome and processing of caspase-1 and IL-1beta.	Glycosphingolipids	52-69	NLR family pyrin domain containing 3	Homo sapiens	239-244
26502906-4	2016	The treatment of cells with a chemical inhibitor of glycosphingolipid biosynthesis, which suppresses the expression of the Stx receptor globotriaosylceramide and subsequent endocytosis of the toxin, substantially blocked activation of the NLRP3 inflammasome and processing of caspase-1 and IL-1beta.	globotriaosylceramide	136-157	NLR family pyrin domain containing 3	Homo sapiens	239-244
26502906-8	2016	Taken together, these results suggest that Stxs trigger the NLRP3 inflammasome pathway to release proinflammatory IL-1beta as well as to promote apoptotic cell death.	Saxitoxin	43-47	NLR family pyrin domain containing 3	Homo sapiens	60-65
26444566-10	2015	Analysis excluding patients with VUR, a well-known risk factor for severe UTIs, revealed a lower frequency of the CC genotype in NLRP3 (rs4612666) in patients with APN and ALN than in controls.	aln	172-175	NLR family pyrin domain containing 3	Homo sapiens	129-134
26282945-8	2015	Multivariate analysis demonstrated that body mass index and serum level of uric acid were predictors of NLRP3 expression in SAT.	Uric Acid	75-84	NLR family pyrin domain containing 3	Homo sapiens	104-109
26332156-0	2015	Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways.	Potassium	0-9	NLR family pyrin domain containing 3	Homo sapiens	102-107
26095630-7	2015	After 24 h of incubation with different concentrations of glucose, our results showed a significant increase in NLRP3 expression.	Glucose	58-65	NLR family pyrin domain containing 3	Homo sapiens	112-117
26173909-8	2015	Furthermore, we show that active caspase-11 leads to a drop of intracellular potassium levels, which is necessary to activate NLRP3.	Potassium	77-86	NLR family pyrin domain containing 3	Homo sapiens	126-131
26332156-0	2015	Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways.	Potassium	34-43	NLR family pyrin domain containing 3	Homo sapiens	102-107
26238426-2	2015	The present study aimed to investigate the role of PPARgamma in regulating NOD-like receptor family, pyrin domain containing 3 (NALP3) inflammasome and interleukin (IL)-1beta levels during monosodium urate (MSU) crystal-induced inflammation.	Uric Acid	189-205	NLR family pyrin domain containing 3	Homo sapiens	128-133
26198480-7	2015	Genetic deletion of NLRP3 reversed the CLP-induced reduction in blood pressure and increases in serum creatinine level and neutrophil infiltration, and attenuated the CLP-induced upregulation of apoptosis-associated speck-like protein, caspase-1 expression and activity, and the secretion of IL-1beta and IL-18, similarly to the effects of caspase-1 inhibition.	Creatinine	102-112	NLR family pyrin domain containing 3	Homo sapiens	20-25
26116704-1	2015	The Nod-like receptor family protein 3 (NLRP3)-inflammasome pathway is known to be activated by danger signals such as monosodium urate (MSU).	Uric Acid	119-135	NLR family pyrin domain containing 3	Homo sapiens	4-38
26116704-1	2015	The Nod-like receptor family protein 3 (NLRP3)-inflammasome pathway is known to be activated by danger signals such as monosodium urate (MSU).	Uric Acid	119-135	NLR family pyrin domain containing 3	Homo sapiens	40-45
26116704-1	2015	The Nod-like receptor family protein 3 (NLRP3)-inflammasome pathway is known to be activated by danger signals such as monosodium urate (MSU).	Uric Acid	137-140	NLR family pyrin domain containing 3	Homo sapiens	4-38
26116704-1	2015	The Nod-like receptor family protein 3 (NLRP3)-inflammasome pathway is known to be activated by danger signals such as monosodium urate (MSU).	Uric Acid	137-140	NLR family pyrin domain containing 3	Homo sapiens	40-45
26116704-2	2015	We investigated the role of P2 purinergic receptors in the activation of NLRP3-inflammasome pathway after MSU treatment of primary human monocyte-derived macrophages (MDMs).	Uric Acid	106-109	NLR family pyrin domain containing 3	Homo sapiens	73-78
26412089-2	2015	Acute (up to 4 hours) LPS stimulation, followed by ATP is frequently used to activate the NLRP3 inflammasome in macrophages.	Adenosine Triphosphate	51-54	NLR family pyrin domain containing 3	Homo sapiens	90-95
26412089-5	2015	Transfer of culture supernatants from macrophages stimulated with LPS for 24 hours dramatically reduced ATP- and nigericin-induced NLRP3 inflammasome activation in naive macrophages.	Adenosine Triphosphate	104-107	NLR family pyrin domain containing 3	Homo sapiens	131-136
26412089-5	2015	Transfer of culture supernatants from macrophages stimulated with LPS for 24 hours dramatically reduced ATP- and nigericin-induced NLRP3 inflammasome activation in naive macrophages.	Nigericin	113-122	NLR family pyrin domain containing 3	Homo sapiens	131-136
25684031-5	2015	Additionally, we investigate the role of the NLRP3/caspase-1 inflammasome pathway in human dental pulp fibroblasts and show that ATP activates the P2X7 receptor on the cell membrane triggering K(+) efflux and inducing the gradual recruitment of the membrane pore pannexin-1.	Adenosine Triphosphate	129-132	NLR family pyrin domain containing 3	Homo sapiens	45-50
26385789-6	2015	NLRP3 function (IL-1beta secretion) was assessed upon priming of TLR2 (Pam(3)CysSK(4), TLR3 (poly(I:C)) or TLR4 (LPS) and ATP sequential treatment.	Adenosine Triphosphate	122-125	NLR family pyrin domain containing 3	Homo sapiens	0-5
26385789-10	2015	Upon priming with TLR4 (LPS) and ATP, RA-derived cell extracts (n = 7) displayed increased expression of NLRP3 (p &lt; 0.01) and active caspase-1 (p &lt; 0.001).	Adenosine Triphosphate	33-36	NLR family pyrin domain containing 3	Homo sapiens	105-110
26212544-0	2015	A new pharmacological effect of levornidazole: Inhibition of NLRP3 inflammasome activation.	Ornidazole Levo-	32-45	NLR family pyrin domain containing 3	Homo sapiens	61-66
26212544-2	2015	In this study, we investigated the possible modulation by levornidazole of NOD-like receptor protein 3 (NLRP3) inflammasome-mediated IL-1beta and IL-18 release from macrophages.	Ornidazole Levo-	58-71	NLR family pyrin domain containing 3	Homo sapiens	75-102
26212544-2	2015	In this study, we investigated the possible modulation by levornidazole of NOD-like receptor protein 3 (NLRP3) inflammasome-mediated IL-1beta and IL-18 release from macrophages.	Ornidazole Levo-	58-71	NLR family pyrin domain containing 3	Homo sapiens	104-109
26212544-3	2015	The NLRP3 inflammasome could be activated by lipopolysaccharide (LPS) plus ATP or monosodium urate (MSU) in PMA-pretreated THP-1 macrophages.	Adenosine Triphosphate	75-78	NLR family pyrin domain containing 3	Homo sapiens	4-9
26212544-3	2015	The NLRP3 inflammasome could be activated by lipopolysaccharide (LPS) plus ATP or monosodium urate (MSU) in PMA-pretreated THP-1 macrophages.	Uric Acid	82-98	NLR family pyrin domain containing 3	Homo sapiens	4-9
26212544-3	2015	The NLRP3 inflammasome could be activated by lipopolysaccharide (LPS) plus ATP or monosodium urate (MSU) in PMA-pretreated THP-1 macrophages.	Uric Acid	100-103	NLR family pyrin domain containing 3	Homo sapiens	4-9
26212544-4	2015	Surprisingly, an in vitro study showed that levornidazole suppressed IL-1beta and IL-18 secretion by blocking the activation of the NLRP3 inflammasome.	Ornidazole Levo-	44-57	NLR family pyrin domain containing 3	Homo sapiens	132-137
26212544-5	2015	However, dextrornidazole barely suppressed the NLRP3 inflammasome.	dextrornidazole	9-24	NLR family pyrin domain containing 3	Homo sapiens	47-52
26212544-8	2015	Therefore, we used the widely applied NLRP3 inflammasome-related models of dextran sodium sulfate (DSS)-induced colitis and LPS-induced endotoxin shock to confirm the novel pharmacological effect of levornidazole in vivo.	dss	99-102	NLR family pyrin domain containing 3	Homo sapiens	38-43
26212544-8	2015	Therefore, we used the widely applied NLRP3 inflammasome-related models of dextran sodium sulfate (DSS)-induced colitis and LPS-induced endotoxin shock to confirm the novel pharmacological effect of levornidazole in vivo.	Ornidazole Levo-	199-212	NLR family pyrin domain containing 3	Homo sapiens	38-43
26212544-9	2015	The in vivo studies verified the novel activity of levornidazole because the inhibition of NLRP3 inflammasome by levornidazole contributed to a better ameliorating effect than that of dextrornidazole in the in vivo models tested.	Ornidazole Levo-	51-64	NLR family pyrin domain containing 3	Homo sapiens	91-96
26212544-9	2015	The in vivo studies verified the novel activity of levornidazole because the inhibition of NLRP3 inflammasome by levornidazole contributed to a better ameliorating effect than that of dextrornidazole in the in vivo models tested.	Ornidazole Levo-	113-126	NLR family pyrin domain containing 3	Homo sapiens	91-96
26212544-11	2015	In summary, these data describe a new pharmacological effect of levornidazole as an inhibitor of NLRP3 inflammasome activation.	Ornidazole Levo-	64-77	NLR family pyrin domain containing 3	Homo sapiens	97-102
26097125-6	2015	The results identify that a low-dose SWCNT treatment serves a protective function for the E. coli- and S. aureus-infected Caco-2 cells by negatively regulating mitochondrial reactive oxygen species-mediated NLRP3 inflammasome activation.	Reactive Oxygen Species	174-197	NLR family pyrin domain containing 3	Homo sapiens	207-212
26096886-0	2015	Fumaric acid esters prevent the NLRP3 inflammasome-mediated and ATP-triggered pyroptosis of differentiated THP-1 cells.	Fumarates	0-19	NLR family pyrin domain containing 3	Homo sapiens	32-37
26102024-0	2015	Inhibition of autophagy induces IL-1beta release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress.	ros	72-75	NLR family pyrin domain containing 3	Homo sapiens	85-90
26102024-0	2015	Inhibition of autophagy induces IL-1beta release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress.	Glucose	126-133	NLR family pyrin domain containing 3	Homo sapiens	85-90
26102024-5	2015	3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1beta secretion.	3-methyladenine	0-15	NLR family pyrin domain containing 3	Homo sapiens	152-157
26102024-5	2015	3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1beta secretion.	3-methyladenine	17-21	NLR family pyrin domain containing 3	Homo sapiens	152-157
26200133-7	2015	Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells.	Titanium	50-52	NLR family pyrin domain containing 3	Homo sapiens	262-267
26200133-7	2015	Detailed characterization revealed that increased Ti and Al doping could reduce surface silanol density and expression of three-membered siloxane rings, leading to dose-dependent reduction in hydroxyl radical generation, membrane perturbation, potassium efflux, NLRP3 inflammasome activation, and cytotoxicity in THP-1 cells.	Aluminum	57-59	NLR family pyrin domain containing 3	Homo sapiens	262-267
26332984-12	2015	Cumulatively, our findings provide the first example of EPEC-mediated suppression of inflammasome activity in which NieA plays a novel role in controlling the host immune response through targeting of NLRP3.	NIEA	116-120	NLR family pyrin domain containing 3	Homo sapiens	201-206
25855661-0	2015	Resveratrol inhibits the acetylated alpha-tubulin-mediated assembly of the NLRP3-inflammasome.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	75-80
25855661-3	2015	We show that resveratrol, a natural polyphenol in grapes and wine, is a safe and effective phytochemical that inhibits NLRP3-inflammasome activation.	Resveratrol	13-24	NLR family pyrin domain containing 3	Homo sapiens	119-124
25855661-4	2015	Resveratrol inhibits the accumulation of acetylated alpha-tubulin caused by mitochondrial damage in macrophages stimulated with inducers of the NLRP3-inflammasome.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	144-149
25855661-5	2015	Consequently, resveratrol inhibits the acetylated-alpha-tubulin-mediated spatial arrangement of mitochondria and their subsequent contact with the endoplasmic reticulum (ER), causing insufficient assembly of ASC on the mitochondria and NLRP3 on the ER.	Resveratrol	14-25	NLR family pyrin domain containing 3	Homo sapiens	236-241
25855661-6	2015	These findings indicate that resveratrol targets the generation of an optimal site for the assembly of NLRP3 and ASC, thus inhibiting NLRP3-inflammasome activation.	Resveratrol	29-40	NLR family pyrin domain containing 3	Homo sapiens	103-108
25855661-6	2015	These findings indicate that resveratrol targets the generation of an optimal site for the assembly of NLRP3 and ASC, thus inhibiting NLRP3-inflammasome activation.	Resveratrol	29-40	NLR family pyrin domain containing 3	Homo sapiens	134-139
25855661-7	2015	Therefore, resveratrol could be an effective medication for the treatment of NLRP3-related inflammatory diseases.	Resveratrol	11-22	NLR family pyrin domain containing 3	Homo sapiens	77-82
26202987-4	2015	LPS from Gram-negative bacteria is a prototypical first signal inducing pro-IL-1beta synthesis, whereas extracellular ATP is a typical second signal sensed by the ATP receptor P2X7 that triggers activation of the NLRP3-containing inflammasome, proteolytic cleavage of pro-IL-1beta by caspase-1, and release of mature IL-1beta.	Adenosine Triphosphate	118-121	NLR family pyrin domain containing 3	Homo sapiens	213-218
26234731-0	2015	Protective Effects of Catechin against Monosodium Urate-Induced Inflammation through the Modulation of NLRP3 Inflammasome Activation.	Catechin	22-30	NLR family pyrin domain containing 3	Homo sapiens	103-108
26234731-0	2015	Protective Effects of Catechin against Monosodium Urate-Induced Inflammation through the Modulation of NLRP3 Inflammasome Activation.	Uric Acid	39-55	NLR family pyrin domain containing 3	Homo sapiens	103-108
26234731-10	2015	It also suggests that catechin has the potential to protect gout attack by modulation of NLRP3 inflammasome activation.	Catechin	22-30	NLR family pyrin domain containing 3	Homo sapiens	89-94
26304941-2	2015	Colchicine is believed to block the NLRP3 inflammasome, a cytosolic complex responsible for the production of IL-1beta and IL-18.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	36-41
25979856-0	2015	An experimental study on amelioration of dyslipidemia-induced atherosclesis by Clematichinenoside through regulating Peroxisome proliferator-activated receptor-alpha mediated apolipoprotein A-I, A-II and C-III.	clematichinenoside	79-97	NLR family pyrin domain containing 3	Homo sapiens	195-209
25979856-2	2015	The aim of the study was to scrutinize the effect of Clematichinenoside (AR) on dyslipidemia-induced atherosclerosis and explore its capability on expression of Peroxisome proliferator-activated receptor-alpha (PPAR-alpha), apolipoprotein A-I (APOA1) and A-II (APOA2), and suppression of apolipoprotein C-III (APOC3) genes and proteins.	clematichinenoside	53-71	NLR family pyrin domain containing 3	Homo sapiens	255-259
25946654-2	2015	In this study, we aimed to evaluate the effect of the dose of rosuvastatin on NLRP3 and cathepsin-B expression in peripheral blood monocytes in patients with acute coronary syndrome.	Rosuvastatin Calcium	62-74	NLR family pyrin domain containing 3	Homo sapiens	78-83
25946654-9	2015	Rosuvastatin at a concentration of 20 mg led to a significant decrease (P&lt;0.05) in the expressions of NLRP3, cathepsin-B, and their downstream cytokines as compared with 5 mg rosuvastatin (P&gt;0.05) from baseline to 4 weeks.	Rosuvastatin Calcium	0-12	NLR family pyrin domain containing 3	Homo sapiens	105-110
25946654-12	2015	A high dose of rosuvastatin can modulate the inflammatory process of atherosclerosis by downregulating the expression of NLRP3, cathepsin-B, and their downstream mediators.	Rosuvastatin Calcium	15-27	NLR family pyrin domain containing 3	Homo sapiens	121-126
25684031-7	2015	Furthermore, the low intracellular K(+) concentration in the cytosol triggers reactive oxygen species generation, which also induces the NLRP3 inflammasome.	Reactive Oxygen Species	78-101	NLR family pyrin domain containing 3	Homo sapiens	137-142
25575547-0	2015	The anti-inflammatory effects of acetaminophen and N-acetylcysteine through suppression of the NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes.	Acetaminophen	33-46	NLR family pyrin domain containing 3	Homo sapiens	95-100
25743943-0	2015	Effects of dimethyl sulfoxide on the NLRP3 inflammasome.	Dimethyl Sulfoxide	11-29	NLR family pyrin domain containing 3	Homo sapiens	37-42
25575547-0	2015	The anti-inflammatory effects of acetaminophen and N-acetylcysteine through suppression of the NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes.	Acetylcysteine	51-67	NLR family pyrin domain containing 3	Homo sapiens	95-100
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetaminophen	0-3	NLR family pyrin domain containing 3	Homo sapiens	177-182
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	NLR family pyrin domain containing 3	Homo sapiens	177-182
25575547-8	2015	The combined use of AAP plus NAC had better inhibition action on the NLRP3 inflammasome pathway.	Acetylcysteine	29-32	NLR family pyrin domain containing 3	Homo sapiens	69-74
25575547-9	2015	These results indicate that the anti-inflammatory effects of AAP and NAC occur via the regulation on mRNA expression of NLRP3 and activation of caspase-1.	Acetylcysteine	69-72	NLR family pyrin domain containing 3	Homo sapiens	120-125
25575547-10	2015	The anti-inflammatory activity of AAP and NAC could be related to the suppression of NLRP3 inflammasome pathway under LPS stimulation.	Acetylcysteine	42-45	NLR family pyrin domain containing 3	Homo sapiens	85-90
25863775-15	2015	ATP promoted the generation of ROS and activated the NLRP3 inflammasome in a ROS-dependent manner.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	53-58
25858687-0	2015	Lentinan exerts synergistic apoptotic effects with paclitaxel in A549 cells via activating ROS-TXNIP-NLRP3 inflammasome.	Lentinan	0-8	NLR family pyrin domain containing 3	Homo sapiens	101-106
25858687-0	2015	Lentinan exerts synergistic apoptotic effects with paclitaxel in A549 cells via activating ROS-TXNIP-NLRP3 inflammasome.	Paclitaxel	51-61	NLR family pyrin domain containing 3	Homo sapiens	101-106
25858687-0	2015	Lentinan exerts synergistic apoptotic effects with paclitaxel in A549 cells via activating ROS-TXNIP-NLRP3 inflammasome.	Reactive Oxygen Species	91-94	NLR family pyrin domain containing 3	Homo sapiens	101-106
25858687-7	2015	Moreover, co-treatment with paclitaxel and lentinan enhanced TXNIP-NLRP3 interaction, and activated NLRP3 inflammasome whereat interleukin-1beta levels were increased and cell apoptosis was induced.	Paclitaxel	28-38	NLR family pyrin domain containing 3	Homo sapiens	67-72
25858687-7	2015	Moreover, co-treatment with paclitaxel and lentinan enhanced TXNIP-NLRP3 interaction, and activated NLRP3 inflammasome whereat interleukin-1beta levels were increased and cell apoptosis was induced.	Paclitaxel	28-38	NLR family pyrin domain containing 3	Homo sapiens	100-105
25858687-9	2015	Taken together, co-treatment with paclitaxel and lentinan exerts synergistic apoptotic effects in A549 cells through inducing ROS production, and activating NLRP3 inflammasome and ASK1/p38 MAPK signal pathway.	Paclitaxel	34-44	NLR family pyrin domain containing 3	Homo sapiens	157-162
25783493-0	2015	Light induces NLRP3 inflammasome activation in retinal pigment epithelial cells via lipofuscin-mediated photooxidative damage.	Lipofuscin	84-94	NLR family pyrin domain containing 3	Homo sapiens	14-19
25783493-5	2015	Interleukin secretion was dependent on the activity of NLRP3, caspase-1, and lysosomal proteases cathepsin B and L. These results demonstrate that accumulation of lipofuscin-like material in vitro renders RPE cells susceptible to phototoxic destabilization of lysosomes, resulting in NLRP3 inflammasome activation and secretion of inflammatory cytokines.	Lipofuscin	163-173	NLR family pyrin domain containing 3	Homo sapiens	55-60
25783493-5	2015	Interleukin secretion was dependent on the activity of NLRP3, caspase-1, and lysosomal proteases cathepsin B and L. These results demonstrate that accumulation of lipofuscin-like material in vitro renders RPE cells susceptible to phototoxic destabilization of lysosomes, resulting in NLRP3 inflammasome activation and secretion of inflammatory cytokines.	Lipofuscin	163-173	NLR family pyrin domain containing 3	Homo sapiens	284-289
25863775-13	2015	CONCLUSIONS: Our results demonstrated that the NLRP3 inflammasome in HDPFs is crucial for IL-1beta secretion in response to LPS plus ATP.	Adenosine Triphosphate	133-136	NLR family pyrin domain containing 3	Homo sapiens	47-52
25863775-15	2015	ATP promoted the generation of ROS and activated the NLRP3 inflammasome in a ROS-dependent manner.	Reactive Oxygen Species	77-80	NLR family pyrin domain containing 3	Homo sapiens	53-58
25791922-0	2015	Curcumin attenuates glutamate neurotoxicity in the hippocampus by suppression of ER stress-associated TXNIP/NLRP3 inflammasome activation in a manner dependent on AMPK.	Curcumin	0-8	NLR family pyrin domain containing 3	Homo sapiens	108-113
26005910-6	2015	Immunofluorescence studies showed that Ang II increased the expression of NLRP3 and ASC, which was inhibited by telmisartan.	Telmisartan	112-123	NLR family pyrin domain containing 3	Homo sapiens	74-79
26005910-8	2015	Moreover, Ang II-induced increases in the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 were significantly inhibited by pretreatment with the ERS inhibitor 4-PBA (5 mmol/L).	4-phenylbutylamine	167-172	NLR family pyrin domain containing 3	Homo sapiens	56-61
25109682-3	2015	Reactive oxygen species (ROS) are major mediators of the NLRP3/IL-1beta interaction.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	57-62
25109682-3	2015	Reactive oxygen species (ROS) are major mediators of the NLRP3/IL-1beta interaction.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	57-62
25109682-9	2015	MSU-induced IL-1beta secretion and NLRP3 inflammasome activation were inhibited by the knockdown of Nrf2 and via the HO-1 inhibitor zinc (II) protoporphyrin IX (ZnPP).	zinc;3-[7,12-bis(ethenyl)-18-(3-hydroperoxyprop-1-en-2-yl)-3,8,13,17-tetramethylporphyrin-21,23-diid-2-yl]propanoic acid	132-159	NLR family pyrin domain containing 3	Homo sapiens	35-40
25109682-9	2015	MSU-induced IL-1beta secretion and NLRP3 inflammasome activation were inhibited by the knockdown of Nrf2 and via the HO-1 inhibitor zinc (II) protoporphyrin IX (ZnPP).	zinc protoporphyrin	161-165	NLR family pyrin domain containing 3	Homo sapiens	35-40
25467233-0	2015	Muramyl dipeptide activates human beta defensin 2 and pro-inflammatory mediators through Toll-like receptors and NLRP3 inflammasomes in human dental pulp cells.	Acetylmuramyl-Alanyl-Isoglutamine	0-17	NLR family pyrin domain containing 3	Homo sapiens	113-118
25467233-8	2015	Furthermore, silencing of the NLRP3 gene using a siRNA significantly decreased the MDP-induced expression of hBD2 and cytokines, such as iNOS-derived NO, COX2, PGE2, TNF-alpha, IL-6, and IL-8.	Dinoprostone	160-164	NLR family pyrin domain containing 3	Homo sapiens	30-35
25909495-9	2015	TLR4 inhibitor TAK242 significantly blocked the up-regulation of NLRP3, IL-1beta, HLA-DR and CD40 induced by soluble MSU while no TAK242 suppression effect on MSU crystals induced IL-1beta up-regulation was found.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	15-21	NLR family pyrin domain containing 3	Homo sapiens	65-70
26133028-0	2015	Retraction: Hyaluronan activation of the Nlrp3 inflammasome contributes to the development of airway hyperresponsiveness.	Hyaluronic Acid	12-22	NLR family pyrin domain containing 3	Homo sapiens	41-46
26006022-8	2015	Our data reveal that treatment with 17beta-estradiol (E2) significantly inhibited the malignant behavior of HCC cells through E2/ERbeta/MAPK pathway-mediated upregulation of the NLRP3 inflammasome.	Estradiol	36-52	NLR family pyrin domain containing 3	Homo sapiens	178-183
25791922-0	2015	Curcumin attenuates glutamate neurotoxicity in the hippocampus by suppression of ER stress-associated TXNIP/NLRP3 inflammasome activation in a manner dependent on AMPK.	Glutamic Acid	20-29	NLR family pyrin domain containing 3	Homo sapiens	108-113
25791922-3	2015	Glutamate stimulation induced reactive oxygen species (ROS), endoplasmic reticulum stress (ER stress) and TXNIP/NLRP3 inflammasome activation, leading to damage in the hippocampus.	Glutamic Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	112-117
25791922-6	2015	As a result, curcumin reduced TXNIP expression and inhibited NLRP3 inflammasome activation by downregulation of NLRP3 and cleaved caspase-1 induction, and thus reduced IL-1beta secretion.	Curcumin	13-21	NLR family pyrin domain containing 3	Homo sapiens	61-66
25791922-6	2015	As a result, curcumin reduced TXNIP expression and inhibited NLRP3 inflammasome activation by downregulation of NLRP3 and cleaved caspase-1 induction, and thus reduced IL-1beta secretion.	Curcumin	13-21	NLR family pyrin domain containing 3	Homo sapiens	112-117
25791922-9	2015	Immunohistochemistry showed that curcumin inhibited p-IRE1alpha, p-PERK and NLRP3 expression in hippocampus CA1 region.	Curcumin	33-41	NLR family pyrin domain containing 3	Homo sapiens	76-81
25791922-10	2015	Together, these results showed that curcumin attenuated glutamate neurotoxicity by inhibiting ER stress-associated TXNIP/NLRP3 inflammasome activation via the regulation of AMPK, and thereby protected the hippocampus from ischemic insult.	Curcumin	36-44	NLR family pyrin domain containing 3	Homo sapiens	121-126
25791922-10	2015	Together, these results showed that curcumin attenuated glutamate neurotoxicity by inhibiting ER stress-associated TXNIP/NLRP3 inflammasome activation via the regulation of AMPK, and thereby protected the hippocampus from ischemic insult.	Glutamic Acid	56-65	NLR family pyrin domain containing 3	Homo sapiens	121-126
26114647-10	2015	Leishmania-dependent suppression of IL-1beta secretion is accompanied by an inhibition of reactive oxygen species (ROS) production that has previously been shown to be associated with NLRP3 inflammasome activation.	Reactive Oxygen Species	90-113	NLR family pyrin domain containing 3	Homo sapiens	184-189
26114647-0	2015	PKC/ROS-Mediated NLRP3 Inflammasome Activation Is Attenuated by Leishmania Zinc-Metalloprotease during Infection.	Reactive Oxygen Species	4-7	NLR family pyrin domain containing 3	Homo sapiens	17-22
26114647-5	2015	The NLRP3 inflammasome has been shown to be of pivotal importance in the detection of danger molecules such as inorganic crystals like asbestos, silica and malarial hemozoin, (HZ) as well as infectious agents.	Silicon Dioxide	145-151	NLR family pyrin domain containing 3	Homo sapiens	4-9
26114647-10	2015	Leishmania-dependent suppression of IL-1beta secretion is accompanied by an inhibition of reactive oxygen species (ROS) production that has previously been shown to be associated with NLRP3 inflammasome activation.	Reactive Oxygen Species	115-118	NLR family pyrin domain containing 3	Homo sapiens	184-189
25938942-2	2015	To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters.	Prednisolone	72-84	NLR family pyrin domain containing 3	Homo sapiens	378-383
26053021-0	2015	Endogenous and Uric Acid-Induced Activation of NLRP3 Inflammasome in Pregnant Women with Preeclampsia.	Uric Acid	15-24	NLR family pyrin domain containing 3	Homo sapiens	47-52
26053021-12	2015	These cells stimulation with MSU demonstrates that uric acid plays a role in NLRP3 inflammasome activation, suggesting the participation of this inflammatory complex in the pathogenesis of preeclampsia.	Uric Acid	51-60	NLR family pyrin domain containing 3	Homo sapiens	77-82
25917098-0	2015	Prostaglandin E2 Inhibits NLRP3 Inflammasome Activation through EP4 Receptor and Intracellular Cyclic AMP in Human Macrophages.	Dinoprostone	0-16	NLR family pyrin domain containing 3	Homo sapiens	26-31
25917098-0	2015	Prostaglandin E2 Inhibits NLRP3 Inflammasome Activation through EP4 Receptor and Intracellular Cyclic AMP in Human Macrophages.	Cyclic AMP	95-105	NLR family pyrin domain containing 3	Homo sapiens	26-31
25917098-4	2015	In this study, we showed that NLRP3 inflammasome activation is inhibited by PGE2 in human primary monocyte-derived macrophages.	Dinoprostone	76-80	NLR family pyrin domain containing 3	Homo sapiens	30-35
25917098-6	2015	A specific agonist of EP4 mimicked, whereas its antagonist or EP4 knockdown reversed, PGE2-mediated NLRP3 inhibition.	Dinoprostone	86-90	NLR family pyrin domain containing 3	Homo sapiens	100-105
25917098-8	2015	Blockade of adenylate cyclase by its inhibitor reversed PGE2-mediated NLRP3 inhibition.	Dinoprostone	56-60	NLR family pyrin domain containing 3	Homo sapiens	70-75
25917098-9	2015	Increase of intracellular cAMP by an activator of adenylate cyclase or an analog of cAMP, or a blockade of cAMP degradation by phosphodiesterase inhibitor decreased NLRP3 activation.	Cyclic AMP	26-30	NLR family pyrin domain containing 3	Homo sapiens	165-170
25917098-9	2015	Increase of intracellular cAMP by an activator of adenylate cyclase or an analog of cAMP, or a blockade of cAMP degradation by phosphodiesterase inhibitor decreased NLRP3 activation.	Cyclic AMP	84-88	NLR family pyrin domain containing 3	Homo sapiens	165-170
25917098-9	2015	Increase of intracellular cAMP by an activator of adenylate cyclase or an analog of cAMP, or a blockade of cAMP degradation by phosphodiesterase inhibitor decreased NLRP3 activation.	Cyclic AMP	84-88	NLR family pyrin domain containing 3	Homo sapiens	165-170
25917098-11	2015	Additionally, constitutive IL-1beta secretion from LPS-primed PBMCs of cryopyrin-associated periodic fever syndromes patients was substantially reduced by high doses of PGE2.	Dinoprostone	169-173	NLR family pyrin domain containing 3	Homo sapiens	71-80
25917098-12	2015	Moreover, blocking cytosolic phospholipase A2alpha by its inhibitor or small interfering RNA or inhibiting cyclooxygenase 2, resulting in inhibition of endogenous PGE2 production, caused an increase in NLRP3 inflammasome activation.	Dinoprostone	163-167	NLR family pyrin domain containing 3	Homo sapiens	202-207
25938942-2	2015	To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters.	Prednisolone	72-84	NLR family pyrin domain containing 3	Homo sapiens	256-261
26104484-1	2015	TLR2 promotes NLRP3 inflammasome activation via an early MyD88-IRAK1-dependent pathway that provides a priming signal (signal 1) necessary for activation of the inflammasome by a second potassium-depleting signal (signal 2).	Potassium	186-195	NLR family pyrin domain containing 3	Homo sapiens	14-19
25330206-7	2015	Increasing evidence seeks to understand how this spatiotemporal action of ROS occurs during NLRP3 inflammasome activation, which will be a major focus of this review.	Reactive Oxygen Species	74-77	NLR family pyrin domain containing 3	Homo sapiens	92-97
25834143-0	2015	Helicobacter pylori induces IL-1beta and IL-18 production in human monocytic cell line through activation of NLRP3 inflammasome via ROS signaling pathway.	Reactive Oxygen Species	132-135	NLR family pyrin domain containing 3	Homo sapiens	109-114
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	41-46
25770182-0	2015	Carbon monoxide negatively regulates NLRP3 inflammasome activation in macrophages.	Carbon Monoxide	0-15	NLR family pyrin domain containing 3	Homo sapiens	37-42
25770182-6	2015	CO also inhibited IL-18 secretion in response to LPS and nigericin treatment, another NLRP3 inflammasome activation model.	Nigericin	57-66	NLR family pyrin domain containing 3	Homo sapiens	86-91
25770182-8	2015	LPS and ATP stimulation induced the formation of complexes between NLRP3 and apoptosis-associated speck-like protein, or NLRP3 and caspase-1.	Adenosine Triphosphate	8-11	NLR family pyrin domain containing 3	Homo sapiens	67-72
25770182-8	2015	LPS and ATP stimulation induced the formation of complexes between NLRP3 and apoptosis-associated speck-like protein, or NLRP3 and caspase-1.	Adenosine Triphosphate	8-11	NLR family pyrin domain containing 3	Homo sapiens	121-126
25330206-0	2015	Redox regulation of NLRP3 inflammasomes: ROS as trigger or effector?	Reactive Oxygen Species	41-44	NLR family pyrin domain containing 3	Homo sapiens	20-25
25330206-5	2015	Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS).	Reactive Oxygen Species	233-256	NLR family pyrin domain containing 3	Homo sapiens	51-56
25330206-5	2015	Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS).	Reactive Oxygen Species	258-261	NLR family pyrin domain containing 3	Homo sapiens	51-56
25330206-6	2015	CRITICAL ISSUES: ROS may serve as a "kindling" or triggering factor to activate NLRP3 inflammasomes as well as "bonfire" or "effector" molecules, resulting in pathological processes.	Reactive Oxygen Species	17-20	NLR family pyrin domain containing 3	Homo sapiens	80-85
25991463-2	2015	Two recent studies identified the sulfonylurea MCC950 and the ketone metabolite beta-hydroxybutyrate as specific inhibitors of the Nlrp3 inflammasome, with promising therapeutic potential for the treatment of auto-inflammatory diseases.	Ketones	62-68	NLR family pyrin domain containing 3	Homo sapiens	131-136
25991463-2	2015	Two recent studies identified the sulfonylurea MCC950 and the ketone metabolite beta-hydroxybutyrate as specific inhibitors of the Nlrp3 inflammasome, with promising therapeutic potential for the treatment of auto-inflammatory diseases.	3-Hydroxybutyric Acid	80-100	NLR family pyrin domain containing 3	Homo sapiens	131-136
25651569-2	2015	We investigated the role of soluble uric acid in NLRP3 inflammasome activation in macrophages to demonstrate the effect of systemic hyperuricemia on progressive kidney damage in type 2 diabetes.	Uric Acid	36-45	NLR family pyrin domain containing 3	Homo sapiens	49-54
25651569-5	2015	Soluble uric acid stimulated NLRP3 inflammasomes to produce IL-1beta in macrophages.	Uric Acid	8-17	NLR family pyrin domain containing 3	Homo sapiens	29-34
25651569-6	2015	Uric acid-induced MitoSOX mediates NLRP3 activation and IL-1beta secretion.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	35-40
25330206-8	2015	FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases.	Reactive Oxygen Species	68-71	NLR family pyrin domain containing 3	Homo sapiens	85-90
25330206-8	2015	FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases.	Reactive Oxygen Species	68-71	NLR family pyrin domain containing 3	Homo sapiens	195-200
26121854-0	2015	[Sodium Ferulate Attenuates Oxidative Stress Induced Inflammation via Suppressing NALP3 and NF-kappaB Signal Pathway].	ferulic acid	1-16	NLR family pyrin domain containing 3	Homo sapiens	82-87
25813103-0	2015	Soluble uric acid increases NALP3 inflammasome and interleukin-1beta expression in human primary renal proximal tubule epithelial cells through the Toll-like receptor 4-mediated pathway.	Uric Acid	8-17	NLR family pyrin domain containing 3	Homo sapiens	28-33
25813103-1	2015	Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1beta expression in gout.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	120-167
25813103-1	2015	Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1beta expression in gout.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	169-174
25813103-1	2015	Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1beta expression in gout.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	243-248
25813103-1	2015	Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1beta expression in gout.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	254-263
25813103-5	2015	Soluble UA significantly enhanced TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	Uric Acid	8-10	NLR family pyrin domain containing 3	Homo sapiens	40-45
25813103-6	2015	The TLR4 inhibitor, TAK242 effectively blocked the soluble UA-induced upregulation of TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	20-26	NLR family pyrin domain containing 3	Homo sapiens	92-97
25813103-6	2015	The TLR4 inhibitor, TAK242 effectively blocked the soluble UA-induced upregulation of TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	Uric Acid	59-61	NLR family pyrin domain containing 3	Homo sapiens	92-97
25813103-7	2015	Our findings indicate that soluble UA enhances NALP3 expression, caspase-1 activation, IL-1beta and ICAM-1 production in renal proximal tubule epithelial cells in a TLR4-dependent manner, suggesting the activation of innate immunity in human primary renal proximal tubule epithelial cells by soluble UA.	Uric Acid	35-37	NLR family pyrin domain containing 3	Homo sapiens	47-52
25589411-5	2015	While endosomal superoxide production induces caspase-1 and NLRP3 transcription, it does not affect prae-IL-1beta transcription.	Superoxides	16-26	NLR family pyrin domain containing 3	Homo sapiens	60-65
25701684-0	2015	Reactive oxygen species activated NLRP3 inflammasomes initiate inflammation in hyperosmolarity stressed human corneal epithelial cells and environment-induced dry eye patients.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	34-39
25701684-2	2015	These immune reactions might be mediated by inflammasomes, macromolecular complexes mounted around the NLRP3 protein and can be activated by reactive oxygen species (ROS) over-generation.	Reactive Oxygen Species	141-164	NLR family pyrin domain containing 3	Homo sapiens	103-108
25701684-2	2015	These immune reactions might be mediated by inflammasomes, macromolecular complexes mounted around the NLRP3 protein and can be activated by reactive oxygen species (ROS) over-generation.	Reactive Oxygen Species	166-169	NLR family pyrin domain containing 3	Homo sapiens	103-108
25701684-3	2015	Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE.	Reactive Oxygen Species	45-48	NLR family pyrin domain containing 3	Homo sapiens	59-64
25701684-3	2015	Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE.	Reactive Oxygen Species	45-48	NLR family pyrin domain containing 3	Homo sapiens	182-187
25701684-3	2015	Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE.	Reactive Oxygen Species	178-181	NLR family pyrin domain containing 3	Homo sapiens	59-64
25701684-3	2015	Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE.	Reactive Oxygen Species	178-181	NLR family pyrin domain containing 3	Homo sapiens	182-187
25701684-11	2015	NAC suppressed hyperosmolarity-induced rises in ROS levels, NLRP3 inflammasome formation and activation, caspase-1 activity and IL-1beta release.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	60-65
25701684-14	2015	Taken together, NLRP3 mediated innate immune responses triggered by rises in ROS generation induce inflammation in hyperosmotic stressed HCECs.	Reactive Oxygen Species	77-80	NLR family pyrin domain containing 3	Homo sapiens	16-21
25701684-15	2015	ROS-NLRP3-IL-1beta signaling pathway might play a priming role in environment-induced DE development.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	4-9
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Adenosine Triphosphate	182-185	NLR family pyrin domain containing 3	Homo sapiens	4-9
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Glucose	194-201	NLR family pyrin domain containing 3	Homo sapiens	4-9
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Ceramides	203-212	NLR family pyrin domain containing 3	Homo sapiens	4-9
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Uric Acid	224-229	NLR family pyrin domain containing 3	Homo sapiens	4-9
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Cholesterol	235-246	NLR family pyrin domain containing 3	Homo sapiens	4-9
25639477-0	2015	Vitamin D3 metabolites enhance the NLRP3-dependent secretion of IL-1beta from human THP-1 monocytic cells.	Cholecalciferol	0-10	NLR family pyrin domain containing 3	Homo sapiens	35-40
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	Calcitriol	5-16	NLR family pyrin domain containing 3	Homo sapiens	163-168
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	Calcifediol	23-31	NLR family pyrin domain containing 3	Homo sapiens	163-168
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	Glyburide	180-189	NLR family pyrin domain containing 3	Homo sapiens	163-168
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	194-205	NLR family pyrin domain containing 3	Homo sapiens	163-168
25639477-7	2015	Interestingly, 1,25 (OH)2D3 exposure reduced NLRP3 protein expression but had no effect on ASC or pro-caspase-1 protein levels.	Calcitriol	15-27	NLR family pyrin domain containing 3	Homo sapiens	45-50
26121854-1	2015	OBJECTIVE: To study the effects of sodium ferulate on inflammation in human lung epithelial cells (A549) under oxidative stress and itsinfluence onthe expression of inflammasome NACHT-PYD-containing protein 3 (NALP3) and nuclear factor kappa B (NF-kappaB).	ferulic acid	35-50	NLR family pyrin domain containing 3	Homo sapiens	210-215
26121854-5	2015	RESULTS: H2O2 not only increased the mRNA and protein expression levels of NALP3, but also enhanced the secretion of ILbeta1p in human lung epithelial cells A549 (P&lt;0.	Hydrogen Peroxide	9-13	NLR family pyrin domain containing 3	Homo sapiens	75-80
26121854-7	2015	NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P&lt;0.	Sodium	28-34	NLR family pyrin domain containing 3	Homo sapiens	137-142
26121854-7	2015	NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P&lt;0.	Hydrogen Peroxide	67-71	NLR family pyrin domain containing 3	Homo sapiens	137-142
25816776-3	2015	We report that virus activation of the NLRP3 inflammasome involves the 2",5"-oligoadenylate (2-5A) synthetase(OAS)/RNase L system, a component of the interferon-induced antiviral response that senses double-stranded RNA and activates endoribonuclease RNase L to cleave viral and cellular RNAs.	2',5'-oligoadenylate	71-91	NLR family pyrin domain containing 3	Homo sapiens	39-44
25786687-7	2015	Furthermore, CT, mmCT, and dmLT induced IL-1beta production and caspase-1 activation in monocytes, which was associated with increased expression of key proinflammatory and inflammasome-related genes, including NLRP1, NLRP3, and NLRC4.	dmlt	27-31	NLR family pyrin domain containing 3	Homo sapiens	218-223
25897296-0	2015	Role of the NLRP3 inflammasome in the transient release of IL-1beta induced by monosodium urate crystals in human fibroblast-like synoviocytes.	Uric Acid	79-95	NLR family pyrin domain containing 3	Homo sapiens	12-17
25897296-6	2015	Simultaneously, intercellular pro-IL-1beta was detected at 6 h. Furthermore, MSU crystals also induced NLRP3 mRNA and protein expression at 6 h to 48 h after MSU treatment.	Uric Acid	77-80	NLR family pyrin domain containing 3	Homo sapiens	103-108
25394884-6	2015	Excess glucose-induced trophoblast IL-1beta production was inhibited by disabling the Nalp3/ASC inflammasome.	Glucose	7-14	NLR family pyrin domain containing 3	Homo sapiens	86-91
25681192-6	2015	Amylosin may thus trigger the activation of the NLRP3 inflammasome and subsequently cytokine release by causing potassium efflux from exposed cells.	amylosin	0-8	NLR family pyrin domain containing 3	Homo sapiens	48-53
25681192-6	2015	Amylosin may thus trigger the activation of the NLRP3 inflammasome and subsequently cytokine release by causing potassium efflux from exposed cells.	Potassium	112-121	NLR family pyrin domain containing 3	Homo sapiens	48-53
25686105-2	2015	We describe the development of MCC950, a potent, selective, small-molecule inhibitor of NLRP3.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	31-37	NLR family pyrin domain containing 3	Homo sapiens	88-93
25800347-1	2015	Activation of the NLRP3 inflammasome by microbial ligands or tissue damage requires intracellular generation of reactive oxygen species (ROS).	Reactive Oxygen Species	112-135	NLR family pyrin domain containing 3	Homo sapiens	18-23
25800347-1	2015	Activation of the NLRP3 inflammasome by microbial ligands or tissue damage requires intracellular generation of reactive oxygen species (ROS).	Reactive Oxygen Species	137-140	NLR family pyrin domain containing 3	Homo sapiens	18-23
25677765-10	2015	Furthermore, wogonoside markedly decreased production of IL-1beta, TNF-alpha and IL-6 and suppressed mRNA expression of pro-IL-1beta and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-kappaB and NLRP3 inflammasome.	wogonoside	13-23	NLR family pyrin domain containing 3	Homo sapiens	137-142
25677765-10	2015	Furthermore, wogonoside markedly decreased production of IL-1beta, TNF-alpha and IL-6 and suppressed mRNA expression of pro-IL-1beta and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-kappaB and NLRP3 inflammasome.	wogonoside	13-23	NLR family pyrin domain containing 3	Homo sapiens	262-267
25677765-10	2015	Furthermore, wogonoside markedly decreased production of IL-1beta, TNF-alpha and IL-6 and suppressed mRNA expression of pro-IL-1beta and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-kappaB and NLRP3 inflammasome.	Tetradecanoylphorbol Acetate	146-171	NLR family pyrin domain containing 3	Homo sapiens	137-142
25677765-10	2015	Furthermore, wogonoside markedly decreased production of IL-1beta, TNF-alpha and IL-6 and suppressed mRNA expression of pro-IL-1beta and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-kappaB and NLRP3 inflammasome.	Tetradecanoylphorbol Acetate	173-176	NLR family pyrin domain containing 3	Homo sapiens	137-142
25677765-10	2015	Furthermore, wogonoside markedly decreased production of IL-1beta, TNF-alpha and IL-6 and suppressed mRNA expression of pro-IL-1beta and NLRP3 in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells via inhibiting the activation of NF-kappaB and NLRP3 inflammasome.	Tetradecanoylphorbol Acetate	173-176	NLR family pyrin domain containing 3	Homo sapiens	262-267
25761061-6	2015	We also demonstrated that NLRP3 could activate NF-kappaB and induce cytokines in response to sterile signals, monosodium urate crystals and aluminum adjuvant.	Uric Acid	110-126	NLR family pyrin domain containing 3	Homo sapiens	26-31
25761061-6	2015	We also demonstrated that NLRP3 could activate NF-kappaB and induce cytokines in response to sterile signals, monosodium urate crystals and aluminum adjuvant.	Aluminum	140-148	NLR family pyrin domain containing 3	Homo sapiens	26-31
25499441-6	2015	Mangiferin treatment attenuated the expressions of TXNIP and NLRP3 and reduced IL-1beta and IL-6 production, demonstrating its inhibitory effects on TXNIP/NLRP3 inflammasome activation.	mangiferin	0-10	NLR family pyrin domain containing 3	Homo sapiens	61-66
25499441-6	2015	Mangiferin treatment attenuated the expressions of TXNIP and NLRP3 and reduced IL-1beta and IL-6 production, demonstrating its inhibitory effects on TXNIP/NLRP3 inflammasome activation.	mangiferin	0-10	NLR family pyrin domain containing 3	Homo sapiens	155-160
25686106-11	2015	Our findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be linked to BHB-mediated inhibition of the NLRP3 inflammasome.	3-Hydroxybutyric Acid	115-118	NLR family pyrin domain containing 3	Homo sapiens	146-151
25730877-0	2015	Cell stress increases ATP release in NLRP3 inflammasome-mediated autoinflammatory diseases, resulting in cytokine imbalance.	Adenosine Triphosphate	22-25	NLR family pyrin domain containing 3	Homo sapiens	37-42
25686106-0	2015	The ketone metabolite beta-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.	Ketones	4-10	NLR family pyrin domain containing 3	Homo sapiens	50-55
25686106-0	2015	The ketone metabolite beta-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.	3-Hydroxybutyric Acid	22-42	NLR family pyrin domain containing 3	Homo sapiens	50-55
25686106-4	2015	We report that BHB, but neither AcAc nor the structurally related short-chain fatty acids butyrate and acetate, suppresses activation of the NLRP3 inflammasome in response to urate crystals, ATP and lipotoxic fatty acids.	3-Hydroxybutyric Acid	15-18	NLR family pyrin domain containing 3	Homo sapiens	141-146
25686106-4	2015	We report that BHB, but neither AcAc nor the structurally related short-chain fatty acids butyrate and acetate, suppresses activation of the NLRP3 inflammasome in response to urate crystals, ATP and lipotoxic fatty acids.	Uric Acid	175-180	NLR family pyrin domain containing 3	Homo sapiens	141-146
25686106-4	2015	We report that BHB, but neither AcAc nor the structurally related short-chain fatty acids butyrate and acetate, suppresses activation of the NLRP3 inflammasome in response to urate crystals, ATP and lipotoxic fatty acids.	Adenosine Triphosphate	191-194	NLR family pyrin domain containing 3	Homo sapiens	141-146
25686106-6	2015	Mechanistically, BHB inhibits the NLRP3 inflammasome by preventing K(+) efflux and reducing ASC oligomerization and speck formation.	3-Hydroxybutyric Acid	17-20	NLR family pyrin domain containing 3	Homo sapiens	34-39
25686106-7	2015	The inhibitory effects of BHB on NLRP3 are not dependent on chirality or starvation-regulated mechanisms like AMP-activated protein kinase (AMPK), reactive oxygen species (ROS), autophagy or glycolytic inhibition.	3-Hydroxybutyric Acid	26-29	NLR family pyrin domain containing 3	Homo sapiens	33-38
25686106-8	2015	BHB blocks the NLRP3 inflammasome without undergoing oxidation in the TCA cycle, and independently of uncoupling protein-2 (UCP2), sirtuin-2 (SIRT2), the G protein-coupled receptor GPR109A or hydrocaboxylic acid receptor 2 (HCAR2).	3-Hydroxybutyric Acid	0-3	NLR family pyrin domain containing 3	Homo sapiens	15-20
25686106-9	2015	BHB reduces NLRP3 inflammasome-mediated interleukin (IL)-1beta and IL-18 production in human monocytes.	3-Hydroxybutyric Acid	0-3	NLR family pyrin domain containing 3	Homo sapiens	12-17
25709906-7	2015	Furthermore, in the SV40-immortalized human corneal epithelial cells, NLRP3 was exclusively located in the nucleus, and treatment of the cells with high concentration of extracellular potassium (known as an inhibitor of NLRP3 activation) effectively drove NLRP3 back to the cytoplasm as reflected by both immunohistochemistry and Western blot.	Potassium	184-193	NLR family pyrin domain containing 3	Homo sapiens	70-75
25593314-0	2015	Silver nanoparticles induce degradation of the endoplasmic reticulum stress sensor activating transcription factor-6 leading to activation of the NLRP-3 inflammasome.	Silver	0-6	NLR family pyrin domain containing 3	Homo sapiens	146-152
25593314-5	2015	Also, AgNP15 induced pyroptosis and activation of the NLRP-3 inflammasome as demonstrated by the processing and increased activity of caspase-1 and secretion of IL-1beta and ASC (apoptosis-associated speck-like protein containing a CARD domain) pyroptosome formation.	agnp15	6-12	NLR family pyrin domain containing 3	Homo sapiens	54-60
25593314-10	2015	We conclude that AgNP15 induce degradation of the ER stress sensor ATF-6, leading to activation of the NLRP-3 inflammasome regulated by caspase-4 in human monocytes.	agnp15	17-23	NLR family pyrin domain containing 3	Homo sapiens	103-109
25709906-7	2015	Furthermore, in the SV40-immortalized human corneal epithelial cells, NLRP3 was exclusively located in the nucleus, and treatment of the cells with high concentration of extracellular potassium (known as an inhibitor of NLRP3 activation) effectively drove NLRP3 back to the cytoplasm as reflected by both immunohistochemistry and Western blot.	Potassium	184-193	NLR family pyrin domain containing 3	Homo sapiens	220-225
25709906-7	2015	Furthermore, in the SV40-immortalized human corneal epithelial cells, NLRP3 was exclusively located in the nucleus, and treatment of the cells with high concentration of extracellular potassium (known as an inhibitor of NLRP3 activation) effectively drove NLRP3 back to the cytoplasm as reflected by both immunohistochemistry and Western blot.	Potassium	184-193	NLR family pyrin domain containing 3	Homo sapiens	220-225
25654762-6	2015	Downstream of these receptors, our results show that nanoparticles activate the NLRP3 inflammasome via activation of PLC-InsP3 and/or inhibition of adenylate cyclase (ADCY)-cAMP pathways.	Cyclic AMP	173-177	NLR family pyrin domain containing 3	Homo sapiens	80-85
25654762-8	2015	In summary, we show for the first time that extracellular adenosine activates the NLRP3 inflammasome by two ways: by interacting with adenosine receptors at nanomolar/micromolar concentrations and through cellular uptake by equilibrative nucleoside transporters at millimolar concentrations.	Adenosine	58-67	NLR family pyrin domain containing 3	Homo sapiens	82-87
25654762-0	2015	The NLRP3 inflammasome is activated by nanoparticles through ATP, ADP and adenosine.	Adenosine Triphosphate	61-64	NLR family pyrin domain containing 3	Homo sapiens	4-9
25231464-9	2015	The mechanism of SAA-triggered NLRP3 activation and subsequent IL-1beta secretion was found to involve the generation of reactive oxygen species.	Reactive Oxygen Species	121-144	NLR family pyrin domain containing 3	Homo sapiens	31-36
25654762-0	2015	The NLRP3 inflammasome is activated by nanoparticles through ATP, ADP and adenosine.	Adenosine Diphosphate	66-69	NLR family pyrin domain containing 3	Homo sapiens	4-9
25654762-0	2015	The NLRP3 inflammasome is activated by nanoparticles through ATP, ADP and adenosine.	Adenosine	74-83	NLR family pyrin domain containing 3	Homo sapiens	4-9
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	metal oxides	33-45	NLR family pyrin domain containing 3	Homo sapiens	127-132
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	silica dioxide	54-68	NLR family pyrin domain containing 3	Homo sapiens	127-132
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	Silicon Dioxide	75-79	NLR family pyrin domain containing 3	Homo sapiens	127-132
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	titanium dioxide	85-101	NLR family pyrin domain containing 3	Homo sapiens	127-132
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	titanium dioxide	108-112	NLR family pyrin domain containing 3	Homo sapiens	127-132
25654762-2	2015	Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO2) and titanium dioxide (nano-TiO2) activate the NLRP3 inflammasome in macrophages similarly to silica or asbestos micro-sized particles.	Silicon Dioxide	54-60	NLR family pyrin domain containing 3	Homo sapiens	127-132
25461402-0	2015	Methylsulfonylmethane inhibits NLRP3 inflammasome activation.	dimethyl sulfone	0-21	NLR family pyrin domain containing 3	Homo sapiens	31-36
25325516-0	2015	Hyperglucose contributes to periodontitis: involvement of the NLRP3 pathway by engaging the innate immunity of oral gingival epithelium.	hyperglucose	0-12	NLR family pyrin domain containing 3	Homo sapiens	62-67
25325516-8	2015	The expression of NLRP3 was significantly upregulated in HGECs when stimulated in vitro by LPS or high glucose (P = 0.00).	Glucose	103-110	NLR family pyrin domain containing 3	Homo sapiens	18-23
25325516-9	2015	The simultaneous stimulation of LPS and high glucose contributed to significant upregulation of NLRP3 expression versus LPS or high glucose alone (P = 0.00).	Glucose	45-52	NLR family pyrin domain containing 3	Homo sapiens	96-101
25325516-9	2015	The simultaneous stimulation of LPS and high glucose contributed to significant upregulation of NLRP3 expression versus LPS or high glucose alone (P = 0.00).	Glucose	132-139	NLR family pyrin domain containing 3	Homo sapiens	96-101
25825956-3	2015	Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IkappaBalpha kinase/nuclear factor-kappaB (IKK/NF- kappaB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling.	Fatty Acids, Nonesterified	136-152	NLR family pyrin domain containing 3	Homo sapiens	471-491
25379992-7	2015	Furthermore, procyanidin B2 decreases NLRP3 and pro-IL-1beta cytoplasmic pools, limiting components of inflammasome activation and impeding inflammasome assembly and caspase-1 activation, and finally secretion of active IL-1beta.	procyanidin B2	13-27	NLR family pyrin domain containing 3	Homo sapiens	38-43
25378535-4	2015	Subsequent gene set enrichment analysis showed that many genes associated with the high iron cluster were involved in the toll-like receptor system (TLR4, TLR7, and TLR8) and inflammasome complex pathway (NLRP3, NLRC4, and CASP1).	Iron	88-92	NLR family pyrin domain containing 3	Homo sapiens	205-210
25594175-0	2015	Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome.	Dopamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	62-67
25594175-3	2015	Here, we report that the neurotransmitter dopamine (DA) inhibits NLRP3 inflammasome activation via dopamine D1 receptor (DRD1).	Dopamine	42-50	NLR family pyrin domain containing 3	Homo sapiens	65-70
25594175-3	2015	Here, we report that the neurotransmitter dopamine (DA) inhibits NLRP3 inflammasome activation via dopamine D1 receptor (DRD1).	Dopamine	52-54	NLR family pyrin domain containing 3	Homo sapiens	65-70
25594175-4	2015	DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7.	Cyclic AMP	78-108	NLR family pyrin domain containing 3	Homo sapiens	36-41
25594175-4	2015	DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7.	Cyclic AMP	78-108	NLR family pyrin domain containing 3	Homo sapiens	132-137
25594175-4	2015	DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7.	Cyclic AMP	110-114	NLR family pyrin domain containing 3	Homo sapiens	36-41
25594175-4	2015	DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7.	Cyclic AMP	110-114	NLR family pyrin domain containing 3	Homo sapiens	132-137
25594175-5	2015	Importantly, in vivo data show that DA and DRD1 signaling prevent NLRP3 inflammasome-dependent inflammation, including neurotoxin-induced neuroinflammation, LPS-induced systemic inflammation, and monosodium urate crystal (MSU)-induced peritoneal inflammation.	Uric Acid	196-212	NLR family pyrin domain containing 3	Homo sapiens	66-71
25825956-3	2015	Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IkappaBalpha kinase/nuclear factor-kappaB (IKK/NF- kappaB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling.	Fatty Acids, Nonesterified	136-152	NLR family pyrin domain containing 3	Homo sapiens	493-498
25692535-5	2015	Current explanations for the mode of action of aluminum hydroxide-based adjuvants include, among others, the repository effect, pro-phagocytic effect, and activation of the pro-inflammatory NLRP3 pathway.	Aluminum Hydroxide	47-65	NLR family pyrin domain containing 3	Homo sapiens	190-195
25327779-9	2015	The depletion of Kupffer cells with gadolinium chloride markedly decreased NLRP3 and AIM2 inflammasome expression and activation of their signaling pathways, and also reduced the level of caspase-1 protein in F4/80-positive cells.	gadolinium chloride	36-55	NLR family pyrin domain containing 3	Homo sapiens	75-80
25327779-10	2015	Our findings suggest that reactive-oxygen-species-mediated activation of NLRP3 and AIM2 inflammasomes leads to I/R-induced inflammatory responses in which Kupffer cells play a crucial role.	Reactive Oxygen Species	26-49	NLR family pyrin domain containing 3	Homo sapiens	73-78
26435646-0	2015	Urate crystals induce NLRP3 inflammasome-dependent IL-1beta secretion and proliferation in isolated primary human T-cells.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	22-27
26435646-11	2015	CONCLUSIONS: Urate, a well defined danger signal, stimulates directly human T-cells in a NLRP3 infmmasomela-dependent way.	Uric Acid	13-18	NLR family pyrin domain containing 3	Homo sapiens	89-94
26075098-3	2015	Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3).	Reactive Oxygen Species	59-62	NLR family pyrin domain containing 3	Homo sapiens	134-177
25864748-4	2015	This study was undertaken to analyze whether disrupting the microtubule cytoskeleton by colchicine modulates transcriptional levels of MEFV, NF-kappaB p65, NLRP3, HMGB1, and caspase-3 in neutrophils from patients with familial Mediterranean fever (FMF) and healthy subjects.	Colchicine	88-98	NLR family pyrin domain containing 3	Homo sapiens	156-161
25864748-5	2015	In the present study, colchicine caused increased expression of NLRP3 (p=0.007) and MEFV (p=0.03), but had no effect on caspase-3, NF-kappaB p65 and HMGB1 genes in healthy neutrophils.	Colchicine	22-32	NLR family pyrin domain containing 3	Homo sapiens	64-69
26160272-2	2015	The present study was designed to test the hypothesis that the formation and activation of NLRP3 (Nod-like receptor family pyrin domain containing 3) inflammasomes is an important initiating mechanism resulting in PGN.	pgn	214-217	NLR family pyrin domain containing 3	Homo sapiens	91-96
26160272-6	2015	RESULTS: RT-PCR analyses demonstrated that the mRNA levels of NLRP3 and caspase-1 genes were elevated significantly in renal tissues of PGN patients compared to those from normal pericarcinoma tissues.	pgn	136-139	NLR family pyrin domain containing 3	Homo sapiens	62-67
26160272-8	2015	Immunofluorescence analysis also showed the protein expressions of NLRP3 and caspase-1 were increased in the glomeruli of PGN patients.	pgn	122-125	NLR family pyrin domain containing 3	Homo sapiens	67-72
26160272-12	2015	CONCLUSIONS: The formation and activation of NLRP3 inflammasomes in podocytes has been importantly implicated in the development of PGN-associated glomerular injury.	pgn	132-135	NLR family pyrin domain containing 3	Homo sapiens	45-50
26075098-3	2015	Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3).	Reactive Oxygen Species	59-62	NLR family pyrin domain containing 3	Homo sapiens	179-184
26075098-4	2015	Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade.	Reactive Oxygen Species	38-41	NLR family pyrin domain containing 3	Homo sapiens	43-48
26075098-4	2015	Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade.	Reactive Oxygen Species	38-41	NLR family pyrin domain containing 3	Homo sapiens	63-68
25446924-9	2014	In conclusion, quercetin, luteolin and EGCG inhibited ER stress-associated TXNIP and NLRP3 inflammasome activation, and thereby protected endothelial cells from inflammatory and apoptotic damage.	Quercetin	15-24	NLR family pyrin domain containing 3	Homo sapiens	85-90
25790542-8	2015	Guanine was transformed to adenine at the 732nd nucleotide position of the CIAS1 gene in the cDNA of chromosome 1.	Guanine	0-7	NLR family pyrin domain containing 3	Homo sapiens	75-80
25790542-8	2015	Guanine was transformed to adenine at the 732nd nucleotide position of the CIAS1 gene in the cDNA of chromosome 1.	Adenine	27-34	NLR family pyrin domain containing 3	Homo sapiens	75-80
25450671-0	2014	Procyanidin B2 inhibits NLRP3 inflammasome activation in human vascular endothelial cells.	procyanidin B2	0-14	NLR family pyrin domain containing 3	Homo sapiens	24-29
25450671-5	2014	Since aberrant activation of NLRP3 inflammasome is implicated in the pathogeneses of pro-inflammatory diseases such as diabetes, atherosclerosis and arthritis, we aimed to investigate whether procyanidin B2 (PCB2), the most widely distributed natural procyanidins, inhibits the activation of NLRP3 inflammasome in endothelial cells (ECs).	Proanthocyanidins	251-263	NLR family pyrin domain containing 3	Homo sapiens	29-34
25450671-9	2014	In conclusion, we demonstrated for the first time that procyanidin B2 inhibits NLRP3 inflammasome activation via suppression of AP-1 pathway in ECs.	procyanidin B2	55-69	NLR family pyrin domain containing 3	Homo sapiens	79-84
25446924-0	2014	Quercetin, luteolin and epigallocatechin gallate alleviate TXNIP and NLRP3-mediated inflammation and apoptosis with regulation of AMPK in endothelial cells.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	69-74
25446924-0	2014	Quercetin, luteolin and epigallocatechin gallate alleviate TXNIP and NLRP3-mediated inflammation and apoptosis with regulation of AMPK in endothelial cells.	Luteolin	11-19	NLR family pyrin domain containing 3	Homo sapiens	69-74
25446924-9	2014	In conclusion, quercetin, luteolin and EGCG inhibited ER stress-associated TXNIP and NLRP3 inflammasome activation, and thereby protected endothelial cells from inflammatory and apoptotic damage.	Luteolin	26-34	NLR family pyrin domain containing 3	Homo sapiens	85-90
25446924-0	2014	Quercetin, luteolin and epigallocatechin gallate alleviate TXNIP and NLRP3-mediated inflammation and apoptosis with regulation of AMPK in endothelial cells.	epigallocatechin gallate	24-48	NLR family pyrin domain containing 3	Homo sapiens	69-74
25446924-9	2014	In conclusion, quercetin, luteolin and EGCG inhibited ER stress-associated TXNIP and NLRP3 inflammasome activation, and thereby protected endothelial cells from inflammatory and apoptotic damage.	epigallocatechin gallate	39-43	NLR family pyrin domain containing 3	Homo sapiens	85-90
25446924-4	2014	Palmitate stimulation evoked oxidative stress and then induced TXNIP and NLRP3 inflammasome activation in the endothelial cells.	Palmitates	0-9	NLR family pyrin domain containing 3	Homo sapiens	73-78
25486008-4	2014	METHODS AND RESULTS: IFNT dose-dependently inhibited IL-1beta secretion induced by nano-silica, a well-known activators of NLRP3 inflammasomes, in human macrophages primed with lipopolysaccharide (LPS, TLR4 agonist) and Pam3CSK4 (TLR1/2 agonist).	Silicon Dioxide	88-94	NLR family pyrin domain containing 3	Homo sapiens	123-128
25446924-5	2014	Quercetin, luteolin and EGCG reduced reactive oxygen species production and inhibited TXNIP and NLRP3 inflammasome activation, lead to the downregulation of IL-1beta expression.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	96-101
25446924-5	2014	Quercetin, luteolin and EGCG reduced reactive oxygen species production and inhibited TXNIP and NLRP3 inflammasome activation, lead to the downregulation of IL-1beta expression.	Luteolin	11-19	NLR family pyrin domain containing 3	Homo sapiens	96-101
25446924-5	2014	Quercetin, luteolin and EGCG reduced reactive oxygen species production and inhibited TXNIP and NLRP3 inflammasome activation, lead to the downregulation of IL-1beta expression.	epigallocatechin gallate	24-28	NLR family pyrin domain containing 3	Homo sapiens	96-101
25281528-0	2014	Activation of the Nlrp3 inflammasome by mitochondrial reactive oxygen species: a novel mechanism of albumin-induced tubulointerstitial inflammation.	Reactive Oxygen Species	54-77	NLR family pyrin domain containing 3	Homo sapiens	18-23
25445147-4	2014	Silica and monosodium urate crystal-treated macrophages with undisturbed lysosomes demonstrated strong co-localization of ASC and Caspase-1, indicative of NLRP3 inflammasome activation.	Silicon Dioxide	0-6	NLR family pyrin domain containing 3	Homo sapiens	155-160
25445147-4	2014	Silica and monosodium urate crystal-treated macrophages with undisturbed lysosomes demonstrated strong co-localization of ASC and Caspase-1, indicative of NLRP3 inflammasome activation.	Uric Acid	11-27	NLR family pyrin domain containing 3	Homo sapiens	155-160
25445147-5	2014	Importantly, we provided evidence to suggest that macrophage cell membrane binding to immobilized crystals was sufficient to induce IL-1beta release, and this activation of the NLRP3 inflammasome was inhibited by blocking potassium efflux.	Potassium	222-231	NLR family pyrin domain containing 3	Homo sapiens	177-182
25281528-2	2014	In this study, we determined whether activation of the Nlrp3 inflammasome is involved in albuminuria induced-TIF and the underlying mechanisms of inflammasome activation by mitochondrial reactive oxygen species (mROS).	Reactive Oxygen Species	187-210	NLR family pyrin domain containing 3	Homo sapiens	55-60
25131433-11	2014	Inhibited activation of NLRP3 inflammasome in lung by steroid treatment could reverse R-ILD and block subsequent lung fibrosis.	Steroids	54-61	NLR family pyrin domain containing 3	Homo sapiens	24-29
25619352-8	2014	Gene analysis showed T1702T/A in exon 4 of NLRP3 gene, which causes Phe568lle.	phe568lle	68-77	NLR family pyrin domain containing 3	Homo sapiens	43-48
25396345-2	2014	This results in excessive production of reactive oxygen species and subsequent activation of the NLRP3 inflammasome.	Reactive Oxygen Species	40-63	NLR family pyrin domain containing 3	Homo sapiens	97-102
25868270-6	2014	This article reviews the activation and regulation of NL-RP3 inflammasome, and the effect of NLRP3 inflammasome on glucose metabolism and its targeted therapy in diabetes.	Glucose	115-122	NLR family pyrin domain containing 3	Homo sapiens	93-98
25017793-3	2014	In our study, we confirmed that high glucose (HG) concentrations induced NALP3 inflammasome activation both in vivo and in vitro.	Glucose	37-44	NLR family pyrin domain containing 3	Homo sapiens	73-78
25355909-6	2014	In addition, we also found that 20-guanosine ssRNA can activate the NLRP3 inflammasome in human macrophages but not in murine macrophages.	20-guanosine	32-44	NLR family pyrin domain containing 3	Homo sapiens	68-73
25389767-5	2014	Incubating the cells with 5-FU increased the expression of nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) and caspase-1.	Fluorouracil	26-30	NLR family pyrin domain containing 3	Homo sapiens	127-132
25389767-7	2014	The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death.	Fluorouracil	70-74	NLR family pyrin domain containing 3	Homo sapiens	22-27
25389767-7	2014	The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death.	Fluorouracil	70-74	NLR family pyrin domain containing 3	Homo sapiens	126-131
25389767-7	2014	The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death.	Fluorouracil	159-163	NLR family pyrin domain containing 3	Homo sapiens	22-27
25389767-7	2014	The inhibition of the NLRP3 pathway slightly decreased the effects of 5-FU on cell viability and LDH release, suggesting that NLRP3 may be in part involved in 5-FU-induced cell death.	Fluorouracil	159-163	NLR family pyrin domain containing 3	Homo sapiens	126-131
25091898-6	2014	In addition, we critically evaluate controversial evidence suggesting a specific role for mitochondrial reactive oxygen species in the activation of the NLRP3 inflammasome, a multiprotein complex that mediates the production of IL-1beta and IL-18.	Reactive Oxygen Species	104-127	NLR family pyrin domain containing 3	Homo sapiens	153-158
25175736-0	2014	Free fatty acids as modulators of the NLRP3 inflammasome in obesity/type 2 diabetes.	Fatty Acids, Nonesterified	0-16	NLR family pyrin domain containing 3	Homo sapiens	38-43
25175736-5	2014	SFAs (saturated fatty acids), unlike UFAs (unsaturated fatty acids), have recently been proposed as triggers of the NLRP3 inflammasome, a molecular platform mediating the processing of IL-1beta in response to infection and stress conditions.	Fatty Acids	6-27	NLR family pyrin domain containing 3	Homo sapiens	116-121
25175736-6	2014	Interestingly, UFAs, especially omega-3 FAs, inhibit NLRP3 inflammasome activation in various settings.	Fatty Acids, Unsaturated	15-19	NLR family pyrin domain containing 3	Homo sapiens	53-58
25175736-6	2014	Interestingly, UFAs, especially omega-3 FAs, inhibit NLRP3 inflammasome activation in various settings.	omega-3 fas	32-43	NLR family pyrin domain containing 3	Homo sapiens	53-58
25065288-0	2014	Suppression of the pro-inflammatory NLRP3/interleukin-1beta pathway in macrophages by the thioredoxin reductase inhibitor auranofin.	Auranofin	122-131	NLR family pyrin domain containing 3	Homo sapiens	36-41
24217221-7	2014	Enhanced IL-1beta secretion depended on the activation of the NLRP3 inflammasome through a mechanism involving reactive oxygen species formation and activation of thioredoxin-interacting protein.	Reactive Oxygen Species	111-134	NLR family pyrin domain containing 3	Homo sapiens	62-67
25251502-1	2014	Engineered nanomaterials (ENMs) including multiwall carbon nanotubes (MWCNTs) and rare earth oxide (REO) nanoparticles, which are capable of activating the NLRP3 inflammasome and inducing IL-1beta production, have the potential to cause chronic lung toxicity.	Carbon	52-58	NLR family pyrin domain containing 3	Homo sapiens	156-161
25225670-1	2014	The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (Nlrp3) inflammasome plays an important role in inflammation by controlling the maturation and secretion of the cytokines IL-1beta and IL-18 in response to multiple stimuli including pore-forming toxins, particulate matter, and ATP.	Adenosine Triphosphate	314-317	NLR family pyrin domain containing 3	Homo sapiens	4-85
25225670-1	2014	The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (Nlrp3) inflammasome plays an important role in inflammation by controlling the maturation and secretion of the cytokines IL-1beta and IL-18 in response to multiple stimuli including pore-forming toxins, particulate matter, and ATP.	Adenosine Triphosphate	314-317	NLR family pyrin domain containing 3	Homo sapiens	87-92
25225670-3	2014	In this study, we found that cytosolic poly(I:C), but not total RNA from healthy macrophages, macrophages undergoing pyroptosis, or mitochondrial RNA, induces caspase-1 activation and IL-1beta release through the Nlrp3 inflammasome.	poly	39-43	NLR family pyrin domain containing 3	Homo sapiens	213-218
25225670-5	2014	Further analyses revealed that the cytosolic sensors Rig-I and melanoma differentiation-associated gene 5 act redundantly via the common adaptor mitochondrial antiviral signaling (Mavs) to induce Nlrp3 activation in response to poly(I:C), but not ATP or nigericin.	Adenosine Triphosphate	247-250	NLR family pyrin domain containing 3	Homo sapiens	196-201
25225670-5	2014	Further analyses revealed that the cytosolic sensors Rig-I and melanoma differentiation-associated gene 5 act redundantly via the common adaptor mitochondrial antiviral signaling (Mavs) to induce Nlrp3 activation in response to poly(I:C), but not ATP or nigericin.	Nigericin	254-263	NLR family pyrin domain containing 3	Homo sapiens	196-201
25225670-6	2014	Mechanistically, Mavs triggered membrane permeabilization and K(+) efflux independently of the inflammasome which were required for poly(I:C)-induced Nlrp3 activation.	Poly I-C	132-141	NLR family pyrin domain containing 3	Homo sapiens	150-155
25225670-7	2014	We conclude that poly (I:C) activates the inflammasome through an Mavs-dependent surveillance pathway that converges into a common K(+) lowering step in the cytosol that is essential for the induction of Nlrp3 activation.	Poly I-C	17-26	NLR family pyrin domain containing 3	Homo sapiens	204-209
24820890-7	2014	The activation of the NLRP3 inflammasome by P. acnes was dependent on protease activity and reactive oxygen species generation.	Reactive Oxygen Species	92-115	NLR family pyrin domain containing 3	Homo sapiens	22-27
25065288-8	2014	In addition, qPCR and Western blot analyses showed that auranofin impaired TLR4-dependent induction of the inflammasome receptor NLRP3, which plays a critical role in IL-1beta processing.	Auranofin	56-65	NLR family pyrin domain containing 3	Homo sapiens	129-134
25046000-5	2014	When delivered in combination with doxorubicin, one of the drugs, vincristine, was also capable of synergistically activating the NLRP3-dependent inflammasome and increasing expression of IL-1beta, IL-6, and CXCL1.	Doxorubicin	35-46	NLR family pyrin domain containing 3	Homo sapiens	130-135
25046000-5	2014	When delivered in combination with doxorubicin, one of the drugs, vincristine, was also capable of synergistically activating the NLRP3-dependent inflammasome and increasing expression of IL-1beta, IL-6, and CXCL1.	Vincristine	66-77	NLR family pyrin domain containing 3	Homo sapiens	130-135
25022544-7	2014	To determine the role of PKC activation in the effects of DPP-4 inhibitors, cells were treated with PMA- which blocked the effect of DPP-4 inhibitors on NLRP3 and IL-1beta as well as TLR4 and GLP-1R.	Tetradecanoylphorbol Acetate	100-103	NLR family pyrin domain containing 3	Homo sapiens	153-158
25048991-0	2014	NLRP3 inflammasome activation and interleukin-1beta release in macrophages require calcium but are independent of calcium-activated NADPH oxidases.	Calcium	83-90	NLR family pyrin domain containing 3	Homo sapiens	0-5
25041941-0	2014	Vinpocetine inhibits amyloid-beta induced activation of NF-kappaB, NLRP3 inflammasome and cytokine production in retinal pigment epithelial cells.	vinpocetine	0-11	NLR family pyrin domain containing 3	Homo sapiens	67-72
25048991-1	2014	OBJECTIVE AND DESIGN: We studied the involvement of calcium and calcium-activated NADPH oxidases in NLRP3 inflammasome activation and IL-1beta release to better understand inflammasome signaling in macrophages.	Calcium	52-59	NLR family pyrin domain containing 3	Homo sapiens	100-105
25048991-4	2014	TREATMENT: Murine or human macrophages were treated in vitro with NLRP3 inflammasome agonists (ATP, silica crystals) or calcium agonists (thapsigargin, ionomycin) in calcium-containing or calcium-free medium.	Calcium	166-173	NLR family pyrin domain containing 3	Homo sapiens	66-71
25048991-4	2014	TREATMENT: Murine or human macrophages were treated in vitro with NLRP3 inflammasome agonists (ATP, silica crystals) or calcium agonists (thapsigargin, ionomycin) in calcium-containing or calcium-free medium.	Calcium	166-173	NLR family pyrin domain containing 3	Homo sapiens	66-71
24814218-0	2014	Type AII lantibiotic bovicin HJ50 with a rare disulfide bond: structure, structure-activity relationships and mode of action.	Disulfides	46-55	NLR family pyrin domain containing 3	Homo sapiens	5-8
25172487-6	2014	The ubiquitination of DHX33 by TRIM33 is lysine 63 specific and is required for the formation of the DHX33-NLRP3 inflammasome complex.	Lysine	41-47	NLR family pyrin domain containing 3	Homo sapiens	107-112
24703401-4	2014	Activation of the NLRP3-inflammasome by microcrystals, such as monosodium urate (MSU) and basic calcium phosphate (BCP) crystals, leads to IL1beta release, which in turn triggers local inflammation.	Uric Acid	63-79	NLR family pyrin domain containing 3	Homo sapiens	18-23
24703401-4	2014	Activation of the NLRP3-inflammasome by microcrystals, such as monosodium urate (MSU) and basic calcium phosphate (BCP) crystals, leads to IL1beta release, which in turn triggers local inflammation.	Uric Acid	81-84	NLR family pyrin domain containing 3	Homo sapiens	18-23
24703401-4	2014	Activation of the NLRP3-inflammasome by microcrystals, such as monosodium urate (MSU) and basic calcium phosphate (BCP) crystals, leads to IL1beta release, which in turn triggers local inflammation.	basic calcium phosphate	90-113	NLR family pyrin domain containing 3	Homo sapiens	18-23
25225402-4	2014	We found that heme, but not porphyrins without iron, activated LPS-primed macrophages promoting the processing of IL-1beta dependent on nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3).	Heme	14-18	NLR family pyrin domain containing 3	Homo sapiens	232-237
25225402-5	2014	The activation of NLRP3 by heme required spleen tyrosine kinase, NADPH oxidase-2, mitochondrial reactive oxygen species, and K(+) efflux, whereas it was independent of heme internalization, lysosomal damage, ATP release, the purinergic receptor P2X7, and cell death.	Heme	27-31	NLR family pyrin domain containing 3	Homo sapiens	18-23
25225402-5	2014	The activation of NLRP3 by heme required spleen tyrosine kinase, NADPH oxidase-2, mitochondrial reactive oxygen species, and K(+) efflux, whereas it was independent of heme internalization, lysosomal damage, ATP release, the purinergic receptor P2X7, and cell death.	Reactive Oxygen Species	96-119	NLR family pyrin domain containing 3	Homo sapiens	18-23
25225402-5	2014	The activation of NLRP3 by heme required spleen tyrosine kinase, NADPH oxidase-2, mitochondrial reactive oxygen species, and K(+) efflux, whereas it was independent of heme internalization, lysosomal damage, ATP release, the purinergic receptor P2X7, and cell death.	Adenosine Triphosphate	208-211	NLR family pyrin domain containing 3	Homo sapiens	18-23
25181346-0	2014	High-temperature calcined fullerene nanowhiskers as well as long needle-like multi-wall carbon nanotubes have abilities to induce NLRP3-mediated IL-1beta secretion.	Fullerenes	26-35	NLR family pyrin domain containing 3	Homo sapiens	130-135
25181346-0	2014	High-temperature calcined fullerene nanowhiskers as well as long needle-like multi-wall carbon nanotubes have abilities to induce NLRP3-mediated IL-1beta secretion.	Carbon	88-94	NLR family pyrin domain containing 3	Homo sapiens	130-135
25181346-3	2014	In this study, we employed high-temperature calcined fullerene nanowhiskers (HTCFNWs), which are needle-like nanofibers composed of amorphous carbon having similar sizes to MWCNTs but neither metal impurities nor tubular structures, and investigated their ability to induce production a major proinflammatory cytokine IL-1beta via the Nod-like receptor pyrin domain containing 3 (NLRP3)-containing flammasome-mediated mechanism.	Fullerenes	53-62	NLR family pyrin domain containing 3	Homo sapiens	380-385
25181346-5	2014	IL-1beta release induced by long-HTCFNW as well as by long, needle-like MWCNTs was abolished by a caspase-1 inhibitor or siRNA-knockdown of NLRP3, indicating that NLRP3-inflammasome-mediated IL-1beta production by these carbon nanofibers.	Carbon	220-226	NLR family pyrin domain containing 3	Homo sapiens	140-145
25181346-5	2014	IL-1beta release induced by long-HTCFNW as well as by long, needle-like MWCNTs was abolished by a caspase-1 inhibitor or siRNA-knockdown of NLRP3, indicating that NLRP3-inflammasome-mediated IL-1beta production by these carbon nanofibers.	Carbon	220-226	NLR family pyrin domain containing 3	Homo sapiens	163-168
24849809-7	2014	Together, these findings reveal a novel neurotransmitter-mediated signaling pathway: acetylcholine translocates into the cytoplasm of immune cells during inflammation and inhibits NLRP3 inflammasome activation by preventing mitochondrial DNA release.	Acetylcholine	85-98	NLR family pyrin domain containing 3	Homo sapiens	180-185
24703401-4	2014	Activation of the NLRP3-inflammasome by microcrystals, such as monosodium urate (MSU) and basic calcium phosphate (BCP) crystals, leads to IL1beta release, which in turn triggers local inflammation.	bcp	115-118	NLR family pyrin domain containing 3	Homo sapiens	18-23
24776598-6	2014	To study the LOX-1-NLRP3 inflammasome signalling, we performed studies using ROS inhibitors and an autophagy inducer, and found that both decreased the expression of NLRP3.	Reactive Oxygen Species	77-80	NLR family pyrin domain containing 3	Homo sapiens	166-171
24700466-6	2014	We conclude that AQP-mediated water transport in macrophages constitutes a general danger signal required for NLRP3-related inflammation.	Water	30-35	NLR family pyrin domain containing 3	Homo sapiens	110-115
25202950-6	2014	RESULTS: Compared with the THP-1 macrophages without palmitic acid, the level of ROS, NALP3 protein and caspase-1 protein, and the expression of IL-1beta were increased after palmitic acid treatment in a dose dependent manner (P&lt;0.05).	Palmitic Acid	175-188	NLR family pyrin domain containing 3	Homo sapiens	86-91
25202950-8	2014	CONCLUSION: ROS induced by free fatty acid can regulate the activation of NALP3 inflammasome signaling pathway leading to the release of inflammatory cytokines.	ros	12-15	NLR family pyrin domain containing 3	Homo sapiens	74-79
25202950-8	2014	CONCLUSION: ROS induced by free fatty acid can regulate the activation of NALP3 inflammasome signaling pathway leading to the release of inflammatory cytokines.	Fatty Acids, Nonesterified	27-42	NLR family pyrin domain containing 3	Homo sapiens	74-79
24915862-7	2014	RESULTS: MWCNT induced NLRP3 inflammasome dependent pyroptosis in HBE cells in a time- and dose-dependent manner.	mwcnt	9-14	NLR family pyrin domain containing 3	Homo sapiens	23-28
24307525-0	2014	Mesenchymal stem/stromal cells inhibit the NLRP3 inflammasome by decreasing mitochondrial reactive oxygen species.	Reactive Oxygen Species	90-113	NLR family pyrin domain containing 3	Homo sapiens	43-48
24894187-7	2014	The ability of dendritic cells to respond to the signals required for IL-1beta secretion can be tested using a synthetic purine, R848, which is sensed by TLR8 in human monocyte derived dendritic cells (moDCs) to prime cells, followed by activation of the NLRP3 inflammasome with the bacterial toxin and potassium ionophore, nigericin.	purine	121-127	NLR family pyrin domain containing 3	Homo sapiens	255-260
25202950-0	2014	[Effect of free fatty acid on NALP3 inflammasome signaling pathway in THP-1 macrophages].	Fatty Acids, Nonesterified	11-26	NLR family pyrin domain containing 3	Homo sapiens	30-35
25054228-13	2014	Glioblastoma IL-1beta processing occurred by the NLRP3 inflammasome, and ATP and nigericin increased IL-1beta processing by upregulating NLRP3 expression, similar to macrophages.	Adenosine Triphosphate	73-76	NLR family pyrin domain containing 3	Homo sapiens	137-142
25054228-13	2014	Glioblastoma IL-1beta processing occurred by the NLRP3 inflammasome, and ATP and nigericin increased IL-1beta processing by upregulating NLRP3 expression, similar to macrophages.	Nigericin	81-90	NLR family pyrin domain containing 3	Homo sapiens	137-142
24607329-8	2014	Apolipoprotein A-I/A-II and B changed respectively in accordance with HDL-cholesterol and LDL-cholesterol changes.	Cholesterol	74-85	NLR family pyrin domain containing 3	Homo sapiens	19-29
24607329-8	2014	Apolipoprotein A-I/A-II and B changed respectively in accordance with HDL-cholesterol and LDL-cholesterol changes.	Cholesterol	94-105	NLR family pyrin domain containing 3	Homo sapiens	19-29
24850149-6	2014	Following exposure to extracellular ATP, stimulation of the P2X purinoreceptor-7 (P2X7R), which results in K(+) efflux, is required as a second signal for NLRP3 inflammasome formation.	Adenosine Triphosphate	36-39	NLR family pyrin domain containing 3	Homo sapiens	155-160
24850149-7	2014	Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and/or mitochondria-dependent reactive oxygen species (ROS) production.	Reactive Oxygen Species	133-156	NLR family pyrin domain containing 3	Homo sapiens	23-28
24850149-7	2014	Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and/or mitochondria-dependent reactive oxygen species (ROS) production.	Reactive Oxygen Species	158-161	NLR family pyrin domain containing 3	Homo sapiens	23-28
24307525-4	2014	Here we demonstrate that human MSCs (hMSCs) negatively regulate NLRP3 inflammasome activation in human or mouse macrophages stimulated with LPS and ATP.	Adenosine Triphosphate	148-151	NLR family pyrin domain containing 3	Homo sapiens	64-69
24307525-12	2014	Together, our results reveal that hMSCs inhibit NLRP3 inflammasome activation in macrophages primarily by secreting STC-1 in response to activated macrophages and thus by decreasing mitochondrial ROS.	Reactive Oxygen Species	196-199	NLR family pyrin domain containing 3	Homo sapiens	48-53
24646829-0	2014	Calcium signaling and mitochondrial destabilization in the triggering of the NLRP3 inflammasome.	Calcium	0-7	NLR family pyrin domain containing 3	Homo sapiens	77-82
24806599-7	2014	All tested haptens, but not irritants, can induce Syk activation, leading to both the CARD9/BCL10-dependent pro-IL-1 synthesis (signal1) and reactive oxygen species-mediated NLRP3 inflammasome activation (signal2), required for IL-1 secretion.	Reactive Oxygen Species	141-164	NLR family pyrin domain containing 3	Homo sapiens	174-179
24158569-0	2014	Nickel induces interleukin-1beta secretion via the NLRP3-ASC-caspase-1 pathway.	Nickel	0-6	NLR family pyrin domain containing 3	Homo sapiens	51-56
24252030-6	2014	RESULTS: DHMEQ inhibited expression of proIL-1beta and NLRP3 by normal PBMCs primed with LPS, resulting in inhibition of caspase-1 activation and IL-1beta secretion by the cells after subsequent stimulation with ATP.	dehydroxymethylepoxyquinomicin	9-14	NLR family pyrin domain containing 3	Homo sapiens	55-60
24472059-0	2014	Involvement of purinergic receptors and NOD-like receptor-family protein 3-inflammasome pathway in the adenosine triphosphate-induced cytokine release from macrophages.	Adenosine Triphosphate	103-125	NLR family pyrin domain containing 3	Homo sapiens	40-74
24472059-1	2014	Adenosine triphosphate (ATP) has been described as a danger signal activating the NOD-like receptor-family protein 3 (NLRP3)-inflammasome leading to the pro-inflammatory cytokine, interleukin (IL)-1beta, release in the lung.	Adenosine Triphosphate	0-22	NLR family pyrin domain containing 3	Homo sapiens	82-116
24472059-1	2014	Adenosine triphosphate (ATP) has been described as a danger signal activating the NOD-like receptor-family protein 3 (NLRP3)-inflammasome leading to the pro-inflammatory cytokine, interleukin (IL)-1beta, release in the lung.	Adenosine Triphosphate	0-22	NLR family pyrin domain containing 3	Homo sapiens	118-123
24472059-1	2014	Adenosine triphosphate (ATP) has been described as a danger signal activating the NOD-like receptor-family protein 3 (NLRP3)-inflammasome leading to the pro-inflammatory cytokine, interleukin (IL)-1beta, release in the lung.	Adenosine Triphosphate	24-27	NLR family pyrin domain containing 3	Homo sapiens	82-116
24472059-1	2014	Adenosine triphosphate (ATP) has been described as a danger signal activating the NOD-like receptor-family protein 3 (NLRP3)-inflammasome leading to the pro-inflammatory cytokine, interleukin (IL)-1beta, release in the lung.	Adenosine Triphosphate	24-27	NLR family pyrin domain containing 3	Homo sapiens	118-123
24472059-3	2014	The aim of the present study was to investigate the role of the NLRP3 inflammasome pathway and P2X7 purinergic receptor in the activation of human macrophages in vitro by ATP.	Adenosine Triphosphate	171-174	NLR family pyrin domain containing 3	Homo sapiens	64-69
24472059-7	2014	NLRP3 and IL-1beta mRNA expression were induced from LPS-primed macrophages, but also after 5-h treatment of BzATP as analysed by reverse transcription quantitative polymerase chain reaction.	BzATP	109-114	NLR family pyrin domain containing 3	Homo sapiens	0-5
24472059-10	2014	The present results showed the involvement of the P2X7 R-NLRP3 inflammasome pathway in the secretion of IL-1beta from ATP-stimulated human macrophages, and suggest that P2X7 R were not involved in IL-1alpha and IL-6 release.	Adenosine Triphosphate	118-121	NLR family pyrin domain containing 3	Homo sapiens	57-62
24758928-5	2014	Our results show that isoprenoids acted in different ways, mainly increasing the expression of the evaluated markers [apoptosis, mitochondrial dysfunction, nucleotide-binding oligomerization-domain protein-like receptors 3 (NALP3), cytokines and nitric oxide (NO)].	Terpenes	22-33	NLR family pyrin domain containing 3	Homo sapiens	156-222
24758928-5	2014	Our results show that isoprenoids acted in different ways, mainly increasing the expression of the evaluated markers [apoptosis, mitochondrial dysfunction, nucleotide-binding oligomerization-domain protein-like receptors 3 (NALP3), cytokines and nitric oxide (NO)].	Terpenes	22-33	NLR family pyrin domain containing 3	Homo sapiens	224-229
24623131-6	2014	Within minutes of endotoxin priming, the NLRP3 inflammasome is licensed for ATP-induced release of processed IL-18, apoptosis-associated speck-forming complex containing CARD, and active caspase-1, independent of new mRNA or protein synthesis.	Adenosine Triphosphate	76-79	NLR family pyrin domain containing 3	Homo sapiens	41-46
24623131-11	2014	These findings suggest that ERK1-mediated posttranslational modifications license the NLRP3 inflammasome to respond to the second signal ATP by inducing posttranslational events that are independent of new production of pro-IL-1beta and NOD-like receptor components.	Adenosine Triphosphate	137-140	NLR family pyrin domain containing 3	Homo sapiens	86-91
24380723-0	2014	Dimethyl sulfoxide inhibits NLRP3 inflammasome activation.	Dimethyl Sulfoxide	0-18	NLR family pyrin domain containing 3	Homo sapiens	28-33
24380723-4	2014	In the present study, we prove that DMSO attenuated IL-1beta maturation, Casp1 activity, and ASC pyroptosome formation via NLRP3 inflammasome activators.	Dimethyl Sulfoxide	36-40	NLR family pyrin domain containing 3	Homo sapiens	123-128
24380723-5	2014	Further, NLRC4 and AIM2 inflammasome activity were not affected, suggesting that DMSO is a selective inhibitor of the NLRP3 inflammasomes.	Dimethyl Sulfoxide	81-85	NLR family pyrin domain containing 3	Homo sapiens	118-123
24380723-8	2014	Taken together, DMSO shows anti-inflammatory characteristics, attenuates NLRP3 inflammasome activation, and mediates inhibition of IL-1s transcription.	Dimethyl Sulfoxide	16-20	NLR family pyrin domain containing 3	Homo sapiens	73-78
24158569-3	2014	Here we report that Ni(2+) activates the NLRP3-ASC-caspase-1 immune signaling pathway in antigen-presenting cells, leading to the proteolytic processing and secretion of a proinflammatory cytokine, interleukin-1beta (IL-1beta).	Nickel(2+)	20-26	NLR family pyrin domain containing 3	Homo sapiens	41-46
24158569-5	2014	Instead, Ni(2+) induces mitochondrial reactive oxygen species accumulation and cation fluxes, both of which are required for activating the NLRP3-ASC-caspase-1 pathway.	Nickel(2+)	9-15	NLR family pyrin domain containing 3	Homo sapiens	140-145
24158569-6	2014	Together, these results identified a novel innate immune signaling pathway (NLRP3-ASC-caspase-1-IL-1beta) activated by Ni(2+) and provided a mechanistic basis for optimizing the therapeutic intervention against Ni(2+)-induced allergy in patients.	Nickel(2+)	119-125	NLR family pyrin domain containing 3	Homo sapiens	76-81
24158569-6	2014	Together, these results identified a novel innate immune signaling pathway (NLRP3-ASC-caspase-1-IL-1beta) activated by Ni(2+) and provided a mechanistic basis for optimizing the therapeutic intervention against Ni(2+)-induced allergy in patients.	Nickel(2+)	211-217	NLR family pyrin domain containing 3	Homo sapiens	76-81
23944632-0	2014	NLRP3 inflammasome activation in coronary artery disease: results from prospective and randomized study of treatment with atorvastatin or rosuvastatin.	Rosuvastatin Calcium	138-150	NLR family pyrin domain containing 3	Homo sapiens	0-5
24513871-9	2014	Interestingly, amitriptyline treatment reduced NLRP3 and caspase-1 gene expression, and IL-1beta and IL-18 serum levels.	Amitriptyline	15-28	NLR family pyrin domain containing 3	Homo sapiens	47-52
24513871-12	2014	CONCLUSIONS: These findings provide new insight into the pathogenesis of MDD and the effects of amitriptyline treatment on NLRP3 inflammasome activation and IL-1beta and IL-18 serum levels.	Amitriptyline	96-109	NLR family pyrin domain containing 3	Homo sapiens	123-128
24532802-6	2014	We demonstrate that palmitate-loaded primary macrophages challenged with LPS activate the NLRP3 inflammasome through a mechanism that involves the lysosome.	Palmitates	20-29	NLR family pyrin domain containing 3	Homo sapiens	90-95
23944632-2	2014	The aim of the present study was to determine whether NLRP3 inflammasome is expressed in patients with CAD (coronary artery disease) and whether statins (atorvastatin or rosuvastatin) might affect NLRP3 levels.	Atorvastatin	154-166	NLR family pyrin domain containing 3	Homo sapiens	197-202
23944632-0	2014	NLRP3 inflammasome activation in coronary artery disease: results from prospective and randomized study of treatment with atorvastatin or rosuvastatin.	Atorvastatin	122-134	NLR family pyrin domain containing 3	Homo sapiens	0-5
23944632-2	2014	The aim of the present study was to determine whether NLRP3 inflammasome is expressed in patients with CAD (coronary artery disease) and whether statins (atorvastatin or rosuvastatin) might affect NLRP3 levels.	Rosuvastatin Calcium	170-182	NLR family pyrin domain containing 3	Homo sapiens	197-202
23944632-10	2014	A randomized clinical study has shown that atorvastatin markedly diminished NLRP3 inflammasome levels, whereas rosuvastatin had no impact on these levels.	Atorvastatin	43-55	NLR family pyrin domain containing 3	Homo sapiens	76-81
23944632-11	2014	Levels of NLRP3 inflammasome decreased in THP-1 cells treated with statins compared with those treated with vehicle, and the fold changes in NLRP3 inflammasome were higher in THP-1 cells treated with atorvastatin compared with those treated with rosuvastatin.	Atorvastatin	200-212	NLR family pyrin domain containing 3	Homo sapiens	10-15
23944632-11	2014	Levels of NLRP3 inflammasome decreased in THP-1 cells treated with statins compared with those treated with vehicle, and the fold changes in NLRP3 inflammasome were higher in THP-1 cells treated with atorvastatin compared with those treated with rosuvastatin.	Atorvastatin	200-212	NLR family pyrin domain containing 3	Homo sapiens	141-146
23944632-11	2014	Levels of NLRP3 inflammasome decreased in THP-1 cells treated with statins compared with those treated with vehicle, and the fold changes in NLRP3 inflammasome were higher in THP-1 cells treated with atorvastatin compared with those treated with rosuvastatin.	Rosuvastatin Calcium	246-258	NLR family pyrin domain containing 3	Homo sapiens	10-15
23944632-11	2014	Levels of NLRP3 inflammasome decreased in THP-1 cells treated with statins compared with those treated with vehicle, and the fold changes in NLRP3 inflammasome were higher in THP-1 cells treated with atorvastatin compared with those treated with rosuvastatin.	Rosuvastatin Calcium	246-258	NLR family pyrin domain containing 3	Homo sapiens	141-146
23944632-12	2014	The present study suggests that atorvastatin down-regulates NLRP3 inflammasome expression in CAD, possibly contributing to the inhibitory effects of atorvastatin on chronic inflammation and atherogenic progression in this disorder.	Atorvastatin	32-44	NLR family pyrin domain containing 3	Homo sapiens	60-65
23944632-12	2014	The present study suggests that atorvastatin down-regulates NLRP3 inflammasome expression in CAD, possibly contributing to the inhibitory effects of atorvastatin on chronic inflammation and atherogenic progression in this disorder.	Atorvastatin	149-161	NLR family pyrin domain containing 3	Homo sapiens	60-65
23884315-7	2014	The mechanism of P. acnes-induced NLRP3 activation and subsequent IL-1beta secretion was found to involve potassium efflux.	Potassium	106-115	NLR family pyrin domain containing 3	Homo sapiens	34-39
24269698-0	2014	Trichothecene mycotoxins activate NLRP3 inflammasome through a P2X7 receptor and Src tyrosine kinase dependent pathway.	trichothecene mycotoxins	0-24	NLR family pyrin domain containing 3	Homo sapiens	34-39
24269698-5	2014	Here, we show that the trichothecene-induced IL-1beta secretion is dependent on NLRP3 inflammasome in human primary macrophages.	Trichothecenes	23-36	NLR family pyrin domain containing 3	Homo sapiens	80-85
24269698-6	2014	Pharmacological inhibition and small interfering RNA approach showed that the trichothecene-induced NLRP3 inflammasome activation is mediated through ATP-gated P2X7 receptor.	Trichothecenes	78-91	NLR family pyrin domain containing 3	Homo sapiens	100-105
24269698-7	2014	Moreover, we show that trichothecene-triggered NLRP3 inflammasome activation is dependent on Src tyrosine kinase activity.	Trichothecenes	23-36	NLR family pyrin domain containing 3	Homo sapiens	47-52
24269698-9	2014	In conclusion, our results suggest that roridin A, a fungal trichothecene mycotoxin, acts as microbial danger signals that trigger activation of NLRP3 inflammasome through P2X7R and Src tyrosine kinase signaling dependent pathway in human primary macrophages.	roridin A	40-49	NLR family pyrin domain containing 3	Homo sapiens	145-150
24265316-0	2014	3,4-methylenedioxy-beta-nitrostyrene inhibits NLRP3 inflammasome activation by blocking assembly of the inflammasome.	3,4-methylenedioxy-beta-nitrostyrene	0-36	NLR family pyrin domain containing 3	Homo sapiens	46-51
24265316-4	2014	In this study, we explored the role of kinases in NLRP3 inflammasome activation by screening a kinase inhibitor library and identified 3,4-methylenedioxy-beta-nitrostyrene (MNS) as an inhibitor for NLRP3 inflammasome activation.	3,4-methylenedioxy-beta-nitrostyrene	135-171	NLR family pyrin domain containing 3	Homo sapiens	50-55
24265316-4	2014	In this study, we explored the role of kinases in NLRP3 inflammasome activation by screening a kinase inhibitor library and identified 3,4-methylenedioxy-beta-nitrostyrene (MNS) as an inhibitor for NLRP3 inflammasome activation.	3,4-methylenedioxy-beta-nitrostyrene	135-171	NLR family pyrin domain containing 3	Homo sapiens	198-203
24265316-4	2014	In this study, we explored the role of kinases in NLRP3 inflammasome activation by screening a kinase inhibitor library and identified 3,4-methylenedioxy-beta-nitrostyrene (MNS) as an inhibitor for NLRP3 inflammasome activation.	3,4-methylenedioxy-beta-nitrostyrene	173-176	NLR family pyrin domain containing 3	Homo sapiens	50-55
24265316-4	2014	In this study, we explored the role of kinases in NLRP3 inflammasome activation by screening a kinase inhibitor library and identified 3,4-methylenedioxy-beta-nitrostyrene (MNS) as an inhibitor for NLRP3 inflammasome activation.	3,4-methylenedioxy-beta-nitrostyrene	173-176	NLR family pyrin domain containing 3	Homo sapiens	198-203
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	18-21	NLR family pyrin domain containing 3	Homo sapiens	37-42
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	18-21	NLR family pyrin domain containing 3	Homo sapiens	100-105
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	18-21	NLR family pyrin domain containing 3	Homo sapiens	100-105
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	18-21	NLR family pyrin domain containing 3	Homo sapiens	100-105
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	85-88	NLR family pyrin domain containing 3	Homo sapiens	37-42
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	85-88	NLR family pyrin domain containing 3	Homo sapiens	100-105
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	85-88	NLR family pyrin domain containing 3	Homo sapiens	100-105
24265316-10	2014	Administration of MNS also inhibited NLRP3 ATPase activity in vitro, suggesting that MNS blocks the NLRP3 inflammasome by directly targeting NLRP3 or NLRP3-associated complexes.	3,4-methylenedioxy-beta-nitrostyrene	85-88	NLR family pyrin domain containing 3	Homo sapiens	100-105
24261790-3	2013	Other than being comprised of micrometer-sized aggregates that include nanoscale particulates, Alum lacks specific physicochemical properties to explain activation of the innate immune system, including the mechanism by which aluminum-based adjuvants engage the NLRP3 inflammasome and IL-1beta production.	Aluminum	226-234	NLR family pyrin domain containing 3	Homo sapiens	262-267
24400125-7	2014	CONCLUSIONS: Our results indicate that HCV RNA activates the NLRP3 inflammasome in a ROS-dependent manner, and RIG-I is not required for this process.	Reactive Oxygen Species	85-88	NLR family pyrin domain containing 3	Homo sapiens	61-66
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Uric Acid	63-79	NLR family pyrin domain containing 3	Homo sapiens	132-137
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Ceramides	81-89	NLR family pyrin domain containing 3	Homo sapiens	132-137
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Cholesterol	91-102	NLR family pyrin domain containing 3	Homo sapiens	132-137
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Glucose	108-115	NLR family pyrin domain containing 3	Homo sapiens	132-137
24261790-6	2013	Using comparison to commercial Alum, we demonstrate that the crystallinity and surface hydroxyl group display of AlOOH nanoparticles quantitatively impact the activation of the NLRP3 inflammasome in human THP-1 myeloid cells or murine bone marrow-derived dendritic cells (BMDCs).	alooh	113-118	NLR family pyrin domain containing 3	Homo sapiens	177-182
24261790-8	2013	These results demonstrate that shape, crystallinity, and hydroxyl content play an important role in NLRP3 inflammasome activation and are therefore useful for quantitative boosting of antigen-specific immune responses.	Hydroxyl Radical	57-65	NLR family pyrin domain containing 3	Homo sapiens	100-105
24456929-0	2013	NLRP3 promotes autophagy of urate crystals phagocytized by human osteoblasts.	Uric Acid	28-33	NLR family pyrin domain containing 3	Homo sapiens	0-5
23815151-0	2013	Rhinovirus-induced calcium flux triggers NLRP3 and NLRC5 activation in bronchial cells.	Calcium	19-26	NLR family pyrin domain containing 3	Homo sapiens	41-46
24089192-0	2013	Mitochondrial reactive oxygen species induces NLRP3-dependent lysosomal damage and inflammasome activation.	Reactive Oxygen Species	14-37	NLR family pyrin domain containing 3	Homo sapiens	46-51
24089192-3	2013	Macrophages triggered by the NLRP3 inflammasome activator nigericin show reduced mitochondrial function and decreased cellular ATP.	Nigericin	58-67	NLR family pyrin domain containing 3	Homo sapiens	29-34
24089192-3	2013	Macrophages triggered by the NLRP3 inflammasome activator nigericin show reduced mitochondrial function and decreased cellular ATP.	Adenosine Triphosphate	127-130	NLR family pyrin domain containing 3	Homo sapiens	29-34
24089192-5	2013	NLRP3-deficient macrophages show comparable reduced mitochondrial function and ATP loss, but maintain lysosomal acidity, demonstrating that LMP is NLRP3 dependent.	Adenosine Triphosphate	79-82	NLR family pyrin domain containing 3	Homo sapiens	0-5
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	148-171	NLR family pyrin domain containing 3	Homo sapiens	123-128
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	173-176	NLR family pyrin domain containing 3	Homo sapiens	123-128
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	218-221	NLR family pyrin domain containing 3	Homo sapiens	123-128
23512739-1	2013	The NLRP3 inflammasome, which consists of the NLRP3 (nucleotide-binding oligomerization domain (Nod)-like receptor 3) scaffold, the ASC (apoptosis-associated speck-like protein containing a CARD) adaptor and procaspase- 1, is assembled after the cytoplasmic LRRs (leucine-rich repeats) of NLRP3 sense pathogens or danger signals.	Leucine	264-271	NLR family pyrin domain containing 3	Homo sapiens	4-9
24235127-6	2013	Release of ATP is a rate-limiting step for activating caspase-1, as extracellular ATP triggers the P2X7 purinergic receptor to initiate oligomerization of NLRP3.	Adenosine Triphosphate	11-14	NLR family pyrin domain containing 3	Homo sapiens	155-160
24235127-6	2013	Release of ATP is a rate-limiting step for activating caspase-1, as extracellular ATP triggers the P2X7 purinergic receptor to initiate oligomerization of NLRP3.	Adenosine Triphosphate	82-85	NLR family pyrin domain containing 3	Homo sapiens	155-160
24244322-0	2013	Ethanol inhibits activation of NLRP3 and AIM2 inflammasomes in human macrophages--a novel anti-inflammatory action of alcohol.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	31-36
24244322-0	2013	Ethanol inhibits activation of NLRP3 and AIM2 inflammasomes in human macrophages--a novel anti-inflammatory action of alcohol.	Alcohols	118-125	NLR family pyrin domain containing 3	Homo sapiens	31-36
24244322-4	2013	RESULTS: Ethanol decreased dose-dependently the production of mature IL-1beta induced by activators of the NLRP3 inflammasome, i.e. ATP, cholesterol crystals, serum amyloid A and nigericin.	Ethanol	9-16	NLR family pyrin domain containing 3	Homo sapiens	107-112
24244322-4	2013	RESULTS: Ethanol decreased dose-dependently the production of mature IL-1beta induced by activators of the NLRP3 inflammasome, i.e. ATP, cholesterol crystals, serum amyloid A and nigericin.	Nigericin	179-188	NLR family pyrin domain containing 3	Homo sapiens	107-112
24244322-10	2013	CONCLUSION: Ethanol-induced inhibition of the NLRP3 inflammasome activation in macrophages may represent a biological pathway underlying the protective effect of moderate alcohol consumption on coronary heart disease.	Ethanol	12-19	NLR family pyrin domain containing 3	Homo sapiens	46-51
24244322-10	2013	CONCLUSION: Ethanol-induced inhibition of the NLRP3 inflammasome activation in macrophages may represent a biological pathway underlying the protective effect of moderate alcohol consumption on coronary heart disease.	Alcohols	171-178	NLR family pyrin domain containing 3	Homo sapiens	46-51
24456929-1	2013	INTRODUCTION: Monosodium urate (MSU) microcrystals present in bone tissues of chronic gout can be ingested by nonprofessional phagocytes like osteoblasts (OBs) that express NLRP3 (nucleotide-binding domain and leucine-rich repeat region containing family of receptor protein 3).	Uric Acid	14-30	NLR family pyrin domain containing 3	Homo sapiens	173-178
24043885-6	2013	Our results reveal mechanistic insight about how palmitic acid activates TLR2, upregulates NALP3 expression, and induces inflammasome-mediated IL-1beta production in human monocytes, which can trigger enhanced inflammation in peripheral tissues, and suggest that these processes are dynamically modulated by the types of dietary fat we consume.	Palmitic Acid	49-62	NLR family pyrin domain containing 3	Homo sapiens	91-96
23454144-6	2013	ROS are also involved in the activation of the NLRP3/NALP3 inflammasome, which is required to direct the proteolytic maturation of inflammatory cytokines such as IL-1beta and IL-18, which are all integral to the process of dendritic cells mobilization, migration and functional maturation.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	47-52
23454144-6	2013	ROS are also involved in the activation of the NLRP3/NALP3 inflammasome, which is required to direct the proteolytic maturation of inflammatory cytokines such as IL-1beta and IL-18, which are all integral to the process of dendritic cells mobilization, migration and functional maturation.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	53-58
24006511-0	2013	Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages.	Fatty Acids, Unsaturated	0-23	NLR family pyrin domain containing 3	Homo sapiens	46-51
24006511-3	2013	Here we reported opposite effects of saturated fatty acids (SFAs) compared with unsaturated fatty acids (UFAs) on NLRP3 inflammasome in human monocytes/macrophages.	Fatty Acids	37-58	NLR family pyrin domain containing 3	Homo sapiens	114-119
24006511-3	2013	Here we reported opposite effects of saturated fatty acids (SFAs) compared with unsaturated fatty acids (UFAs) on NLRP3 inflammasome in human monocytes/macrophages.	Fatty Acids, Unsaturated	80-103	NLR family pyrin domain containing 3	Homo sapiens	114-119
24006511-3	2013	Here we reported opposite effects of saturated fatty acids (SFAs) compared with unsaturated fatty acids (UFAs) on NLRP3 inflammasome in human monocytes/macrophages.	Fatty Acids, Unsaturated	105-109	NLR family pyrin domain containing 3	Homo sapiens	114-119
24006511-4	2013	Palmitate and stearate, both SFAs, triggered IL-1beta secretion in a caspase-1/ASC/NLRP3-dependent pathway.	Palmitates	0-9	NLR family pyrin domain containing 3	Homo sapiens	83-88
24006511-4	2013	Palmitate and stearate, both SFAs, triggered IL-1beta secretion in a caspase-1/ASC/NLRP3-dependent pathway.	Stearates	14-22	NLR family pyrin domain containing 3	Homo sapiens	83-88
24006511-8	2013	These results provide a new anti-inflammatory mechanism of UFAs by preventing the activation of the NLRP3 inflammasome and, therefore, IL-1beta processing.	Fatty Acids, Unsaturated	59-63	NLR family pyrin domain containing 3	Homo sapiens	100-105
24006511-9	2013	By this way, UFAs might play a protective role in NLRP3-associated diseases.	Fatty Acids, Unsaturated	13-17	NLR family pyrin domain containing 3	Homo sapiens	50-55
24127597-4	2013	Recent studies indicate that the reactive oxygen species produced by mitochondrial respiration is critical for the activation of the NLRP3 inflammasome by monosodium urate, alum, and ATP.	Reactive Oxygen Species	33-56	NLR family pyrin domain containing 3	Homo sapiens	133-138
24127597-4	2013	Recent studies indicate that the reactive oxygen species produced by mitochondrial respiration is critical for the activation of the NLRP3 inflammasome by monosodium urate, alum, and ATP.	Uric Acid	155-171	NLR family pyrin domain containing 3	Homo sapiens	133-138
24127597-4	2013	Recent studies indicate that the reactive oxygen species produced by mitochondrial respiration is critical for the activation of the NLRP3 inflammasome by monosodium urate, alum, and ATP.	aluminum sulfate	173-177	NLR family pyrin domain containing 3	Homo sapiens	133-138
24127597-4	2013	Recent studies indicate that the reactive oxygen species produced by mitochondrial respiration is critical for the activation of the NLRP3 inflammasome by monosodium urate, alum, and ATP.	Adenosine Triphosphate	183-186	NLR family pyrin domain containing 3	Homo sapiens	133-138
24048902-2	2013	How NLRP3 senses these various stimuli is still poorly understood, but mitochondria and mitochondrial reactive oxygen species have been proposed to play a critical role in NLRP3 activation.	Reactive Oxygen Species	102-125	NLR family pyrin domain containing 3	Homo sapiens	4-9
24048902-2	2013	How NLRP3 senses these various stimuli is still poorly understood, but mitochondria and mitochondrial reactive oxygen species have been proposed to play a critical role in NLRP3 activation.	Reactive Oxygen Species	102-125	NLR family pyrin domain containing 3	Homo sapiens	172-177
24048902-7	2013	Taken together, our results suggest that MAVS facilitates the recruitment of NLRP3 to the mitochondria and may enhance its oligomerization and activation by bringing it in close proximity to mitochondrial reactive oxygen species.	Reactive Oxygen Species	205-228	NLR family pyrin domain containing 3	Homo sapiens	77-82
23794526-1	2013	Recent investigations indicate that innate immune "danger-signaling" pathways mediate metal implant debris induced-inflammatory responses, for example, NALP3 inflammasome.	Metals	86-91	NLR family pyrin domain containing 3	Homo sapiens	152-157
24008845-0	2013	Cyclic-di-GMP and cyclic-di-AMP activate the NLRP3 inflammasome.	bis(3',5')-cyclic diguanylic acid	0-13	NLR family pyrin domain containing 3	Homo sapiens	45-50
24008845-0	2013	Cyclic-di-GMP and cyclic-di-AMP activate the NLRP3 inflammasome.	cyclic diadenosine phosphate	18-31	NLR family pyrin domain containing 3	Homo sapiens	45-50
24008845-2	2013	Here, we show that physiologically relevant levels of cyclic dinucleotides also stimulate a robust secretion of IL-1beta through the NLRP3 inflammasome.	cyclic dinucleotides	54-74	NLR family pyrin domain containing 3	Homo sapiens	133-138
24008845-6	2013	Thus, cyclic dinucleotides activate the NLRP3 inflammasome through a unique pathway that could have evolved to detect pervasive bacterial pathogen-associated molecular patterns associated with intracellular infections.	cyclic dinucleotides	6-26	NLR family pyrin domain containing 3	Homo sapiens	40-45
23977231-0	2013	S100A8 and S100A9 induce cytokine expression and regulate the NLRP3 inflammasome via ROS-dependent activation of NF-kappaB(1.).	Reactive Oxygen Species	85-88	NLR family pyrin domain containing 3	Homo sapiens	62-67
23462287-7	2013	The NLRP3 expression in aorta was positively correlated with total cholesterol, low density lipoprotein cholesterol, and lipoprotein(a) (P&lt;0.05); but negatively correlated with high density lipoprotein cholesterol (P&lt;0.05).	Cholesterol	67-78	NLR family pyrin domain containing 3	Homo sapiens	4-9
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	101-124	NLR family pyrin domain containing 3	Homo sapiens	43-48
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	101-124	NLR family pyrin domain containing 3	Homo sapiens	199-204
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	126-129	NLR family pyrin domain containing 3	Homo sapiens	43-48
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	126-129	NLR family pyrin domain containing 3	Homo sapiens	199-204
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	160-163	NLR family pyrin domain containing 3	Homo sapiens	43-48
23954133-2	2013	All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation.	Reactive Oxygen Species	160-163	NLR family pyrin domain containing 3	Homo sapiens	199-204
23954133-3	2013	Here we have identified the oxazolidinone antibiotic linezolid as a Nlrp3 agonist that activates the Nlrp3 inflammasome independently of ROS.	Oxazolidinones	28-41	NLR family pyrin domain containing 3	Homo sapiens	68-73
23954133-3	2013	Here we have identified the oxazolidinone antibiotic linezolid as a Nlrp3 agonist that activates the Nlrp3 inflammasome independently of ROS.	Oxazolidinones	28-41	NLR family pyrin domain containing 3	Homo sapiens	101-106
23954133-3	2013	Here we have identified the oxazolidinone antibiotic linezolid as a Nlrp3 agonist that activates the Nlrp3 inflammasome independently of ROS.	Linezolid	53-62	NLR family pyrin domain containing 3	Homo sapiens	68-73
23954133-3	2013	Here we have identified the oxazolidinone antibiotic linezolid as a Nlrp3 agonist that activates the Nlrp3 inflammasome independently of ROS.	Linezolid	53-62	NLR family pyrin domain containing 3	Homo sapiens	101-106
23954133-4	2013	The pathways for ROS-dependent and ROS-independent Nlrp3 activation converged upon mitochondrial dysfunction and specifically the mitochondrial lipid cardiolipin.	Reactive Oxygen Species	17-20	NLR family pyrin domain containing 3	Homo sapiens	51-56
23954133-4	2013	The pathways for ROS-dependent and ROS-independent Nlrp3 activation converged upon mitochondrial dysfunction and specifically the mitochondrial lipid cardiolipin.	Reactive Oxygen Species	35-38	NLR family pyrin domain containing 3	Homo sapiens	51-56
23977231-7	2013	S100A8- and S100A9-mediated activation of NF-kappaB, the NLR family, pyrin domain-containing 3 (NLRP3) protein, and pro-IL-1beta expression was dependent on the generation of reactive oxygen species.	Reactive Oxygen Species	175-198	NLR family pyrin domain containing 3	Homo sapiens	57-94
23977231-7	2013	S100A8- and S100A9-mediated activation of NF-kappaB, the NLR family, pyrin domain-containing 3 (NLRP3) protein, and pro-IL-1beta expression was dependent on the generation of reactive oxygen species.	Reactive Oxygen Species	175-198	NLR family pyrin domain containing 3	Homo sapiens	96-101
23880858-0	2013	Resveratrol inhibits ionising irradiation-induced inflammation in MSCs by activating SIRT1 and limiting NLRP-3 inflammasome activation.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	104-110
23937860-4	2013	CONCLUSIONS: These novel data show that asbestos-induced priming and activation of the NLRP3 inflammasome triggers an autocrine feedback loop modulated via the IL-1 receptor in mesothelial cell type targeted in pleural infection, fibrosis, and carcinogenesis.	Asbestos	40-48	NLR family pyrin domain containing 3	Homo sapiens	87-92
23798679-6	2013	In addition, the extracellular overproduction of metabolites such as uric acid and cholesterol crystals acts as a signal sensed by NLRP3, leading to the production of IL-1beta.	Uric Acid	69-78	NLR family pyrin domain containing 3	Homo sapiens	131-136
23798679-6	2013	In addition, the extracellular overproduction of metabolites such as uric acid and cholesterol crystals acts as a signal sensed by NLRP3, leading to the production of IL-1beta.	Cholesterol	83-94	NLR family pyrin domain containing 3	Homo sapiens	131-136
23344781-2	2013	The identification of the role of NLRP3 inflammasome in the recognition of monosodium urate crystals and the subsequent release of IL-1beta was a milestone in the elucidation of the pathogenesis of this disorder.	Uric Acid	75-91	NLR family pyrin domain containing 3	Homo sapiens	34-39
23613465-5	2013	NLRP3 co-localises with the mitochondria, probably sensing the increase in calcium and the resultant mitochondrial dysfunction, leading to caspase activation and apoptosis.	Calcium	75-82	NLR family pyrin domain containing 3	Homo sapiens	0-5
23703389-5	2013	In this study, we established cell lines in which NLRP3 was induced by doxycycline using a tetracycline-inducible expression (Tet-on) system.	Doxycycline	71-82	NLR family pyrin domain containing 3	Homo sapiens	50-55
23809158-3	2013	(2013) suggest that omega-3 fatty acids commonly found in marine oils can suppress activation of NLRP3 and NLRP1b inflammasomes.	Fatty Acids, Omega-3	20-39	NLR family pyrin domain containing 3	Homo sapiens	97-102
23809161-3	2013	We show that NLRP3 activators including bacterial pore-forming toxins, nigericin, ATP, and particulate matter caused mitochondrial perturbation or the opening of a large membrane pore, but this was not required for NLRP3 activation.	Nigericin	71-80	NLR family pyrin domain containing 3	Homo sapiens	13-18
23809161-3	2013	We show that NLRP3 activators including bacterial pore-forming toxins, nigericin, ATP, and particulate matter caused mitochondrial perturbation or the opening of a large membrane pore, but this was not required for NLRP3 activation.	Adenosine Triphosphate	82-85	NLR family pyrin domain containing 3	Homo sapiens	13-18
23809162-0	2013	Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation.	Fatty Acids, Omega-3	0-19	NLR family pyrin domain containing 3	Homo sapiens	86-91
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Fatty Acids, Omega-3	50-61	NLR family pyrin domain containing 3	Homo sapiens	166-171
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Eicosapentaenoic Acid	73-94	NLR family pyrin domain containing 3	Homo sapiens	166-171
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Eicosapentaenoic Acid	96-99	NLR family pyrin domain containing 3	Homo sapiens	166-171
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Docosahexaenoic Acids	102-122	NLR family pyrin domain containing 3	Homo sapiens	166-171
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Docosahexaenoic Acids	124-127	NLR family pyrin domain containing 3	Homo sapiens	166-171
23809162-5	2013	Our results reveal a mechanism through which omega-3 FAs repress inflammation and prevent inflammation-driven diseases and suggest the potential clinical use of omega-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases.	Fatty Acids, Omega-3	45-56	NLR family pyrin domain containing 3	Homo sapiens	219-224
23762324-9	2013	These findings demonstrate that aPL, via TLR4 activation, induce a uric acid response in human trophoblast, which in turn activates the Nalp3/ASC inflammasome leading to IL-1beta processing and secretion.	Uric Acid	67-76	NLR family pyrin domain containing 3	Homo sapiens	136-141
23507714-12	2013	Zymosan increased NLRP3 inflammasome and interleukin-1beta expression in glomus cells (p &lt; 0.01).	Zymosan	0-7	NLR family pyrin domain containing 3	Homo sapiens	18-23
23703389-5	2013	In this study, we established cell lines in which NLRP3 was induced by doxycycline using a tetracycline-inducible expression (Tet-on) system.	Tetracycline	91-103	NLR family pyrin domain containing 3	Homo sapiens	50-55
23703389-5	2013	In this study, we established cell lines in which NLRP3 was induced by doxycycline using a tetracycline-inducible expression (Tet-on) system.	tetramethylenedisulfotetramine	126-129	NLR family pyrin domain containing 3	Homo sapiens	50-55
24376319-1	2013	BACKGROUND: Urate through Nacht Domain, Leucine-Rich Repeat, and pyrin domain-containing protein 3 (NALP3) dependent caspase-1 activation stimulates macrophages to secrete inteleukin-1beta (IL-1beta).	Uric Acid	12-17	NLR family pyrin domain containing 3	Homo sapiens	100-105
23253918-10	2013	Indeed, NLRP3 inflammasome agonists such as uric acid crystal or nigericin induce IL-1alpha cleavage and secretion, leading to the cosecretion of both IL-1beta and IL-1alpha.	Uric Acid	44-53	NLR family pyrin domain containing 3	Homo sapiens	8-13
23253918-10	2013	Indeed, NLRP3 inflammasome agonists such as uric acid crystal or nigericin induce IL-1alpha cleavage and secretion, leading to the cosecretion of both IL-1beta and IL-1alpha.	Nigericin	65-74	NLR family pyrin domain containing 3	Homo sapiens	8-13
23278511-4	2013	Intracellular ROS have been implicated in NLRP3 inflammasome-mediated IL-1beta production, therefore, we aimed to study whether RWE influences the function of NLRP3 inflammasome.	Reactive Oxygen Species	14-17	NLR family pyrin domain containing 3	Homo sapiens	42-47
23434541-3	2013	Extracellular ATP can cause P2X receptors to activate the NOD-like receptor 3 (NLRP3) inflammasome and cause IL-1beta and IL-18 maturation and release.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	58-77
23434541-3	2013	Extracellular ATP can cause P2X receptors to activate the NOD-like receptor 3 (NLRP3) inflammasome and cause IL-1beta and IL-18 maturation and release.	Adenosine Triphosphate	14-17	NLR family pyrin domain containing 3	Homo sapiens	79-84
23434541-8	2013	In vitro culture experiments showed NLRP3 protein expression, cleavage of caspase-1 and IL-1beta, and release of IL-1beta, IL-18 and ATP in HK-2 cells significantly increased after high glucose stimulation.	Glucose	186-193	NLR family pyrin domain containing 3	Homo sapiens	36-41
23434541-10	2013	The P2 receptor antagonist suramin, P2X receptor antagonist TNP-ATP, P2X4 selective antagonist 5-BDBD, and P2X4 gene silencing attenuated NLRP3 expression, cleavage of caspase-1 and IL-1beta, and release of IL-1beta and IL-18 induced by high glucose.	Suramin	27-34	NLR family pyrin domain containing 3	Homo sapiens	138-143
23434541-11	2013	Taken together, these results suggest that ATP-P2X4 signaling mediates high glucose-induced activation of the NLRP3 inflammasome, regulates IL-1 family cytokine secretion, and causes the development of tubulointerstitial inflammation in DN.	Glucose	76-83	NLR family pyrin domain containing 3	Homo sapiens	110-115
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	123-129	NLR family pyrin domain containing 3	Homo sapiens	16-21
23502856-4	2013	Inducers of the NLRP3 inflammasome caused aberrant mitochondrial homeostasis to diminish the concentration of the coenzyme NAD(+), which in turn inactivated the NAD(+)-dependent alpha-tubulin deacetylase sirtuin 2; this resulted in the accumulation of acetylated alpha-tubulin.	NAD	161-167	NLR family pyrin domain containing 3	Homo sapiens	16-21
23430110-10	2013	In addition, downregulation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, suggesting that targeting to PML could be used to treat NLRP3 inflammasome-associated diseases.	Arsenic Trioxide	38-54	NLR family pyrin domain containing 3	Homo sapiens	174-179
23430110-10	2013	In addition, downregulation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, suggesting that targeting to PML could be used to treat NLRP3 inflammasome-associated diseases.	Uric Acid	66-82	NLR family pyrin domain containing 3	Homo sapiens	174-179
23430110-10	2013	In addition, downregulation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, suggesting that targeting to PML could be used to treat NLRP3 inflammasome-associated diseases.	Uric Acid	84-87	NLR family pyrin domain containing 3	Homo sapiens	174-179
24376319-2	2013	Purinergic receptor P2X7 plays a role in the urate induced NALP3 activation.	Uric Acid	45-50	NLR family pyrin domain containing 3	Homo sapiens	59-64
23412688-5	2013	Cholesterol crystals can activate the NLRP3 inflammasome, a multimolecular signaling complex of the innate immune system, resulting in caspase-1 mediated activation and secretion of proinflammatory interleukin-1 family cytokines.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	38-43
23315075-9	2013	These findings provide new insights in lupus pathogenesis by demonstrating that self dsDNA together with its autoantibodies induces IL-1beta production from human monocytes by activating the NLRP3 inflammasome through inducing ROS synthesis and K(+) efflux, leading to the increased Th17 cell response.	Reactive Oxygen Species	227-230	NLR family pyrin domain containing 3	Homo sapiens	191-196
23402370-0	2013	Silica induces NLRP3 inflammasome activation in human lung epithelial cells.	Silicon Dioxide	0-6	NLR family pyrin domain containing 3	Homo sapiens	15-20
23402370-10	2013	CONCLUSION: Our novel data indicate the presence and functional activation of the NLRP3 inflammasome by crystalline silica in human lung epithelial cells, which prolongs an inflammatory signal and affects fibroblast proliferation, mediating a cadre of lung diseases.	Silicon Dioxide	116-122	NLR family pyrin domain containing 3	Homo sapiens	82-87
23267025-6	2013	LL-37 activation of the NLRP3 inflammasome utilizes P2X7 receptor-mediated potassium efflux.	Potassium	75-84	NLR family pyrin domain containing 3	Homo sapiens	24-29
23159926-11	2013	Notably, exogenous ATP-elicited P2X7 activation and consequent IL-1beta release, an index of direct NLRP3 inflammasome activation, were not altered by statins.	Adenosine Triphosphate	19-22	NLR family pyrin domain containing 3	Homo sapiens	100-105
23335921-9	2012	Phagocytosis of aluminum adjuvants followed by disruption of the phagolysosome activates NLRP3-inflammasomes resulting in the release of active IL-1beta and IL-18.	aluminum adjuvants	16-34	NLR family pyrin domain containing 3	Homo sapiens	89-94
23211828-14	2013	Interaction of TLR2/4 with their ligands PGN/LPS is involved in BD pathogenesis, possibly by the induction of IL-1beta through a ROS-NLRP3-dependent pathway.	Reactive Oxygen Species	129-132	NLR family pyrin domain containing 3	Homo sapiens	133-138
23147779-8	2013	A-II had higher levels of glycerophosphocholine and myo-inositol than GBM.	Glycerylphosphorylcholine	26-47	NLR family pyrin domain containing 3	Homo sapiens	0-4
23147779-8	2013	A-II had higher levels of glycerophosphocholine and myo-inositol than GBM.	Inositol	52-64	NLR family pyrin domain containing 3	Homo sapiens	0-4
23211828-0	2013	IL-1beta triggered by peptidoglycan and lipopolysaccharide through TLR2/4 and ROS-NLRP3 inflammasome-dependent pathways is involved in ocular Behcet"s disease.	Reactive Oxygen Species	78-81	NLR family pyrin domain containing 3	Homo sapiens	82-87
23633957-10	2013	HCV uptake concomitantly induces a potassium efflux that activates the NLRP3 inflammasome for IL-1beta processing and secretion.	Potassium	35-44	NLR family pyrin domain containing 3	Homo sapiens	71-76
24073415-2	2013	The consequent shortage of mevalonate-derived isoprenoid compounds results in an inflammatory phenotype, caused by the activation of the NALP3 inflammasome that determines an increased caspase-1 activation and IL-1 beta release.	Mevalonic Acid	27-37	NLR family pyrin domain containing 3	Homo sapiens	137-142
24073415-2	2013	The consequent shortage of mevalonate-derived isoprenoid compounds results in an inflammatory phenotype, caused by the activation of the NALP3 inflammasome that determines an increased caspase-1 activation and IL-1 beta release.	Terpenes	46-56	NLR family pyrin domain containing 3	Homo sapiens	137-142
23086037-7	2013	Taken together, these data suggest that NLRP3 inflammasome activation is elevated in myeloid cells from type 2 diabetic patients and that antidiabetic treatment with metformin contributes to modulation of inflammasome activation in type 2 diabetes.	Metformin	166-175	NLR family pyrin domain containing 3	Homo sapiens	40-45
23316199-0	2012	ATP release and purinergic signaling in NLRP3 inflammasome activation.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	40-45
23316199-4	2012	Importantly some studies have reported roles for extracellular ATP, in NLRP3 inflammasome activation in response to PAMPs and DAMPs.	Adenosine Triphosphate	63-66	NLR family pyrin domain containing 3	Homo sapiens	71-76
23316199-5	2012	In this mini review, we will discuss the link between active ATP release, purinergic signaling and NLRP3 inflammasome activation.	Adenosine Triphosphate	61-64	NLR family pyrin domain containing 3	Homo sapiens	99-104
23316199-6	2012	We will focus on the role of autocrine or paracrine ATP export in particle-induced NLRP3 inflammasome activation and discuss how particle activators are competent to induce maturation and secretion of IL-1beta through a process that involves, as a first event, extracellular release of endogenous ATP through hemichannel opening, and as a second event, signaling through purinergic receptors that trigger NLRP3 inflammasome activation.	Adenosine Triphosphate	52-55	NLR family pyrin domain containing 3	Homo sapiens	83-88
23316199-8	2012	In particular we will discuss how cancer cells dying via autophagy trigger ATP-dependent NLRP3 inflammasome activation in the macrophages engulfing them, eliciting an immunogenic response against tumors.	Adenosine Triphosphate	75-78	NLR family pyrin domain containing 3	Homo sapiens	89-94
23874021-7	2013	Canakinumab is a human monoclonal antibody that selectively neutralizes IL-1beta, a pro-inflammatory cytokine that plays multiple roles in the atherothrombotic process and that undergoes activation by the NLRP3 inflammasome, a process promoted by cholesterol crystals that in turn leads directly to increased production of IL-1 and IL-6.	Cholesterol	247-258	NLR family pyrin domain containing 3	Homo sapiens	205-210
23143333-0	2012	The calcium-sensing receptor regulates the NLRP3 inflammasome through Ca2+ and cAMP.	Cyclic AMP	79-83	NLR family pyrin domain containing 3	Homo sapiens	43-48
23143333-6	2012	CASR activates the NLRP3 inflammasome through phospholipase C, which catalyses inositol-1,4,5-trisphosphate production and thereby induces release of Ca(2+) from endoplasmic reticulum stores.	Inositol 1,4,5-Trisphosphate	79-107	NLR family pyrin domain containing 3	Homo sapiens	19-24
23143333-8	2012	CASR stimulation also results in reduced intracellular cAMP, which independently activates the NLRP3 inflammasome.	Cyclic AMP	55-59	NLR family pyrin domain containing 3	Homo sapiens	95-100
23143333-9	2012	cAMP binds to NLRP3 directly to inhibit inflammasome assembly, and downregulation of cAMP relieves this inhibition.	Cyclic AMP	0-4	NLR family pyrin domain containing 3	Homo sapiens	14-19
23143333-9	2012	cAMP binds to NLRP3 directly to inhibit inflammasome assembly, and downregulation of cAMP relieves this inhibition.	Cyclic AMP	85-89	NLR family pyrin domain containing 3	Homo sapiens	14-19
23143333-10	2012	The binding affinity of cAMP for CAPS-associated mutant NLRP3 is substantially lower than for wild-type NLRP3, and the uncontrolled mature IL-1beta production from CAPS patients" peripheral blood mononuclear cells is attenuated by increasing cAMP.	Cyclic AMP	24-28	NLR family pyrin domain containing 3	Homo sapiens	56-61
23143333-10	2012	The binding affinity of cAMP for CAPS-associated mutant NLRP3 is substantially lower than for wild-type NLRP3, and the uncontrolled mature IL-1beta production from CAPS patients" peripheral blood mononuclear cells is attenuated by increasing cAMP.	Cyclic AMP	24-28	NLR family pyrin domain containing 3	Homo sapiens	104-109
23143333-10	2012	The binding affinity of cAMP for CAPS-associated mutant NLRP3 is substantially lower than for wild-type NLRP3, and the uncontrolled mature IL-1beta production from CAPS patients" peripheral blood mononuclear cells is attenuated by increasing cAMP.	Cyclic AMP	242-246	NLR family pyrin domain containing 3	Homo sapiens	56-61
23143333-11	2012	Taken together, these findings indicate that Ca(2+) and cAMP are two key molecular regulators of the NLRP3 inflammasome that have critical roles in the molecular pathogenesis of CAPS.	Cyclic AMP	56-60	NLR family pyrin domain containing 3	Homo sapiens	101-106
23897115-10	2012	Increased A-II levels in the secretory phase may be responsible for endometrial growth by increasing polyamines and proline products.	Polyamines	101-111	NLR family pyrin domain containing 3	Homo sapiens	10-14
23897115-10	2012	Increased A-II levels in the secretory phase may be responsible for endometrial growth by increasing polyamines and proline products.	Proline	116-123	NLR family pyrin domain containing 3	Homo sapiens	10-14
22997256-6	2012	Activation of NLRP3 required phagocytosis of uromodulin particles into lysosomes, cathepsin leakage, oxidative stress, and potassium efflux from the cell.	Potassium	123-132	NLR family pyrin domain containing 3	Homo sapiens	14-19
23100513-0	2012	Cutting edge: nitric oxide inhibits the NLRP3 inflammasome.	Nitric Oxide	14-26	NLR family pyrin domain containing 3	Homo sapiens	40-45
23100513-4	2012	Furthermore, S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, markedly inhibited NLRP3 inflammasome activation, whereas the AIM2 and NLRC4 inflammasomes were only partially inhibited by SNAP.	S-Nitroso-N-Acetylpenicillamine	13-44	NLR family pyrin domain containing 3	Homo sapiens	85-90
23100513-4	2012	Furthermore, S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, markedly inhibited NLRP3 inflammasome activation, whereas the AIM2 and NLRC4 inflammasomes were only partially inhibited by SNAP.	S-Nitroso-N-Acetylpenicillamine	46-50	NLR family pyrin domain containing 3	Homo sapiens	85-90
23017228-2	2012	Direct treatment of THP-1 cells with Chry caused cell death, activation of caspase-1 and release of IL-1beta, while the addition of caspase-1 inhibitor, Z-YVAD-FMK, reduced IL-1beta, suggesting that Chry activated the caspase-1 mediated Nod-like receptor protein 3 (NLRP3) inflammasome; by comparison, LIB had less effects on all of these parameters.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	153-163	NLR family pyrin domain containing 3	Homo sapiens	237-264
23017228-2	2012	Direct treatment of THP-1 cells with Chry caused cell death, activation of caspase-1 and release of IL-1beta, while the addition of caspase-1 inhibitor, Z-YVAD-FMK, reduced IL-1beta, suggesting that Chry activated the caspase-1 mediated Nod-like receptor protein 3 (NLRP3) inflammasome; by comparison, LIB had less effects on all of these parameters.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	153-163	NLR family pyrin domain containing 3	Homo sapiens	266-271
23065753-5	2012	In tumour cells, AIM2 and RIG-I are required for IL-1beta induction by EBV genomic DNA and EBV-encoded small RNAs, respectively, while NLRP3 responds to extracellular ATP and reactive oxygen species.	Adenosine Triphosphate	167-170	NLR family pyrin domain containing 3	Homo sapiens	135-140
23065753-5	2012	In tumour cells, AIM2 and RIG-I are required for IL-1beta induction by EBV genomic DNA and EBV-encoded small RNAs, respectively, while NLRP3 responds to extracellular ATP and reactive oxygen species.	Reactive Oxygen Species	175-198	NLR family pyrin domain containing 3	Homo sapiens	135-140
23059822-5	2012	Interestingly, not only ATP but also ADP and UTP are involved in IL-1beta production upon these Nlrp3 inflammasome activators through multiple purinergic receptor signaling.	Adenosine Triphosphate	24-27	NLR family pyrin domain containing 3	Homo sapiens	96-101
22869553-3	2012	In this study, we used the isobaric tags for relative and absolute quantification approach to systemically analyze the interactomes of the NLRP3, AIM2, and RIG-I inflammasomes in nasopharyngeal carcinoma cells treated with specific stimuli of these interactomes (H2O2, poly (dA:dT), and EBV noncoding RNA, respectively).	Hydrogen Peroxide	263-267	NLR family pyrin domain containing 3	Homo sapiens	139-144
22869553-3	2012	In this study, we used the isobaric tags for relative and absolute quantification approach to systemically analyze the interactomes of the NLRP3, AIM2, and RIG-I inflammasomes in nasopharyngeal carcinoma cells treated with specific stimuli of these interactomes (H2O2, poly (dA:dT), and EBV noncoding RNA, respectively).	poly	269-273	NLR family pyrin domain containing 3	Homo sapiens	139-144
22869553-3	2012	In this study, we used the isobaric tags for relative and absolute quantification approach to systemically analyze the interactomes of the NLRP3, AIM2, and RIG-I inflammasomes in nasopharyngeal carcinoma cells treated with specific stimuli of these interactomes (H2O2, poly (dA:dT), and EBV noncoding RNA, respectively).	amsonic acid	275-277	NLR family pyrin domain containing 3	Homo sapiens	139-144
22869553-3	2012	In this study, we used the isobaric tags for relative and absolute quantification approach to systemically analyze the interactomes of the NLRP3, AIM2, and RIG-I inflammasomes in nasopharyngeal carcinoma cells treated with specific stimuli of these interactomes (H2O2, poly (dA:dT), and EBV noncoding RNA, respectively).	Thymidine	278-280	NLR family pyrin domain containing 3	Homo sapiens	139-144
23025327-10	2012	On the basis of our data, we propose a model in which apo A-I and apo A-II bind to DMPC via surface defects that disappear at 20 mol % FC.	Dimyristoylphosphatidylcholine	83-87	NLR family pyrin domain containing 3	Homo sapiens	70-74
23025327-11	2012	These data suggest apo A-II-containing HDL formed intrahepatically are likely cholesterol-rich compared to the smaller intracellular lipid-poor apo A-I HDL.	Cholesterol	78-89	NLR family pyrin domain containing 3	Homo sapiens	23-27
22634346-3	2012	In the case of extracellular ATP, some of the immune responses are mediated through activation of the NLRP3 inflammasome and secretion of the cytokine, interleukin-1beta (IL-1beta), through a mechanism dependent on ligation of the P2X7 receptor.	Adenosine Triphosphate	29-32	NLR family pyrin domain containing 3	Homo sapiens	102-107
22948162-3	2012	The assembly of the NLRP3 inflammasome requires a priming signal derived from pattern recognition or cytokine receptors, followed by a second signal derived from extracellular ATP, pore-forming toxins, or crystalline materials.	Adenosine Triphosphate	176-179	NLR family pyrin domain containing 3	Homo sapiens	20-25
22948162-7	2012	We further show that signaling by ATP can also induce deubiquitination of NLRP3 by a mechanism that is not sensitive to antioxidants.	Adenosine Triphosphate	34-37	NLR family pyrin domain containing 3	Homo sapiens	74-79
22948162-9	2012	Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals.	Reactive Oxygen Species	146-169	NLR family pyrin domain containing 3	Homo sapiens	26-31
22948162-9	2012	Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals.	Reactive Oxygen Species	146-169	NLR family pyrin domain containing 3	Homo sapiens	226-231
22948162-9	2012	Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals.	Adenosine Triphosphate	197-200	NLR family pyrin domain containing 3	Homo sapiens	26-31
22948162-9	2012	Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals.	Adenosine Triphosphate	197-200	NLR family pyrin domain containing 3	Homo sapiens	226-231
23059822-5	2012	Interestingly, not only ATP but also ADP and UTP are involved in IL-1beta production upon these Nlrp3 inflammasome activators through multiple purinergic receptor signaling.	Adenosine Diphosphate	37-40	NLR family pyrin domain containing 3	Homo sapiens	96-101
23059822-5	2012	Interestingly, not only ATP but also ADP and UTP are involved in IL-1beta production upon these Nlrp3 inflammasome activators through multiple purinergic receptor signaling.	Uridine Triphosphate	45-48	NLR family pyrin domain containing 3	Homo sapiens	96-101
22924492-6	2012	Hydrogen-bonding and electrostatic interactions of the silanol surfaces of fumed silica aggregates with the extracellular plasma membrane cause membrane perturbations sensed by the Nalp3 inflammasome, whose subsequent activation leads to secretion of the cytokine IL-1beta.	Hydrogen	0-8	NLR family pyrin domain containing 3	Homo sapiens	181-186
23121062-0	2012	[AII antagonists (candesartan and irbesartan) in the treatment of cardiovascular diseases].	candesartan	18-29	NLR family pyrin domain containing 3	Homo sapiens	1-4
23121062-0	2012	[AII antagonists (candesartan and irbesartan) in the treatment of cardiovascular diseases].	Irbesartan	34-44	NLR family pyrin domain containing 3	Homo sapiens	1-4
23031505-3	2012	An additional mechanism of injury related to asbestos exposure in MM development has been recently associated to inflammatory responses, principally driven by interleukin (IL)-1 beta (ss) activated within the inflammasome complex.NLRP3 inflammosome has been described as the intracellular sensor for asbestos able to induce inflammasome activation and IL-1ss secretion while NLRP1 is expressed in lung epithelial cells and alveolar macrophages and contributes to the immune response and to survival/apoptosis balance.	Asbestos	45-53	NLR family pyrin domain containing 3	Homo sapiens	230-235
23031505-4	2012	This study proposes to evaluate the impact of known NLRP3 and NLRP1 polymorphisms in the individual susceptibility to asbestos-induced mesothelioma in subjects from a hyperendemic area for MM.	Asbestos	118-126	NLR family pyrin domain containing 3	Homo sapiens	52-57
22777876-7	2012	When used as an adjuvant, CpG-chitosan induced NLRP3-dependent antigen-specific Th1 and Th17 responses.	cpg-chitosan	26-38	NLR family pyrin domain containing 3	Homo sapiens	47-52
22924492-6	2012	Hydrogen-bonding and electrostatic interactions of the silanol surfaces of fumed silica aggregates with the extracellular plasma membrane cause membrane perturbations sensed by the Nalp3 inflammasome, whose subsequent activation leads to secretion of the cytokine IL-1beta.	silanol	55-62	NLR family pyrin domain containing 3	Homo sapiens	181-186
22924492-6	2012	Hydrogen-bonding and electrostatic interactions of the silanol surfaces of fumed silica aggregates with the extracellular plasma membrane cause membrane perturbations sensed by the Nalp3 inflammasome, whose subsequent activation leads to secretion of the cytokine IL-1beta.	Silicon Dioxide	81-87	NLR family pyrin domain containing 3	Homo sapiens	181-186
22652409-1	2012	P2X7, a damage-associated molecular pattern receptor and adenosine 5"-triphosphate (ATP)-gated cation channel, plays an important role in the activation of the NALP3 inflammasome and subsequent release of interleukin (IL)-1beta from human monocytes; however its role in monocytes from other species including the dog remains poorly defined.	Adenosine Triphosphate	57-82	NLR family pyrin domain containing 3	Homo sapiens	160-165
22726397-0	2012	Monosodium urate (MSU) crystals increase gout associated coronary heart disease (CHD) risk through the activation of NLRP3 inflammasome.	Uric Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	117-122
22726397-0	2012	Monosodium urate (MSU) crystals increase gout associated coronary heart disease (CHD) risk through the activation of NLRP3 inflammasome.	Uric Acid	18-21	NLR family pyrin domain containing 3	Homo sapiens	117-122
22652409-1	2012	P2X7, a damage-associated molecular pattern receptor and adenosine 5"-triphosphate (ATP)-gated cation channel, plays an important role in the activation of the NALP3 inflammasome and subsequent release of interleukin (IL)-1beta from human monocytes; however its role in monocytes from other species including the dog remains poorly defined.	Adenosine Triphosphate	84-87	NLR family pyrin domain containing 3	Homo sapiens	160-165
22100755-0	2012	Double-walled carbon nanotubes trigger IL-1beta release in human monocytes through Nlrp3 inflammasome activation.	Carbon	14-20	NLR family pyrin domain containing 3	Homo sapiens	83-88
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Reactive Oxygen Species	98-121	NLR family pyrin domain containing 3	Homo sapiens	0-27
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Reactive Oxygen Species	98-121	NLR family pyrin domain containing 3	Homo sapiens	29-34
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Ceramides	123-132	NLR family pyrin domain containing 3	Homo sapiens	0-27
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Ceramides	123-132	NLR family pyrin domain containing 3	Homo sapiens	29-34
22798349-1	2012	Angiotensin II (A-II) regulation of aldosterone secretion is initiated by inducing cell membrane depolarization, thereby increasing intracellular calcium and activating the calcium calmodulin/calmodulin kinase cascade.	Calcium	146-153	NLR family pyrin domain containing 3	Homo sapiens	0-20
22796220-0	2012	Oxidized low-density lipoprotein induces secretion of interleukin-1beta by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation.	Reactive Oxygen Species	91-114	NLR family pyrin domain containing 3	Homo sapiens	125-130
22796220-4	2012	Here we show that the phagocytosis of ox-LDL can induce human macrophages to secrete IL-1beta by activating the NLRP3 inflammasome, and we further show that the activation of the NLRP3 inflammasome is dependent on the generation of reactive oxygen species and is related to the cathepsin B pathway.	Reactive Oxygen Species	232-255	NLR family pyrin domain containing 3	Homo sapiens	179-184
22100755-5	2012	We show that DWCNTs-induced IL-1beta secretion is exclusively linked to caspase-1 and to Nlrp3 inflammasome activation in human monocytes.	dwcnts	13-19	NLR family pyrin domain containing 3	Homo sapiens	89-94
22100755-7	2012	Moreover, inhibition of lysosomal acidification or cathepsin-B activation reduces DWCNT-induced IL-1beta secretion, suggesting that Nlrp3 inflammasome activation occurs via lysosomal destabilization.	dwcnt	82-87	NLR family pyrin domain containing 3	Homo sapiens	132-137
22100755-8	2012	Thus, DWCNTs present a health hazard due to their capacity to activate Nlrp3 inflammasome, recalling the inflammation caused by asbestos and hence demonstrating that they should be used with caution.	dwcnts	6-12	NLR family pyrin domain containing 3	Homo sapiens	71-76
22733741-0	2012	Critical role for calcium mobilization in activation of the NLRP3 inflammasome.	Calcium	18-25	NLR family pyrin domain containing 3	Homo sapiens	60-65
22661925-7	2012	Ethanol-impaired neurogenesis is associated with strong induction of IL-1beta and inflammasome proteins NALP1 and NALP3 in both neurons and astrocytes.	Ethanol	0-7	NLR family pyrin domain containing 3	Homo sapiens	114-119
22680980-3	2012	Labeled microparticles induce concentration-dependent production of IL-1beta, with inhibition by the caspase inhibitor Z-VAD-FMK supporting activation of the NLRP3-dependent inflammasome.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	119-128	NLR family pyrin domain containing 3	Homo sapiens	158-163
22870500-6	2012	The potential of colchicine as a prophylactic agent in managing recurrent attacks and the likely mechanisms of its effects on the NACHT, LRR and PYD domains-containing protein 3 (NALP-3) inflammasome of the innate immune system are highlighted.	Colchicine	17-27	NLR family pyrin domain containing 3	Homo sapiens	130-177
22623753-3	2012	The inhibition of Rac1 activation and ROS generation suppressed the activity of the Nod-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome, which resulted in attenuated EAE pathogenicity.	Reactive Oxygen Species	38-41	NLR family pyrin domain containing 3	Homo sapiens	143-148
22608202-1	2012	BACKGROUND: Monosodium urate (MSU) has been shown to promote inflammasome activation and interleukin-1beta (IL-1beta) secretion in monocyte/macrophages, but the cellular pathway and nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation in synovial tissues, remain elusive.	Uric Acid	12-28	NLR family pyrin domain containing 3	Homo sapiens	235-240
22608202-1	2012	BACKGROUND: Monosodium urate (MSU) has been shown to promote inflammasome activation and interleukin-1beta (IL-1beta) secretion in monocyte/macrophages, but the cellular pathway and nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation in synovial tissues, remain elusive.	Uric Acid	30-33	NLR family pyrin domain containing 3	Homo sapiens	235-240
22870500-6	2012	The potential of colchicine as a prophylactic agent in managing recurrent attacks and the likely mechanisms of its effects on the NACHT, LRR and PYD domains-containing protein 3 (NALP-3) inflammasome of the innate immune system are highlighted.	Colchicine	17-27	NLR family pyrin domain containing 3	Homo sapiens	179-185
22534002-3	2012	Phagocytosis of crystalline silica in the lung causes lysosomal damage, activating the NALP3 inflammasome and triggering the inflammatory cascade with subsequent fibrosis.	Silicon Dioxide	28-34	NLR family pyrin domain containing 3	Homo sapiens	87-92
22105559-0	2012	Sphingosine regulates the NLRP3-inflammasome and IL-1beta release from macrophages.	Sphingosine	0-11	NLR family pyrin domain containing 3	Homo sapiens	26-31
22342844-2	2012	NLRP3 secondary signal activators such as ATP induced mitochondrial dysfunction and apoptosis, resulting in release of oxidized mitochondrial DNA (mtDNA) into the cytosol, where it bound to and activated the NLRP3 inflammasome.	Adenosine Triphosphate	42-45	NLR family pyrin domain containing 3	Homo sapiens	0-5
22342844-2	2012	NLRP3 secondary signal activators such as ATP induced mitochondrial dysfunction and apoptosis, resulting in release of oxidized mitochondrial DNA (mtDNA) into the cytosol, where it bound to and activated the NLRP3 inflammasome.	Adenosine Triphosphate	42-45	NLR family pyrin domain containing 3	Homo sapiens	208-213
22342844-5	2012	Both binding of oxidized mtDNA to the NLRP3 inflammasome and IL-1beta secretion could be competitively inhibited by the oxidized nucleoside 8-OH-dG.	Nucleosides	129-139	NLR family pyrin domain containing 3	Homo sapiens	38-43
22342844-5	2012	Both binding of oxidized mtDNA to the NLRP3 inflammasome and IL-1beta secretion could be competitively inhibited by the oxidized nucleoside 8-OH-dG.	8-ohdg	140-147	NLR family pyrin domain containing 3	Homo sapiens	38-43
22411934-4	2012	Nod-like receptor 3 (NLRP3) can be activated by many danger signals, e.g. ROS, cathepsin B released from destabilized lysosomes and aggregated proteins, all of which evoke cellular stress and are involved in the aging process.	Reactive Oxygen Species	74-77	NLR family pyrin domain containing 3	Homo sapiens	0-19
22411934-4	2012	Nod-like receptor 3 (NLRP3) can be activated by many danger signals, e.g. ROS, cathepsin B released from destabilized lysosomes and aggregated proteins, all of which evoke cellular stress and are involved in the aging process.	Reactive Oxygen Species	74-77	NLR family pyrin domain containing 3	Homo sapiens	21-26
22105559-4	2012	Here, we show that the endogenous lipid metabolite sphingosine (Sph) acts as a DAMP by inducing the NLRP3-inflammasome-dependent secretion of IL-1beta from macrophages.	Sphingosine	51-62	NLR family pyrin domain containing 3	Homo sapiens	100-105
22105559-4	2012	Here, we show that the endogenous lipid metabolite sphingosine (Sph) acts as a DAMP by inducing the NLRP3-inflammasome-dependent secretion of IL-1beta from macrophages.	Sphingosine	64-67	NLR family pyrin domain containing 3	Homo sapiens	100-105
22105559-6	2012	IL-1beta release induced by other well-characterized NLRP3-inflammasome activators, such as ATP and uric acid crystals, in addition to NLRC4 and AIM2 inflammasome activators was also blocked by these inhibitors.	Adenosine Triphosphate	92-95	NLR family pyrin domain containing 3	Homo sapiens	53-58
22105559-6	2012	IL-1beta release induced by other well-characterized NLRP3-inflammasome activators, such as ATP and uric acid crystals, in addition to NLRC4 and AIM2 inflammasome activators was also blocked by these inhibitors.	Uric Acid	100-109	NLR family pyrin domain containing 3	Homo sapiens	53-58
22844468-4	2012	The purpose of this study is to investigate the effect of AbM water extracts on the regulation of IL-1beta production and activation of the NLRP3 inflammasome in human THP-1 macrophages.	Water	62-67	NLR family pyrin domain containing 3	Homo sapiens	140-145
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Asbestos	0-8	NLR family pyrin domain containing 3	Homo sapiens	89-94
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Asbestos	139-147	NLR family pyrin domain containing 3	Homo sapiens	89-94
22065079-8	2012	Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species.	Reactive Oxygen Species	170-193	NLR family pyrin domain containing 3	Homo sapiens	89-94
23295692-7	2012	With regard to recent findings identifying small particles such as asbestos and monosodium urate as NLRP3 activators, TiO(2) may be another potential target for inflammasome studies.	Uric Acid	80-96	NLR family pyrin domain containing 3	Homo sapiens	100-105
23295692-8	2012	We found that macrophage-like cells readily take up TiO(2) after 6 h. Incubation of cells with TiO(2) resulted in the assembly of NLRP3 with caspase-1.	titanium dioxide	52-58	NLR family pyrin domain containing 3	Homo sapiens	130-135
23295692-8	2012	We found that macrophage-like cells readily take up TiO(2) after 6 h. Incubation of cells with TiO(2) resulted in the assembly of NLRP3 with caspase-1.	titanium dioxide	95-101	NLR family pyrin domain containing 3	Homo sapiens	130-135
23226314-1	2012	INTRODUCTION: Uric acid released from injured tissue is considered a major endogenous danger signal and local instillation of uric acid crystals induces acute lung inflammation via activation of the NLRP3 inflammasome.	Uric Acid	14-23	NLR family pyrin domain containing 3	Homo sapiens	199-204
23226314-1	2012	INTRODUCTION: Uric acid released from injured tissue is considered a major endogenous danger signal and local instillation of uric acid crystals induces acute lung inflammation via activation of the NLRP3 inflammasome.	Uric Acid	126-135	NLR family pyrin domain containing 3	Homo sapiens	199-204
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Cholesterol	82-93	NLR family pyrin domain containing 3	Homo sapiens	159-164
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Fc(alpha) receptor	95-97	NLR family pyrin domain containing 3	Homo sapiens	159-164
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Ceramides	103-112	NLR family pyrin domain containing 3	Homo sapiens	159-164
22123977-0	2011	Basic calcium phosphate crystals induce NLRP3 inflammasome activation: the in vitro and in vivo face to face.	basic calcium phosphate	0-23	NLR family pyrin domain containing 3	Homo sapiens	40-45
22111911-0	2011	Amino-functionalized polystyrene nanoparticles activate the NLRP3 inflammasome in human macrophages.	Polystyrenes	21-32	NLR family pyrin domain containing 3	Homo sapiens	60-65
22111911-3	2011	Here we demonstrate that amino-functionalized polystyrene nanoparticles (PS-NH(2)) of ~100 nm in diameter, but not carboxyl- or nonfunctionalized particles, trigger NLRP3 inflammasome activation and subsequent release of proinflammatory interleukin 1beta (IL-1beta) by human macrophages.	Polystyrenes	46-57	NLR family pyrin domain containing 3	Homo sapiens	165-170
22768094-7	2012	The inhibition of pro-IL-1beta production and suppression of NLRP3 inflammasome activation by IFNbeta-primed human CD4+CD45RO+ memory T-cells is partly mediated by soluble FasL and is associated with down-regulated P2X7R mRNA expression and reduced response to ATP in monocytes.	Adenosine Triphosphate	261-264	NLR family pyrin domain containing 3	Homo sapiens	61-66
21880711-9	2011	The most interesting aspect of the structure was the unexpected disulfide bond between Cys-8 and Cys-108, which might be important for regulation of the activity of NALP3 by redox potential.	Cysteine	97-100	NLR family pyrin domain containing 3	Homo sapiens	165-170
21957307-6	2011	Activation of the NLRP3 inflammasome and secretion of IL-1beta was also dependent on the release of cathepsin B and production of reactive oxygen species (ROS).	Reactive Oxygen Species	130-153	NLR family pyrin domain containing 3	Homo sapiens	18-23
21957307-6	2011	Activation of the NLRP3 inflammasome and secretion of IL-1beta was also dependent on the release of cathepsin B and production of reactive oxygen species (ROS).	Reactive Oxygen Species	155-158	NLR family pyrin domain containing 3	Homo sapiens	18-23
22003197-0	2011	The NLRP3 inflammasome contributes to brain injury in pneumococcal meningitis and is activated through ATP-dependent lysosomal cathepsin B release.	Adenosine Triphosphate	103-106	NLR family pyrin domain containing 3	Homo sapiens	4-9
21930705-9	2011	In addition, inhibitors of reactive oxygen species, cathepsin B, and K(+) efflux pathways, known to specifically influence NLRP3, substantially but not completely impair the Francisella-elicited IL-1beta response, suggesting the involvement of another inflammasome pathway.	Reactive Oxygen Species	27-50	NLR family pyrin domain containing 3	Homo sapiens	123-128
21880711-9	2011	The most interesting aspect of the structure was the unexpected disulfide bond between Cys-8 and Cys-108, which might be important for regulation of the activity of NALP3 by redox potential.	Disulfides	64-73	NLR family pyrin domain containing 3	Homo sapiens	165-170
22102247-4	2011	In this study, human NALP3 PYD, corresponding to amino acids 3-110, was overexpressed in Escherichia coli using engineered C-terminal His tags.	Histidine	134-137	NLR family pyrin domain containing 3	Homo sapiens	21-26
21880711-9	2011	The most interesting aspect of the structure was the unexpected disulfide bond between Cys-8 and Cys-108, which might be important for regulation of the activity of NALP3 by redox potential.	Cysteine	87-90	NLR family pyrin domain containing 3	Homo sapiens	165-170
21940629-5	2011	The glucocorticoid-dependent induction of NLRP3 sensitizes the cells to extracellular ATP and significantly enhances the ATP-mediated release of proinflammatory molecules, including mature IL-1beta, TNF-alpha, and IL-6.	Adenosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	42-47
21940629-5	2011	The glucocorticoid-dependent induction of NLRP3 sensitizes the cells to extracellular ATP and significantly enhances the ATP-mediated release of proinflammatory molecules, including mature IL-1beta, TNF-alpha, and IL-6.	Adenosine Triphosphate	121-124	NLR family pyrin domain containing 3	Homo sapiens	42-47
21940680-6	2011	In turn, reactive oxygen species derived from NAD(P)H oxidase promote the association of thioredoxin-interacting protein with the nucleotide-binding oligomerization domain-like receptor protein NLRP3 and subsequently induce inflammasome activation and IL-1beta secretion from the EC.	Reactive Oxygen Species	9-32	NLR family pyrin domain containing 3	Homo sapiens	194-199
21862613-3	2011	Our previous studies demonstrated that the ceramides activate the Nod-like receptor family, pyrin domain containing 3 (Nlrp3) inflammasome to cause the generation of mature IL-1beta and ablation of the Nlrp3 inflammasome in diet-induced obesity improves insulin signaling.	Ceramides	43-52	NLR family pyrin domain containing 3	Homo sapiens	119-124
21862613-3	2011	Our previous studies demonstrated that the ceramides activate the Nod-like receptor family, pyrin domain containing 3 (Nlrp3) inflammasome to cause the generation of mature IL-1beta and ablation of the Nlrp3 inflammasome in diet-induced obesity improves insulin signaling.	Ceramides	43-52	NLR family pyrin domain containing 3	Homo sapiens	202-207
21800904-0	2011	Long, needle-like carbon nanotubes and asbestos activate the NLRP3 inflammasome through a similar mechanism.	Carbon	18-24	NLR family pyrin domain containing 3	Homo sapiens	61-66
21800904-8	2011	Moreover, it was noted that CNT-induced NLRP3 inflammasome activation depended on reactive oxygen species (ROS) production, cathepsin B activity, P2X(7) receptor, and Src and Syk tyrosine kinases.	Reactive Oxygen Species	82-105	NLR family pyrin domain containing 3	Homo sapiens	40-45
21800904-8	2011	Moreover, it was noted that CNT-induced NLRP3 inflammasome activation depended on reactive oxygen species (ROS) production, cathepsin B activity, P2X(7) receptor, and Src and Syk tyrosine kinases.	Reactive Oxygen Species	107-110	NLR family pyrin domain containing 3	Homo sapiens	40-45
21352397-3	2011	Uric acid, or monosodium urate (MSU), activates the Nod-like receptor, Nalp3, leading to inflammasome activation and IL-1beta processing.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	71-76
21573893-6	2011	Besides ATP, uric acid or soluble extracellular matrix components are functional danger signals that activate the NLRP3 inflammasome when released from dying cells or from extracellular matrix.	Adenosine Triphosphate	8-11	NLR family pyrin domain containing 3	Homo sapiens	114-119
21573893-6	2011	Besides ATP, uric acid or soluble extracellular matrix components are functional danger signals that activate the NLRP3 inflammasome when released from dying cells or from extracellular matrix.	Uric Acid	13-22	NLR family pyrin domain containing 3	Homo sapiens	114-119
21677136-0	2011	Cutting edge: reactive oxygen species inhibitors block priming, but not activation, of the NLRP3 inflammasome.	Reactive Oxygen Species	14-37	NLR family pyrin domain containing 3	Homo sapiens	91-96
21677136-2	2011	Recently, production of reactive oxygen species (ROS) has been suggested to act as a common event upstream of the NLRP3 inflammasome machinery.	Reactive Oxygen Species	24-47	NLR family pyrin domain containing 3	Homo sapiens	114-119
21677136-2	2011	Recently, production of reactive oxygen species (ROS) has been suggested to act as a common event upstream of the NLRP3 inflammasome machinery.	Reactive Oxygen Species	49-52	NLR family pyrin domain containing 3	Homo sapiens	114-119
21677136-4	2011	Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors.	Reactive Oxygen Species	119-122	NLR family pyrin domain containing 3	Homo sapiens	25-30
21677136-4	2011	Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors.	Reactive Oxygen Species	119-122	NLR family pyrin domain containing 3	Homo sapiens	203-208
21677136-4	2011	Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors.	Reactive Oxygen Species	290-293	NLR family pyrin domain containing 3	Homo sapiens	25-30
21677136-4	2011	Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors.	Reactive Oxygen Species	290-293	NLR family pyrin domain containing 3	Homo sapiens	203-208
21677136-5	2011	Although these data do not exclude a general role for ROS production in the process of NLRP3-triggered inflammation, they would put ROS upstream of NLRP3 induction, but not activation.	Reactive Oxygen Species	132-135	NLR family pyrin domain containing 3	Homo sapiens	148-153
21936977-2	2011	Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ss-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes.	Uric Acid	70-75	NLR family pyrin domain containing 3	Homo sapiens	203-209
21936977-2	2011	Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ss-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes.	Cholesterol	81-92	NLR family pyrin domain containing 3	Homo sapiens	203-209
21936977-2	2011	Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ss-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes.	Silicon Dioxide	103-109	NLR family pyrin domain containing 3	Homo sapiens	203-209
21621776-1	2011	OBJECTIVE: Cholesterol crystals have been shown to cause inflammation, and ultimately atherosclerotic lesions through the activation of the NLRP3 inflammasome.	Cholesterol	11-22	NLR family pyrin domain containing 3	Homo sapiens	140-145
21621776-2	2011	As cholesterol crystals have also been found in the walls of patients with abdominal aortic aneurysms (AAA), it is possible that the NLRP3 inflammasome is involved in AAA and genetic variability within this protein complex could alter disease risk.	Cholesterol	3-14	NLR family pyrin domain containing 3	Homo sapiens	133-138
21352397-3	2011	Uric acid, or monosodium urate (MSU), activates the Nod-like receptor, Nalp3, leading to inflammasome activation and IL-1beta processing.	Uric Acid	14-30	NLR family pyrin domain containing 3	Homo sapiens	71-76
21352397-3	2011	Uric acid, or monosodium urate (MSU), activates the Nod-like receptor, Nalp3, leading to inflammasome activation and IL-1beta processing.	Uric Acid	32-35	NLR family pyrin domain containing 3	Homo sapiens	71-76
21438869-7	2011	NACHT-LRR-PYD-containing protein 3 (NLRP3) activation using MurNAc-L-Ala-D-isoGln (MDP) resulted in increased CD64 expression on PMNs from healthy subjects.	Acetylmuramyl-Alanyl-Isoglutamine	60-81	NLR family pyrin domain containing 3	Homo sapiens	0-34
21438869-7	2011	NACHT-LRR-PYD-containing protein 3 (NLRP3) activation using MurNAc-L-Ala-D-isoGln (MDP) resulted in increased CD64 expression on PMNs from healthy subjects.	Acetylmuramyl-Alanyl-Isoglutamine	60-81	NLR family pyrin domain containing 3	Homo sapiens	36-41
21540455-9	2011	In addition, we elucidated the contributions of MyD88 and TRIF to priming of the NLRP3 inflammasome and demonstrated that TRIF-biased TLR4 activation by MLA was responsible for the defective production of mature IL-1beta.	monophosphoryl lipid A	153-156	NLR family pyrin domain containing 3	Homo sapiens	81-86
21622280-5	2011	Increased extracellular ATP levels amplify inflammation in vivo by promoting leukocyte recruitment and NALP3-inflammasome activation via P2X7.	Adenosine Triphosphate	24-27	NLR family pyrin domain containing 3	Homo sapiens	103-108
21469090-3	2011	These bacterial molecules are detected by nucleotide oligomerization domain 1 (Nod1) and Nod2, and recent evidence suggests that muramyl dipeptide also activates NLRP3 and NLRP1 inflammasomes.	Dipeptides	137-146	NLR family pyrin domain containing 3	Homo sapiens	162-167
21234729-6	2011	Uric acid crystals also have been shown to trigger interleukin-1beta-mediated inflammation via activation of the NOD-like receptor protein (NLRP)3 inflammasome, a multimolecular complex whose activation appears to be central to many pathological inflammatory conditions.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	140-146
21478880-0	2011	Fatty acid-induced NLRP3-ASC inflammasome activation interferes with insulin signaling.	Fatty Acids	0-10	NLR family pyrin domain containing 3	Homo sapiens	19-24
21478880-3	2011	We show that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1beta and IL-18 production.	saturated fatty acid palmitate	17-47	NLR family pyrin domain containing 3	Homo sapiens	107-112
21511178-4	2011	(2011) identify NLRP3 inflammasome-independent signaling to be crucial for the Th2 cell response induced by aluminum salts.	Aluminum	108-116	NLR family pyrin domain containing 3	Homo sapiens	16-21
21428959-4	2011	The discovery that NLRP3 (NLR-related protein 3) can recognize host-derived particulate matter such as uric acid and cholesterol crystals has led to this inflammasome being implicated in a number of inflammatory diseases, including gout, atherosclerosis and Type 2 diabetes.	Uric Acid	103-112	NLR family pyrin domain containing 3	Homo sapiens	19-24
21428959-4	2011	The discovery that NLRP3 (NLR-related protein 3) can recognize host-derived particulate matter such as uric acid and cholesterol crystals has led to this inflammasome being implicated in a number of inflammatory diseases, including gout, atherosclerosis and Type 2 diabetes.	Uric Acid	103-112	NLR family pyrin domain containing 3	Homo sapiens	26-47
21428959-4	2011	The discovery that NLRP3 (NLR-related protein 3) can recognize host-derived particulate matter such as uric acid and cholesterol crystals has led to this inflammasome being implicated in a number of inflammatory diseases, including gout, atherosclerosis and Type 2 diabetes.	Cholesterol	117-128	NLR family pyrin domain containing 3	Homo sapiens	19-24
21428959-4	2011	The discovery that NLRP3 (NLR-related protein 3) can recognize host-derived particulate matter such as uric acid and cholesterol crystals has led to this inflammasome being implicated in a number of inflammatory diseases, including gout, atherosclerosis and Type 2 diabetes.	Cholesterol	117-128	NLR family pyrin domain containing 3	Homo sapiens	26-47
21282379-1	2011	Reactive oxygen species (ROS) have an established role in inflammation and host defense, as they kill intracellular bacteria and have been shown to activate the NLRP3 inflammasome.	Reactive Oxygen Species	0-23	NLR family pyrin domain containing 3	Homo sapiens	161-166
21282379-1	2011	Reactive oxygen species (ROS) have an established role in inflammation and host defense, as they kill intracellular bacteria and have been shown to activate the NLRP3 inflammasome.	Reactive Oxygen Species	25-28	NLR family pyrin domain containing 3	Homo sapiens	161-166
21239716-0	2011	Basic calcium phosphate crystals induce monocyte/macrophage IL-1beta secretion through the NLRP3 inflammasome in vitro.	basic calcium phosphate	0-23	NLR family pyrin domain containing 3	Homo sapiens	91-96
21239716-8	2011	Collectively, these results demonstrate that BCP crystals induce IL-1beta secretion through activating the NLRP3 inflammasome.	bcp	45-48	NLR family pyrin domain containing 3	Homo sapiens	107-112
21124315-2	2011	Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle.	Reactive Oxygen Species	125-148	NLR family pyrin domain containing 3	Homo sapiens	32-37
21257004-0	2011	Comparison of high-density lipoprotein cholesterol to apolipoprotein A-I and A-II to predict coronary calcium and the effect of insulin resistance.	Calcium	102-109	NLR family pyrin domain containing 3	Homo sapiens	77-81
21245324-1	2011	Uric acid (UA) is known to activate the NLRP3 (Nacht, leucine-rich repeat and pyrin domain containing protein 3) inflammasome.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	40-45
21245324-1	2011	Uric acid (UA) is known to activate the NLRP3 (Nacht, leucine-rich repeat and pyrin domain containing protein 3) inflammasome.	Uric Acid	11-13	NLR family pyrin domain containing 3	Homo sapiens	40-45
21124315-2	2011	Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle.	Reactive Oxygen Species	150-153	NLR family pyrin domain containing 3	Homo sapiens	32-37
21124315-3	2011	Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome.	Reactive Oxygen Species	85-88	NLR family pyrin domain containing 3	Homo sapiens	145-150
21596183-2	2011	Cryopyrin recruits different adaptor and effectors proteins into a cytosolic macromolecular complex termed Nalp3-inflammasome, which senses both several pathogen-associated and damage-associated molecular patterns as well as inorganic particles (asbestos, silica), and triggers innate immune and inflammatory responses.	Asbestos	246-254	NLR family pyrin domain containing 3	Homo sapiens	0-9
21051542-0	2011	Sodium overload and water influx activate the NALP3 inflammasome.	Sodium	0-6	NLR family pyrin domain containing 3	Homo sapiens	46-51
21051542-0	2011	Sodium overload and water influx activate the NALP3 inflammasome.	Water	20-25	NLR family pyrin domain containing 3	Homo sapiens	46-51
21051542-1	2011	The NALP3 inflammasome is activated by low intracellular potassium concentrations [K(+)](i), leading to the secretion of the proinflammatory cytokine IL-1beta.	Potassium	57-66	NLR family pyrin domain containing 3	Homo sapiens	4-9
20632067-4	2011	XOD produces uric acid and reactive oxygen species, which could activate Nalp3 and therefore induce activation of caspase 1, known to convert inactive pro-IL-1beta into active IL-1beta.	Uric Acid	13-22	NLR family pyrin domain containing 3	Homo sapiens	73-78
20632067-4	2011	XOD produces uric acid and reactive oxygen species, which could activate Nalp3 and therefore induce activation of caspase 1, known to convert inactive pro-IL-1beta into active IL-1beta.	Reactive Oxygen Species	27-50	NLR family pyrin domain containing 3	Homo sapiens	73-78
21596183-2	2011	Cryopyrin recruits different adaptor and effectors proteins into a cytosolic macromolecular complex termed Nalp3-inflammasome, which senses both several pathogen-associated and damage-associated molecular patterns as well as inorganic particles (asbestos, silica), and triggers innate immune and inflammatory responses.	Asbestos	246-254	NLR family pyrin domain containing 3	Homo sapiens	107-112
21596183-2	2011	Cryopyrin recruits different adaptor and effectors proteins into a cytosolic macromolecular complex termed Nalp3-inflammasome, which senses both several pathogen-associated and damage-associated molecular patterns as well as inorganic particles (asbestos, silica), and triggers innate immune and inflammatory responses.	Silicon Dioxide	256-262	NLR family pyrin domain containing 3	Homo sapiens	0-9
21596183-2	2011	Cryopyrin recruits different adaptor and effectors proteins into a cytosolic macromolecular complex termed Nalp3-inflammasome, which senses both several pathogen-associated and damage-associated molecular patterns as well as inorganic particles (asbestos, silica), and triggers innate immune and inflammatory responses.	Silicon Dioxide	256-262	NLR family pyrin domain containing 3	Homo sapiens	107-112
20974980-5	2010	Unlike other particulate Nlrp3 agonists, nano-TiO(2)-dependent-Nlrp3 activity does not require cytoskeleton-dependent phagocytosis and induces IL-1alpha/beta secretion in nonphagocytic keratinocytes.	titanium dioxide	46-52	NLR family pyrin domain containing 3	Homo sapiens	25-30
20971108-0	2010	Activation of the NLRP3 inflammasome by intracellular poly I:C.	Poly I	54-60	NLR family pyrin domain containing 3	Homo sapiens	18-23
20971108-0	2010	Activation of the NLRP3 inflammasome by intracellular poly I:C.	Carbon	61-62	NLR family pyrin domain containing 3	Homo sapiens	18-23
20971108-3	2010	We show here that transfection of the dsRNA analogue poly I:C activates the NLRP3 inflammasome via a pathway requiring endosomal acidification.	Poly I-C	53-61	NLR family pyrin domain containing 3	Homo sapiens	76-81
20974980-5	2010	Unlike other particulate Nlrp3 agonists, nano-TiO(2)-dependent-Nlrp3 activity does not require cytoskeleton-dependent phagocytosis and induces IL-1alpha/beta secretion in nonphagocytic keratinocytes.	titanium dioxide	46-52	NLR family pyrin domain containing 3	Homo sapiens	63-68
20872576-4	2010	Here we showed that titanium particles stimulate the NALP3 inflammasome.	Titanium	20-28	NLR family pyrin domain containing 3	Homo sapiens	53-58
20872576-9	2010	Together, these results suggest that titanium particle-induced acute inflammation is due to activation of the NALP3 inflammasome, which leads to increased IL-1beta secretion and IL-1-associated signaling, including neutrophil recruitment.	Titanium	37-45	NLR family pyrin domain containing 3	Homo sapiens	110-115
20947763-3	2010	Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids.	Adenosine Triphosphate	0-22	NLR family pyrin domain containing 3	Homo sapiens	66-71
20661219-2	2010	Through the activation of P2X and P2Y receptors, extracellular ATP enhances tissue repair, promotes the recruitment of immune phagocytes and dendritic cells, and acts as a co-activator of NLR family, pyrin domain-containing 3 (NLRP3) inflammasomes.	Adenosine Triphosphate	63-66	NLR family pyrin domain containing 3	Homo sapiens	188-225
21126439-0	2010	[Progress in research on role of inflammasome Nalp3 in silica dusts induced body injuries].	Silicon Dioxide	55-61	NLR family pyrin domain containing 3	Homo sapiens	46-51
20661219-2	2010	Through the activation of P2X and P2Y receptors, extracellular ATP enhances tissue repair, promotes the recruitment of immune phagocytes and dendritic cells, and acts as a co-activator of NLR family, pyrin domain-containing 3 (NLRP3) inflammasomes.	Adenosine Triphosphate	63-66	NLR family pyrin domain containing 3	Homo sapiens	227-232
20407038-3	2010	The precise mode of activation of the NLRP3 inflammasome is still elusive, but has been postulated to be mediated by reactive oxygen species (ROS) generated by an NADPH oxidase.	Reactive Oxygen Species	142-145	NLR family pyrin domain containing 3	Homo sapiens	38-43
20561679-0	2010	The effect of surface modification of amorphous silica particles on NLRP3 inflammasome mediated IL-1beta production, ROS production and endosomal rupture.	Silicon Dioxide	48-54	NLR family pyrin domain containing 3	Homo sapiens	68-73
20561679-0	2010	The effect of surface modification of amorphous silica particles on NLRP3 inflammasome mediated IL-1beta production, ROS production and endosomal rupture.	Reactive Oxygen Species	117-120	NLR family pyrin domain containing 3	Homo sapiens	68-73
20561679-7	2010	Our results reveal a part of NLRP3 activation pathway and provide basic information that should help to create safe and effective forms of SPs.	Silicon Dioxide	139-142	NLR family pyrin domain containing 3	Homo sapiens	29-34
20502971-2	2010	Uric acid crystals, first sensed extracellularly by membrane lipid alterations, are internalized and subsequently activate the NLRP3 inflammasome.	Uric Acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	127-132
20668705-0	2010	Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	34-39
20668705-0	2010	Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation.	Cholesterol	96-107	NLR family pyrin domain containing 3	Homo sapiens	34-39
20668705-8	2010	Silencing of the NLRP3 receptor, the crucial component in NLRP3 inflammasome, completely abolished crystal-induced IL-1beta secretion, thus identifying NLRP3 inflammasome as the cholesterol crystal-responsive element in macrophages.	Cholesterol	178-189	NLR family pyrin domain containing 3	Homo sapiens	17-22
20668705-8	2010	Silencing of the NLRP3 receptor, the crucial component in NLRP3 inflammasome, completely abolished crystal-induced IL-1beta secretion, thus identifying NLRP3 inflammasome as the cholesterol crystal-responsive element in macrophages.	Cholesterol	178-189	NLR family pyrin domain containing 3	Homo sapiens	58-63
20668705-8	2010	Silencing of the NLRP3 receptor, the crucial component in NLRP3 inflammasome, completely abolished crystal-induced IL-1beta secretion, thus identifying NLRP3 inflammasome as the cholesterol crystal-responsive element in macrophages.	Cholesterol	178-189	NLR family pyrin domain containing 3	Homo sapiens	58-63
20668705-9	2010	The crystals were shown to induce leakage of the lysosomal protease cathepsin B into the cytoplasm and inhibition of this enzyme reduced cholesterol crystal-induced IL-1beta secretion, suggesting that NLRP3 inflammasome activation occurred via lysosomal destabilization.	Cholesterol	137-148	NLR family pyrin domain containing 3	Homo sapiens	201-206
20407038-3	2010	The precise mode of activation of the NLRP3 inflammasome is still elusive, but has been postulated to be mediated by reactive oxygen species (ROS) generated by an NADPH oxidase.	Reactive Oxygen Species	117-140	NLR family pyrin domain containing 3	Homo sapiens	38-43
20179743-0	2010	The inhibition of mevalonate pathway induces upregulation of NALP3 expression: new insight in the pathogenesis of mevalonate kinase deficiency.	Mevalonic Acid	18-28	NLR family pyrin domain containing 3	Homo sapiens	61-66
20421639-10	2010	Furthermore, our results suggest that the lysosomal cathepsin B protease, the formation of reactive oxygen species, and the efflux of potassium are needed for beta-glucan-induced NLRP3 inflammasome activation.	Potassium	134-143	NLR family pyrin domain containing 3	Homo sapiens	179-184
20179743-5	2010	In healthy subjects, alendronate alone induced the expression of NALP1 and NALP3, and then together with LPS it induced a dramatic increase in NALP3 expression.	Alendronate	21-32	NLR family pyrin domain containing 3	Homo sapiens	75-80
20179743-5	2010	In healthy subjects, alendronate alone induced the expression of NALP1 and NALP3, and then together with LPS it induced a dramatic increase in NALP3 expression.	Alendronate	21-32	NLR family pyrin domain containing 3	Homo sapiens	143-148
20179743-7	2010	Our results, although preliminary, showed that the inhibition of the mevalonate pathway led to a hyper-expression of NALP3, suggesting a possible involvement of NALP3-inflammasome in the activation of caspase-1 consequent to GGPP decrement.	Mevalonic Acid	69-79	NLR family pyrin domain containing 3	Homo sapiens	117-122
20179743-7	2010	Our results, although preliminary, showed that the inhibition of the mevalonate pathway led to a hyper-expression of NALP3, suggesting a possible involvement of NALP3-inflammasome in the activation of caspase-1 consequent to GGPP decrement.	Mevalonic Acid	69-79	NLR family pyrin domain containing 3	Homo sapiens	161-166
20537229-5	2010	The principal VCD transitions in the NIR region are two combination bands, the amide A-II and B-II bands, of the amide A and B fundamentals with the amide II fundamental, and the second overtone of the amide II, referred to as the amide 3 x II band.	Amides	113-118	NLR family pyrin domain containing 3	Homo sapiens	85-98
20537229-5	2010	The principal VCD transitions in the NIR region are two combination bands, the amide A-II and B-II bands, of the amide A and B fundamentals with the amide II fundamental, and the second overtone of the amide II, referred to as the amide 3 x II band.	Amides	113-118	NLR family pyrin domain containing 3	Homo sapiens	85-98
20537229-5	2010	The principal VCD transitions in the NIR region are two combination bands, the amide A-II and B-II bands, of the amide A and B fundamentals with the amide II fundamental, and the second overtone of the amide II, referred to as the amide 3 x II band.	Amides	113-118	NLR family pyrin domain containing 3	Homo sapiens	85-98
20537229-5	2010	The principal VCD transitions in the NIR region are two combination bands, the amide A-II and B-II bands, of the amide A and B fundamentals with the amide II fundamental, and the second overtone of the amide II, referred to as the amide 3 x II band.	Amides	113-118	NLR family pyrin domain containing 3	Homo sapiens	85-98
20421639-0	2010	(1,3)-beta-glucans activate both dectin-1 and NLRP3 inflammasome in human macrophages.	beta-1,3-glucan	0-18	NLR family pyrin domain containing 3	Homo sapiens	46-51
20421639-8	2010	RNA interference-mediated gene knockdown experiments demonstrated that cytoplasmic NLRP3 inflammasome is essential for beta-glucan-induced IL-1beta secretion.	beta-Glucans	119-130	NLR family pyrin domain containing 3	Homo sapiens	83-88
20421639-9	2010	Moreover, our results suggest that beta-glucan-induced NLRP3 inflammasome activation is dependent on the dectin-1/Syk signaling pathway.	beta-Glucans	35-46	NLR family pyrin domain containing 3	Homo sapiens	55-60
20421639-10	2010	Furthermore, our results suggest that the lysosomal cathepsin B protease, the formation of reactive oxygen species, and the efflux of potassium are needed for beta-glucan-induced NLRP3 inflammasome activation.	Reactive Oxygen Species	91-114	NLR family pyrin domain containing 3	Homo sapiens	179-184
20421639-10	2010	Furthermore, our results suggest that the lysosomal cathepsin B protease, the formation of reactive oxygen species, and the efflux of potassium are needed for beta-glucan-induced NLRP3 inflammasome activation.	beta-Glucans	159-170	NLR family pyrin domain containing 3	Homo sapiens	179-184
20421639-11	2010	In conclusion, our results show that beta-glucans are recognized by membrane-associated dectin-1 and cytoplasmic NLRP3 inflammasome resulting in IL-1beta gene transcription and IL-1beta secretion in human macrophages, respectively.	beta-Glucans	37-49	NLR family pyrin domain containing 3	Homo sapiens	113-118
20093358-5	2010	Additional investigations of other NF-kappaB inhibitors revealed that the synthetic I kappaB kinase-beta inhibitor Bay 11-7082 and structurally related vinyl sulfone compounds selectively inhibit NLRP3 inflammasome activity in macrophages independent of their inhibitory effect on NF-kappaB activity.	3-(4-methylphenylsulfonyl)-2-propenenitrile	115-126	NLR family pyrin domain containing 3	Homo sapiens	196-201
20368800-0	2010	Aspergillus fumigatus stimulates the NLRP3 inflammasome through a pathway requiring ROS production and the Syk tyrosine kinase.	ros	84-87	NLR family pyrin domain containing 3	Homo sapiens	37-42
20368800-6	2010	The ability of Aspergillus hyphae to activate the NLRP3 inflammasome in the monocytes requires K(+) efflux and ROS production.	ros	111-114	NLR family pyrin domain containing 3	Homo sapiens	50-55
20093358-5	2010	Additional investigations of other NF-kappaB inhibitors revealed that the synthetic I kappaB kinase-beta inhibitor Bay 11-7082 and structurally related vinyl sulfone compounds selectively inhibit NLRP3 inflammasome activity in macrophages independent of their inhibitory effect on NF-kappaB activity.	Polyvinyl Chloride	152-157	NLR family pyrin domain containing 3	Homo sapiens	196-201
20093358-5	2010	Additional investigations of other NF-kappaB inhibitors revealed that the synthetic I kappaB kinase-beta inhibitor Bay 11-7082 and structurally related vinyl sulfone compounds selectively inhibit NLRP3 inflammasome activity in macrophages independent of their inhibitory effect on NF-kappaB activity.	Sulfones	158-165	NLR family pyrin domain containing 3	Homo sapiens	196-201
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	parthenolide	33-45	NLR family pyrin domain containing 3	Homo sapiens	88-93
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	parthenolide	33-45	NLR family pyrin domain containing 3	Homo sapiens	158-163
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	parthenolide	33-45	NLR family pyrin domain containing 3	Homo sapiens	158-163
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	3-(4-methylphenylsulfonyl)-2-propenenitrile	50-61	NLR family pyrin domain containing 3	Homo sapiens	88-93
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	3-(4-methylphenylsulfonyl)-2-propenenitrile	50-61	NLR family pyrin domain containing 3	Homo sapiens	158-163
20093358-6	2010	In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3.	3-(4-methylphenylsulfonyl)-2-propenenitrile	50-61	NLR family pyrin domain containing 3	Homo sapiens	158-163
20093358-7	2010	Our results thus elucidate the molecular mechanism for the therapeutic anti-inflammatory activity of parthenolide and identify vinyl sulfones as a new class of potential therapeutics that target the NLRP3 inflammasome.	parthenolide	101-113	NLR family pyrin domain containing 3	Homo sapiens	199-204
20093358-7	2010	Our results thus elucidate the molecular mechanism for the therapeutic anti-inflammatory activity of parthenolide and identify vinyl sulfones as a new class of potential therapeutics that target the NLRP3 inflammasome.	divinyl sulfone	127-141	NLR family pyrin domain containing 3	Homo sapiens	199-204
20201014-4	2010	Recent findings suggest that ROS are produced by NLRP3/NALP3 activators and are essential secondary messengers signaling NLRP3/NALP3 inflammasome activation.	ros	29-32	NLR family pyrin domain containing 3	Homo sapiens	49-54
20201014-4	2010	Recent findings suggest that ROS are produced by NLRP3/NALP3 activators and are essential secondary messengers signaling NLRP3/NALP3 inflammasome activation.	ros	29-32	NLR family pyrin domain containing 3	Homo sapiens	55-60
20201014-4	2010	Recent findings suggest that ROS are produced by NLRP3/NALP3 activators and are essential secondary messengers signaling NLRP3/NALP3 inflammasome activation.	ros	29-32	NLR family pyrin domain containing 3	Homo sapiens	121-126
20201014-4	2010	Recent findings suggest that ROS are produced by NLRP3/NALP3 activators and are essential secondary messengers signaling NLRP3/NALP3 inflammasome activation.	ros	29-32	NLR family pyrin domain containing 3	Homo sapiens	127-132
20038581-6	2010	In contrast, NALP3 functionality in intermediate stage melanoma cells requires activation of the IL-1 receptor to secrete active IL-1beta; cells from an early stage of melanoma require stimulation of the IL-1 receptor plus the co-stimulant muramyl dipeptide.	Acetylmuramyl-Alanyl-Isoglutamine	240-257	NLR family pyrin domain containing 3	Homo sapiens	13-18
20168318-0	2010	NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production?	Reactive Oxygen Species	82-85	NLR family pyrin domain containing 3	Homo sapiens	0-5
20168318-4	2010	In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	225-248	NLR family pyrin domain containing 3	Homo sapiens	107-112
20168318-4	2010	In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	225-248	NLR family pyrin domain containing 3	Homo sapiens	187-192
20168318-4	2010	In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	250-253	NLR family pyrin domain containing 3	Homo sapiens	107-112
20168318-4	2010	In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	250-253	NLR family pyrin domain containing 3	Homo sapiens	187-192
19570822-3	2009	The NLRP3 inflammasome, however, assembles in response to extracellular ATP, pore-forming toxins, or crystals only in the presence of proinflammatory stimuli.	Adenosine Triphosphate	72-75	NLR family pyrin domain containing 3	Homo sapiens	4-9
20086177-5	2010	ATP activates purinergic P2RX7 receptors on DC, thus activating the NLRP3/ASC/caspase-1 inflammasome and driving the secretion of interleukin-1beta (IL-1beta).	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	68-73
20060699-5	2010	Numerous different molecular entities, such as various crystals, pore-forming toxins, or extracellular ATP can trigger the NLRP3 inflammasome.	Adenosine Triphosphate	103-106	NLR family pyrin domain containing 3	Homo sapiens	123-128
20075245-3	2010	In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role.	Reactive Oxygen Species	88-91	NLR family pyrin domain containing 3	Homo sapiens	148-153
19918053-4	2009	Nlrp3 inflammasome activation was triggered in part through ATP produced by mitochondria released from damaged cells.	Adenosine Triphosphate	60-63	NLR family pyrin domain containing 3	Homo sapiens	0-5
19633559-4	2009	In particular, nalp3 mediated inflammasome activation of caspase-1 and conversion of pro-IL-1 to IL-1 play a key role in silica-mediated and bleomycin-mediated pulmonary fibrosis.	Silicon Dioxide	121-127	NLR family pyrin domain containing 3	Homo sapiens	15-20
19633559-4	2009	In particular, nalp3 mediated inflammasome activation of caspase-1 and conversion of pro-IL-1 to IL-1 play a key role in silica-mediated and bleomycin-mediated pulmonary fibrosis.	Bleomycin	141-150	NLR family pyrin domain containing 3	Homo sapiens	15-20
20048709-5	2009	For example, aluminum hydroxide salts were shown to engage Nalp3, a member of the cytosolic NOD-like receptors and activation of B cells via invariant natural killer cell presentation of alpha-galactosylceramide was described.	aluminum hydroxide salts	13-37	NLR family pyrin domain containing 3	Homo sapiens	59-64
20048709-5	2009	For example, aluminum hydroxide salts were shown to engage Nalp3, a member of the cytosolic NOD-like receptors and activation of B cells via invariant natural killer cell presentation of alpha-galactosylceramide was described.	alpha-galactosylceramide	187-211	NLR family pyrin domain containing 3	Homo sapiens	59-64
19536133-1	2009	In acute inflammation, extracellular ATP activates P2X(7) ion channel receptors (P2X(7)R) on M1 polarized macrophages to release pro-inflammatory IL-1beta through activation of the caspase-1/nucleotide-binding domain and leucine-rich repeat receptor containing pyrin domain 3 (NLRP3) inflammasome.	Adenosine Triphosphate	37-40	NLR family pyrin domain containing 3	Homo sapiens	277-282
19542372-0	2009	Cutting edge: TNF-alpha mediates sensitization to ATP and silica via the NLRP3 inflammasome in the absence of microbial stimulation.	Adenosine Triphosphate	50-53	NLR family pyrin domain containing 3	Homo sapiens	73-78
19542372-0	2009	Cutting edge: TNF-alpha mediates sensitization to ATP and silica via the NLRP3 inflammasome in the absence of microbial stimulation.	Silicon Dioxide	58-64	NLR family pyrin domain containing 3	Homo sapiens	73-78
19542372-5	2009	In addition to TNF-alpha, IL-1alpha and IL-1beta promoted caspase-1 activation via Nlrp3 in response to ATP.	Adenosine Triphosphate	104-107	NLR family pyrin domain containing 3	Homo sapiens	83-88
19542372-6	2009	Remarkably, macrophages tolerized to TNF-alpha, but not to LPS, retained full sensitivity to ATP stimulation via Nlrp3.	Adenosine Triphosphate	93-96	NLR family pyrin domain containing 3	Homo sapiens	113-118
19931168-3	2009	A 2-year-old child was affected with a severe atypical form of cryopyrin-associated periodic syndrome, suspected based on the analysis of neopterin in CSF.	Neopterin	138-147	NLR family pyrin domain containing 3	Homo sapiens	63-72
19805629-0	2009	Glyburide inhibits the Cryopyrin/Nalp3 inflammasome.	Glyburide	0-9	NLR family pyrin domain containing 3	Homo sapiens	23-32
19805629-0	2009	Glyburide inhibits the Cryopyrin/Nalp3 inflammasome.	Glyburide	0-9	NLR family pyrin domain containing 3	Homo sapiens	33-38
19805629-5	2009	In this study, we show that the type 2 diabetes drug glyburide prevented activation of the Cryopyrin inflammasome.	Glyburide	53-62	NLR family pyrin domain containing 3	Homo sapiens	91-100
19805629-8	2009	Glyburide analogues inhibit ATP- but not hypothermia-induced IL-1beta secretion from human monocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations, thus suggesting that inhibition occurs upstream of Cryopyrin.	Glyburide	0-9	NLR family pyrin domain containing 3	Homo sapiens	174-183
19805629-8	2009	Glyburide analogues inhibit ATP- but not hypothermia-induced IL-1beta secretion from human monocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations, thus suggesting that inhibition occurs upstream of Cryopyrin.	Glyburide	0-9	NLR family pyrin domain containing 3	Homo sapiens	246-255
19805629-10	2009	Therefore, glyburide is the first identified compound to prevent Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion.	Glyburide	11-20	NLR family pyrin domain containing 3	Homo sapiens	65-74
19767079-0	2009	Associations of functional NLRP3 polymorphisms with susceptibility to food-induced anaphylaxis and aspirin-induced asthma.	Aspirin	99-106	NLR family pyrin domain containing 3	Homo sapiens	27-32
19767079-3	2009	OBJECTIVE: We sought to examine whether NLRP3 polymorphisms are associated with susceptibility to food allergy, food-induced anaphylaxis, and aspirin-induced asthma (AIA).	Aspirin	142-149	NLR family pyrin domain containing 3	Homo sapiens	40-45
19570822-6	2009	Signals provided by NF-kappaB activators are necessary but not sufficient for NLRP3 activation, and a second stimulus such as ATP or crystal-induced damage is required for NLRP3 activation.	Adenosine Triphosphate	126-129	NLR family pyrin domain containing 3	Homo sapiens	172-177
19439372-4	2009	Aluminum adjuvants activate the nucleotide-binding domain and leucine-rich-repeat-containing gene family pyrin-domain-containing 3 (known as NLRP3 or NALP3) inflammasome to activate caspase-1 and to induce proinflammatory cytokines interleukin (IL)-1beta and IL-18 by innate cells.	Aluminum	0-8	NLR family pyrin domain containing 3	Homo sapiens	141-146
19439372-5	2009	Aluminum adjuvants activate NLRP3 by multiple mechanisms such as by causing damage and rupture of the phagolysosomes, generating reactive oxygen species, inducing K(+) efflux and via release from injured tissues of molecules that constitute danger-associated molecular patterns (DAMPs) such as uric acid and ATP.	Aluminum	0-8	NLR family pyrin domain containing 3	Homo sapiens	28-33
18973929-3	2009	RESULTS: Assessment, after review of 1512 publications, is that oral colchicine therapy is being refined by attention to novel targets such as NALP3 and pyrin.	Colchicine	69-79	NLR family pyrin domain containing 3	Homo sapiens	143-148
19439372-5	2009	Aluminum adjuvants activate NLRP3 by multiple mechanisms such as by causing damage and rupture of the phagolysosomes, generating reactive oxygen species, inducing K(+) efflux and via release from injured tissues of molecules that constitute danger-associated molecular patterns (DAMPs) such as uric acid and ATP.	Reactive Oxygen Species	129-152	NLR family pyrin domain containing 3	Homo sapiens	28-33
19439372-4	2009	Aluminum adjuvants activate the nucleotide-binding domain and leucine-rich-repeat-containing gene family pyrin-domain-containing 3 (known as NLRP3 or NALP3) inflammasome to activate caspase-1 and to induce proinflammatory cytokines interleukin (IL)-1beta and IL-18 by innate cells.	Aluminum	0-8	NLR family pyrin domain containing 3	Homo sapiens	150-155
19439372-5	2009	Aluminum adjuvants activate NLRP3 by multiple mechanisms such as by causing damage and rupture of the phagolysosomes, generating reactive oxygen species, inducing K(+) efflux and via release from injured tissues of molecules that constitute danger-associated molecular patterns (DAMPs) such as uric acid and ATP.	Uric Acid	294-303	NLR family pyrin domain containing 3	Homo sapiens	28-33
18390571-10	2009	The synergy between urate crystals and LPS was directed at the level of the NALP3 inflammasome, as it was present only when active IL1 beta was measured, but not at the level of IL1 mRNA or proIL1 beta.	Uric Acid	20-25	NLR family pyrin domain containing 3	Homo sapiens	76-81
19439372-5	2009	Aluminum adjuvants activate NLRP3 by multiple mechanisms such as by causing damage and rupture of the phagolysosomes, generating reactive oxygen species, inducing K(+) efflux and via release from injured tissues of molecules that constitute danger-associated molecular patterns (DAMPs) such as uric acid and ATP.	Adenosine Triphosphate	308-311	NLR family pyrin domain containing 3	Homo sapiens	28-33
19362020-6	2009	Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS).	Reactive Oxygen Species	112-135	NLR family pyrin domain containing 3	Homo sapiens	17-22
19362020-6	2009	Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS).	Reactive Oxygen Species	137-140	NLR family pyrin domain containing 3	Homo sapiens	17-22
19364881-0	2009	Mast cells mediate neutrophil recruitment and vascular leakage through the NLRP3 inflammasome in histamine-independent urticaria.	Histamine	97-106	NLR family pyrin domain containing 3	Homo sapiens	75-80
19364881-7	2009	Our findings implicate MCs as IL-1beta producers in the skin and mediators of histamine-independent urticaria through the NLRP3 inflammasome.	Histamine	78-87	NLR family pyrin domain containing 3	Homo sapiens	122-127
19636440-9	2009	Since arginase AI is a key enzyme of the urea cycle, whereas arginase AII most probably takes part in the biosynthesis of ornithine and polyamines, the defective ammonia inactivation and increased collagen biosynthesis observed in cirrhotic liver may be related to the changes in arginase AI and AII levels, respectively.	Urea	41-45	NLR family pyrin domain containing 3	Homo sapiens	70-73
19636440-9	2009	Since arginase AI is a key enzyme of the urea cycle, whereas arginase AII most probably takes part in the biosynthesis of ornithine and polyamines, the defective ammonia inactivation and increased collagen biosynthesis observed in cirrhotic liver may be related to the changes in arginase AI and AII levels, respectively.	Ornithine	122-131	NLR family pyrin domain containing 3	Homo sapiens	70-73
19636440-9	2009	Since arginase AI is a key enzyme of the urea cycle, whereas arginase AII most probably takes part in the biosynthesis of ornithine and polyamines, the defective ammonia inactivation and increased collagen biosynthesis observed in cirrhotic liver may be related to the changes in arginase AI and AII levels, respectively.	Polyamines	136-146	NLR family pyrin domain containing 3	Homo sapiens	70-73
18667412-8	2008	Interestingly Salmonella- and lipopolysaccharide + ATP-induced activation of caspase-7 was abolished in macrophages deficient in caspase-1, the pattern recognition receptors Ipaf and Cryopyrin, and the inflammasome adaptor ASC, demonstrating an upstream role for the caspase-1 inflammasomes in caspase-7 activation in vivo.	Adenosine Triphosphate	51-54	NLR family pyrin domain containing 3	Homo sapiens	183-192
19381284-3	2009	We also examined expression patterns of Toll-like receptors (TLR1-10) and Nod-like receptors (Nod1, Nod2, and NALP3) in response to BmA.	bma	132-135	NLR family pyrin domain containing 3	Homo sapiens	110-115
18831962-6	2008	Concurrently, the rise of AII can increase the level of polyamines, compounds crucial for cells proliferation.	Polyamines	56-66	NLR family pyrin domain containing 3	Homo sapiens	26-29
19057377-2	2009	More recently, it was shown that uric acid crystals stimulate dendritic cell maturation, activate the NALP3 inflammasome, and enhance antigen-specific immune responses.	Uric Acid	33-42	NLR family pyrin domain containing 3	Homo sapiens	102-107
19302040-6	2009	Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response.	Aluminum	80-88	NLR family pyrin domain containing 3	Homo sapiens	14-19
18566365-4	2008	Other particulate adjuvants, such as QuilA and chitosan, induce inflammasome activation in a NLRP3-dependent fashion, suggesting that activation of the NLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.	Quil A	37-42	NLR family pyrin domain containing 3	Homo sapiens	93-98
19001869-6	2008	Unexpectedly, microarray analysis of PBMC from patients treated with chloroquine reveals a reversal of disease-linked KPNA1-, NLRP1- and NLRP3-gene expression phenotypes, implying that chloroquine could serve as a readily clinically available drug for targeted correction of identified aberrations.	Chloroquine	69-80	NLR family pyrin domain containing 3	Homo sapiens	137-142
19001869-6	2008	Unexpectedly, microarray analysis of PBMC from patients treated with chloroquine reveals a reversal of disease-linked KPNA1-, NLRP1- and NLRP3-gene expression phenotypes, implying that chloroquine could serve as a readily clinically available drug for targeted correction of identified aberrations.	Chloroquine	185-196	NLR family pyrin domain containing 3	Homo sapiens	137-142
19038090-0	2008	[Asbestos triggers inflammation by activating the Nalp3 inflammasome].	Asbestos	1-9	NLR family pyrin domain containing 3	Homo sapiens	50-55
18624356-0	2008	The Nlrp3 inflammasome is critical for aluminium hydroxide-mediated IL-1beta secretion but dispensable for adjuvant activity.	Aluminum Hydroxide	39-58	NLR family pyrin domain containing 3	Homo sapiens	4-9
18624356-8	2008	These results indicate that alum induces IL-1beta via the Nlrp3 inflammasome but this activity is dispensable for alum-mediated adjuvant activity.	Aluminum Hydroxide	28-32	NLR family pyrin domain containing 3	Homo sapiens	58-63
18651701-7	2008	Surprisingly, these three studies reported conflicting results on the requirement of the Nlrp3 inflammasome complex for alum adjuvant effects in vivo.	alum adjuvant	120-133	NLR family pyrin domain containing 3	Homo sapiens	89-94
18638431-3	2008	At micromolar concentrations, it suppresses monosodium urate crystal-induced NACHT-LRR-PYD-containing protein-3 (NALP3) inflammasome-driven caspase-1 activation, IL-1beta processing and release, and L-selectin expression on neutrophils.	Uric Acid	44-60	NLR family pyrin domain containing 3	Homo sapiens	77-111
18638431-3	2008	At micromolar concentrations, it suppresses monosodium urate crystal-induced NACHT-LRR-PYD-containing protein-3 (NALP3) inflammasome-driven caspase-1 activation, IL-1beta processing and release, and L-selectin expression on neutrophils.	Uric Acid	44-60	NLR family pyrin domain containing 3	Homo sapiens	113-118
18715799-3	2008	This is illustrated by the discovery that Nalp3 and Nalp1 are specifically activated by low concentrations of intracellular potassium.	Potassium	124-133	NLR family pyrin domain containing 3	Homo sapiens	42-47
18715799-4	2008	The fact that several stimuli, including bacterial toxins and some viruses, but also sterile crystals made of uric acid, asbestos or aluminium hydroxide, can trigger the Nalp3 inflammasome illustrate the fascinating prospect that microbial infections and certain danger signals may be perceived similarly by host recognition systems.	Uric Acid	110-119	NLR family pyrin domain containing 3	Homo sapiens	170-175
18715799-4	2008	The fact that several stimuli, including bacterial toxins and some viruses, but also sterile crystals made of uric acid, asbestos or aluminium hydroxide, can trigger the Nalp3 inflammasome illustrate the fascinating prospect that microbial infections and certain danger signals may be perceived similarly by host recognition systems.	Aluminum Hydroxide	133-152	NLR family pyrin domain containing 3	Homo sapiens	170-175
18604214-0	2008	Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization.	Silicon Dioxide	0-6	NLR family pyrin domain containing 3	Homo sapiens	48-53
18604214-0	2008	Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization.	aluminum salts	20-34	NLR family pyrin domain containing 3	Homo sapiens	48-53
18604214-4	2008	Here we demonstrate that silica and aluminum salt crystals activated inflammasomes formed by the cytoplasmic receptor NALP3.	Silicon Dioxide	25-31	NLR family pyrin domain containing 3	Homo sapiens	118-123
18604214-4	2008	Here we demonstrate that silica and aluminum salt crystals activated inflammasomes formed by the cytoplasmic receptor NALP3.	aluminum salt	36-49	NLR family pyrin domain containing 3	Homo sapiens	118-123
18566365-4	2008	Other particulate adjuvants, such as QuilA and chitosan, induce inflammasome activation in a NLRP3-dependent fashion, suggesting that activation of the NLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.	Quil A	37-42	NLR family pyrin domain containing 3	Homo sapiens	152-157
18566365-4	2008	Other particulate adjuvants, such as QuilA and chitosan, induce inflammasome activation in a NLRP3-dependent fashion, suggesting that activation of the NLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.	Chitosan	47-55	NLR family pyrin domain containing 3	Homo sapiens	93-98
18566365-4	2008	Other particulate adjuvants, such as QuilA and chitosan, induce inflammasome activation in a NLRP3-dependent fashion, suggesting that activation of the NLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.	Chitosan	47-55	NLR family pyrin domain containing 3	Homo sapiens	152-157
18577586-3	2008	Here we show that the inflammatory response and subsequent development of pulmonary fibrosis after inhalation of silica is dependent on the Nalp3 inflammasome.	Silicon Dioxide	113-119	NLR family pyrin domain containing 3	Homo sapiens	140-145
18577586-4	2008	Stimulation of macrophages with silica results in the activation of caspase-1 in a Nalp3-dependent manner.	Silicon Dioxide	32-38	NLR family pyrin domain containing 3	Homo sapiens	83-88
18577586-5	2008	Macrophages deficient in components of the Nalp3 inflammasome were incapable of secreting the proinflammatory cytokines interleukin (IL)-1beta and IL-18 in response to silica.	Silicon Dioxide	168-174	NLR family pyrin domain containing 3	Homo sapiens	43-48
18577586-7	2008	Activation of the Nalp3 inflammasome by silica required both an efflux of intracellular potassium and the generation of reactive oxygen species.	Silicon Dioxide	40-46	NLR family pyrin domain containing 3	Homo sapiens	18-23
18577586-7	2008	Activation of the Nalp3 inflammasome by silica required both an efflux of intracellular potassium and the generation of reactive oxygen species.	Potassium	88-97	NLR family pyrin domain containing 3	Homo sapiens	18-23
18577586-7	2008	Activation of the Nalp3 inflammasome by silica required both an efflux of intracellular potassium and the generation of reactive oxygen species.	Reactive Oxygen Species	120-143	NLR family pyrin domain containing 3	Homo sapiens	18-23
18322214-0	2008	Pannexin-1-mediated intracellular delivery of muramyl dipeptide induces caspase-1 activation via cryopyrin/NLRP3 independently of Nod2.	Acetylmuramyl-Alanyl-Isoglutamine	46-63	NLR family pyrin domain containing 3	Homo sapiens	97-106
18496530-0	2008	Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminium adjuvants.	Aluminum	79-88	NLR family pyrin domain containing 3	Homo sapiens	21-26
18496530-4	2008	Here we show that aluminium adjuvants activate an intracellular innate immune response system called the Nalp3 (also known as cryopyrin, CIAS1 or NLRP3) inflammasome.	Aluminum	18-27	NLR family pyrin domain containing 3	Homo sapiens	105-110
18496530-4	2008	Here we show that aluminium adjuvants activate an intracellular innate immune response system called the Nalp3 (also known as cryopyrin, CIAS1 or NLRP3) inflammasome.	Aluminum	18-27	NLR family pyrin domain containing 3	Homo sapiens	126-135
18496530-4	2008	Here we show that aluminium adjuvants activate an intracellular innate immune response system called the Nalp3 (also known as cryopyrin, CIAS1 or NLRP3) inflammasome.	Aluminum	18-27	NLR family pyrin domain containing 3	Homo sapiens	137-142
18496530-4	2008	Here we show that aluminium adjuvants activate an intracellular innate immune response system called the Nalp3 (also known as cryopyrin, CIAS1 or NLRP3) inflammasome.	Aluminum	18-27	NLR family pyrin domain containing 3	Homo sapiens	146-151
18496530-7	2008	We identify the Nalp3 inflammasome as a crucial element in the adjuvant effect of aluminium adjuvants; in addition, we show that the innate inflammasome pathway can direct a humoral adaptive immune response.	Aluminum	82-91	NLR family pyrin domain containing 3	Homo sapiens	16-21
18480736-10	2008	Arginase isoenzymes AI and AII have high substrate specifi city, but the affi nity to L-arginine is higher for isoenzyme AI than AII.	Arginine	86-96	NLR family pyrin domain containing 3	Homo sapiens	27-30
18480736-10	2008	Arginase isoenzymes AI and AII have high substrate specifi city, but the affi nity to L-arginine is higher for isoenzyme AI than AII.	Arginine	86-96	NLR family pyrin domain containing 3	Homo sapiens	129-132
18322214-0	2008	Pannexin-1-mediated intracellular delivery of muramyl dipeptide induces caspase-1 activation via cryopyrin/NLRP3 independently of Nod2.	Acetylmuramyl-Alanyl-Isoglutamine	46-63	NLR family pyrin domain containing 3	Homo sapiens	107-112
18322214-7	2008	Caspase-1 activation induced by MDP and ATP required pannexin-1 and Cryopyrin but was independent of Nod2.	Adenosine Triphosphate	40-43	NLR family pyrin domain containing 3	Homo sapiens	68-77
22504451-7	2008	For example, the NLR member cryopyrin/NALP3 induces cytokine secretion and lipid synthesis in response to viral dsRNA and K+ efflux, while another NLR, IPAF, induces IL-1beta?	ipaf	152-156	NLR family pyrin domain containing 3	Homo sapiens	28-37
22504451-7	2008	For example, the NLR member cryopyrin/NALP3 induces cytokine secretion and lipid synthesis in response to viral dsRNA and K+ efflux, while another NLR, IPAF, induces IL-1beta?	ipaf	152-156	NLR family pyrin domain containing 3	Homo sapiens	38-43
18281860-6	2008	Monosodium urate crystals stimulate IL-1beta secretion via cryopyrin, which led to the addition of gout to the spectrum of autoinflammatory diseases.	Uric Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	59-68
17977705-3	2007	Amongst the various inflammasomes, the NALP3 inflammasome is particularly qualified to sense a plethora of diverse molecules, ranging from bacterial muramyldipeptide to monosodium urate crystals.	Uric Acid	169-185	NLR family pyrin domain containing 3	Homo sapiens	39-44
17714972-11	2007	Urate monosodium crystals are specifically detected via the NALP3 inflammasome, which results in marked IL-1beta overproduction and initiation of an inflammatory response.	Uric Acid	0-5	NLR family pyrin domain containing 3	Homo sapiens	60-65
17714972-11	2007	Urate monosodium crystals are specifically detected via the NALP3 inflammasome, which results in marked IL-1beta overproduction and initiation of an inflammatory response.	Sodium	6-16	NLR family pyrin domain containing 3	Homo sapiens	60-65
17495597-5	2007	Apolipoproteins A-I, A-II and E are components of the donor lipoprotein particles that participate in the transfer of cholesteryl esters from high-density lipoprotein to apolipoprotein B-containing lipoproteins.	Cholesterol Esters	118-136	NLR family pyrin domain containing 3	Homo sapiens	0-25
17763411-7	2007	CONCLUSION: Our results showed that the requirements of ATP stimulation for IL-1beta release observed in healthy individuals are bypassed in patients bearing CIAS1 mutations.	Adenosine Triphosphate	56-59	NLR family pyrin domain containing 3	Homo sapiens	158-163
17763411-8	2007	This indicates that cryopyrin is the direct target of ATP and that the mutations release the protein from the requirement of ATP for activation.	Adenosine Triphosphate	54-57	NLR family pyrin domain containing 3	Homo sapiens	20-29
17763411-8	2007	This indicates that cryopyrin is the direct target of ATP and that the mutations release the protein from the requirement of ATP for activation.	Adenosine Triphosphate	125-128	NLR family pyrin domain containing 3	Homo sapiens	20-29
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	imidazoquinolines	98-115	NLR family pyrin domain containing 3	Homo sapiens	0-9
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	imidazoquinolines	98-115	NLR family pyrin domain containing 3	Homo sapiens	10-15
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	Uric Acid	157-166	NLR family pyrin domain containing 3	Homo sapiens	0-9
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	Uric Acid	157-166	NLR family pyrin domain containing 3	Homo sapiens	10-15
17530866-2	2007	Chaotropic perturbation (CP) with guanidinium chloride (Gdm-Cl) reveals HDL instability by inducing the unfolding and transfer of apo A-I but not apo A-II into the aqueous phase while forming larger apo A-I deficient HDL-like particles and small amounts of cholesteryl ester-rich microemulsions (CERMs).	Guanidine	56-62	NLR family pyrin domain containing 3	Homo sapiens	150-154
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	Adenosine Triphosphate	22-25	NLR family pyrin domain containing 3	Homo sapiens	0-9
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	Adenosine Triphosphate	22-25	NLR family pyrin domain containing 3	Homo sapiens	10-15
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	2'-deoxyadenosine triphosphate	50-54	NLR family pyrin domain containing 3	Homo sapiens	29-38
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	2'-deoxyadenosine triphosphate	26-30	NLR family pyrin domain containing 3	Homo sapiens	0-9
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	ATP-sepharose	60-71	NLR family pyrin domain containing 3	Homo sapiens	29-38
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	2'-deoxyadenosine triphosphate	26-30	NLR family pyrin domain containing 3	Homo sapiens	10-15
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	Cytidine Triphosphate	81-84	NLR family pyrin domain containing 3	Homo sapiens	29-38
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	0-9
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	Guanosine Triphosphate	86-89	NLR family pyrin domain containing 3	Homo sapiens	29-38
17483456-0	2007	Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	10-15
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	Uridine Triphosphate	94-97	NLR family pyrin domain containing 3	Homo sapiens	29-38
17483456-5	2007	We demonstrate that purified cryopyrin binds ATP, dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.	Adenosine Triphosphate	45-48	NLR family pyrin domain containing 3	Homo sapiens	29-38
17511266-4	2007	On the other hand, HDL-induced nitric oxide production and inhibition of adhesion molecule expression were mediated by two pathways, i.e, HDL-associated apoprotein A-I, A-II/SR-BI and S1P/S1P receptors in endothelial cells.	Nitric Oxide	31-43	NLR family pyrin domain containing 3	Homo sapiens	138-173
17433728-1	2007	Cryopyrin is essential for caspase-1 activation triggered by Toll-like receptor (TLR) ligands in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	113-135	NLR family pyrin domain containing 3	Homo sapiens	0-9
17433728-1	2007	Cryopyrin is essential for caspase-1 activation triggered by Toll-like receptor (TLR) ligands in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	137-140	NLR family pyrin domain containing 3	Homo sapiens	0-9
17433728-2	2007	However, the events linking bacterial products and ATP to cryopyrin remain unclear.	Adenosine Triphosphate	51-54	NLR family pyrin domain containing 3	Homo sapiens	58-67
17008311-6	2006	Finally, cryopyrin was required for IL-1beta production in response to poly(I:C) in vivo.	Poly I-C	71-79	NLR family pyrin domain containing 3	Homo sapiens	9-18
17352828-1	2007	Monosodium urate crystals stimulate monocytes and macrophages to release IL-1beta through the NALP3 component of the inflammasome.	Uric Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	94-99
17916949-5	2007	Sodium selenite administration resulted in significant decline of Bcl-2 level after therapy in group A-II (8.6 +/- 6.9 ng/ml vs 3 6.9 +/- 7.9 ng/ml, P &lt; 0.05).	Sodium Selenite	0-15	NLR family pyrin domain containing 3	Homo sapiens	101-105
17132626-3	2007	Cleavage and secretion of the cytokines is mediated by caspase-1, in association with an inflammasome containing Nalp3, which can be activated by binding of extracellular ATP to purinergic receptors.	Adenosine Triphosphate	171-174	NLR family pyrin domain containing 3	Homo sapiens	113-118
16935537-3	2007	The elevated arginine levels induce the second arginase (AII) in patient kidney and kidney tissue culture.	Arginine	13-21	NLR family pyrin domain containing 3	Homo sapiens	57-60
16407888-6	2006	Cryopyrin and ASC are essential for caspase-1 activation and IL-1beta and IL-18 production in response to bacterial RNA and the imidazoquinoline compounds R837 and R848.	THOS Streptonigrin	128-144	NLR family pyrin domain containing 3	Homo sapiens	0-9
16711179-4	2006	AII were treated with collagenase-based ointments once daily (Noruxol or Iruxol, Smith and Nephew).	noruxol	62-69	NLR family pyrin domain containing 3	Homo sapiens	0-3
16711179-4	2006	AII were treated with collagenase-based ointments once daily (Noruxol or Iruxol, Smith and Nephew).	iruxol	73-79	NLR family pyrin domain containing 3	Homo sapiens	0-3
17441374-13	2006	In group AI the inverse leptin/DHEAS relation remained, while in group AII inverse leptin/HDL-cholesterol relation remained and reverse leptin/IGFBP-1 relation was significant.	Cholesterol	94-105	NLR family pyrin domain containing 3	Homo sapiens	71-74
16544581-4	2006	Muckle wells syndrome and Familial cold urticaria are related to CIAS1 gene mutations which are located on the long arm of the chromosome 1 and encodes cryopirine involved in apoptosis.	cryopirine	152-162	NLR family pyrin domain containing 3	Homo sapiens	65-70
16081838-5	2005	These results further link mutations in cryopyrin with abnormal caspase-1 activation, and support the clinical testing of caspase-1 inhibitors such as VX-765 in autoinflammatory disorders.	belnacasan	151-157	NLR family pyrin domain containing 3	Homo sapiens	40-49
16323982-5	2005	CONCLUSIONS: Ischaemic coronary arteriosclerosis with an incidence rate of 16.6% as caused by prolonged CPA therapy is mediated through changes in HDL cholesterol, Apo A-I and Apo A-II pro fi les, other than the well-known hyperglyceridemic effect caused by estrogen.	Cyproterone Acetate	104-107	NLR family pyrin domain containing 3	Homo sapiens	180-184
20878027-1	2005	The purpose of this study was to evaluate the microhardness of dental enamel around composite restorations bonded with fluoride-containing adhesive systems (FCAS), after thermo- and pH-cycling protocols.	Fluorides	119-127	NLR family pyrin domain containing 3	Homo sapiens	157-161
15669855-5	2005	The three species were identified as the N7 (A-I), N3 (A-II), and N1 (A-III) linkage isomers of [Pt(en)(ACRAMTU-S)(adenine)]3+ (A).	acramtu-s)(adenine)	104-123	NLR family pyrin domain containing 3	Homo sapiens	55-59
15669855-9	2005	A-II crystallizes in the triclinic space group P in the form of centrosymmetric dimers, {[Pt(en)(ACRAMTU-S)(adenine-N3)]2}6+.	[pt(en)(acramtu-s)(adenine-n3)	89-119	NLR family pyrin domain containing 3	Homo sapiens	0-4
15629544-5	2005	AII infused via the portal pathway promotes calcium-dependent PHR but not a hypertensive response in the arterial pathway (AHR); when infused into the arterial pathway AII promotes calcium-dependent PHR and AHR.	Calcium	44-51	NLR family pyrin domain containing 3	Homo sapiens	0-3
15629544-5	2005	AII infused via the portal pathway promotes calcium-dependent PHR but not a hypertensive response in the arterial pathway (AHR); when infused into the arterial pathway AII promotes calcium-dependent PHR and AHR.	Calcium	181-188	NLR family pyrin domain containing 3	Homo sapiens	168-171
15629544-6	2005	Losartan infused into the portal vein abolishes PHR to AII but not the metabolic response; when infused via both pathways it abolishes the hypertensive responses and inhibits the metabolic effects.	Losartan	0-8	NLR family pyrin domain containing 3	Homo sapiens	55-58
15629544-11	2005	Hemodynamic responses to AII are losartan-dependent but metabolic responses are partially losartan-independent.	Losartan	33-41	NLR family pyrin domain containing 3	Homo sapiens	25-28
15218032-6	2004	The ABCA1 flippase activity, apolipoprotein AI and AII binding, and cellular phospholipid and cholesterol efflux were enhanced by mutations preventing CK2 phosphorylation of the threonine and serine residues.	Threonine	178-187	NLR family pyrin domain containing 3	Homo sapiens	51-54
15530394-0	2004	Identification of bacterial muramyl dipeptide as activator of the NALP3/cryopyrin inflammasome.	muramyl	28-35	NLR family pyrin domain containing 3	Homo sapiens	66-71
15530394-0	2004	Identification of bacterial muramyl dipeptide as activator of the NALP3/cryopyrin inflammasome.	muramyl	28-35	NLR family pyrin domain containing 3	Homo sapiens	72-81
15530394-0	2004	Identification of bacterial muramyl dipeptide as activator of the NALP3/cryopyrin inflammasome.	Dipeptides	36-45	NLR family pyrin domain containing 3	Homo sapiens	66-71
15530394-0	2004	Identification of bacterial muramyl dipeptide as activator of the NALP3/cryopyrin inflammasome.	Dipeptides	36-45	NLR family pyrin domain containing 3	Homo sapiens	72-81
15631484-1	2005	The structural properties of a second, apparently amorphous phase (aII) of the molecular glass former triphenyl phosphite were studied by means of multidimensional solid-state NMR spectroscopy and X-ray diffraction.	triphenyl phosphite	102-121	NLR family pyrin domain containing 3	Homo sapiens	67-70
15631484-5	2005	Our data strongly suggest that some of the TPP molecules in phase aII tend toward a parallel alignment.	tetraphenylporphine sulfonate	43-46	NLR family pyrin domain containing 3	Homo sapiens	66-69
15241749-10	2004	RESULTS: Intragroup comparison of different phases of the trial in both groups showed that donepezil significantly increased the testing scores of the AII and VII, as well as PASAT scores, compared with baseline.	Donepezil	91-100	NLR family pyrin domain containing 3	Homo sapiens	151-162
15334500-0	2004	Variant chronic infantile neurologic, cutaneous, articular syndrome due to a mutation within the leucine-rich repeat domain of CIAS1.	Leucine	97-104	NLR family pyrin domain containing 3	Homo sapiens	127-132
15276021-8	2004	- HUVEC showed a baseline arginase activity and expression of both arginase isoforms (arginase I and II (A-I and A-II, respectively)) which resulted in l-norvaline-inhibitable cellular polyamine synthesis.	norvaline	152-163	NLR family pyrin domain containing 3	Homo sapiens	113-117
15276021-8	2004	- HUVEC showed a baseline arginase activity and expression of both arginase isoforms (arginase I and II (A-I and A-II, respectively)) which resulted in l-norvaline-inhibitable cellular polyamine synthesis.	Polyamines	185-194	NLR family pyrin domain containing 3	Homo sapiens	113-117
15231984-0	2004	A novel CIAS1 mutation and plasma/cerebrospinal fluid cytokine profile in a German patient with neonatal-onset multisystem inflammatory disease responsive to methotrexate therapy.	Methotrexate	158-170	NLR family pyrin domain containing 3	Homo sapiens	8-13
15226620-4	2004	The inhibitory effects of telmisartan on AII-induced contraction persisted even after wash-out procedures.	Telmisartan	26-37	NLR family pyrin domain containing 3	Homo sapiens	41-44
15128284-8	2004	Increased binding of SF-1 to its response element in the presence of forskolin, A-II and insulin was observed.	Colforsin	69-78	NLR family pyrin domain containing 3	Homo sapiens	80-96
12943873-3	2003	In the TG &gt;/=200 mg/dl stratum, gemcabene significantly increased serum HDL cholesterol by 18% with corresponding significant increases of 6% in both apolipoprotein A-I and A-II levels at the 150-mg dose.	gemcabene	35-44	NLR family pyrin domain containing 3	Homo sapiens	176-180
15017086-5	2004	For mixed metal compounds (x not equal to 0) the partitioning of calcium and lead over the AI(4f) and AII(6h) positions is nonstoichiometric, with lead preferentially favouring the larger AII site at a partitioning coefficient kPb(AI/AII) approximately 0.33 for all x &lt; 7.	Calcium	65-72	NLR family pyrin domain containing 3	Homo sapiens	102-105
15017086-5	2004	For mixed metal compounds (x not equal to 0) the partitioning of calcium and lead over the AI(4f) and AII(6h) positions is nonstoichiometric, with lead preferentially favouring the larger AII site at a partitioning coefficient kPb(AI/AII) approximately 0.33 for all x &lt; 7.	Calcium	65-72	NLR family pyrin domain containing 3	Homo sapiens	188-191
15017086-5	2004	For mixed metal compounds (x not equal to 0) the partitioning of calcium and lead over the AI(4f) and AII(6h) positions is nonstoichiometric, with lead preferentially favouring the larger AII site at a partitioning coefficient kPb(AI/AII) approximately 0.33 for all x &lt; 7.	Calcium	65-72	NLR family pyrin domain containing 3	Homo sapiens	188-191
15050972-3	2004	A mitochondrial form, AII, has been thought to be more widely expressed and to be involved in the biosynthesis of polyamines, the amino acids ornithine, proline, and glutamate and in the inflammatory process, among others.	Polyamines	114-124	NLR family pyrin domain containing 3	Homo sapiens	22-25
15050972-3	2004	A mitochondrial form, AII, has been thought to be more widely expressed and to be involved in the biosynthesis of polyamines, the amino acids ornithine, proline, and glutamate and in the inflammatory process, among others.	Ornithine	142-151	NLR family pyrin domain containing 3	Homo sapiens	22-25
15050972-3	2004	A mitochondrial form, AII, has been thought to be more widely expressed and to be involved in the biosynthesis of polyamines, the amino acids ornithine, proline, and glutamate and in the inflammatory process, among others.	Proline	153-160	NLR family pyrin domain containing 3	Homo sapiens	22-25
15050972-3	2004	A mitochondrial form, AII, has been thought to be more widely expressed and to be involved in the biosynthesis of polyamines, the amino acids ornithine, proline, and glutamate and in the inflammatory process, among others.	Glutamic Acid	166-175	NLR family pyrin domain containing 3	Homo sapiens	22-25
15025837-0	2004	AII antagonists in hypertension, heart failure, and diabetic nephropathy: focus on losartan.	Losartan	83-91	NLR family pyrin domain containing 3	Homo sapiens	0-3
12752436-2	2003	Conformational analysis of angiotensin I (AI) and II (AII) peptides has been performed through 2D 1H-NMR spectroscopy in dimethylsulfoxide and 2,2,2-trifluoroethanol/H2O.	Hydrogen	98-100	NLR family pyrin domain containing 3	Homo sapiens	54-57
12907170-3	2003	We hypothesized that melatonin may influence retinal light adaptation by acting on AII cells directly and thus investigated whether melatonin receptors were expressed in AII neurons.	Melatonin	21-30	NLR family pyrin domain containing 3	Homo sapiens	83-86
12907170-11	2003	That virtually all AII neurons express the MT(1) receptor in both human and macaque retina, may provide the first evidence demonstrating a role for melatonin in AII regulation, furthering the hypothesis of melatonin function in retinal light adaptation.	Melatonin	206-215	NLR family pyrin domain containing 3	Homo sapiens	19-22
12752436-2	2003	Conformational analysis of angiotensin I (AI) and II (AII) peptides has been performed through 2D 1H-NMR spectroscopy in dimethylsulfoxide and 2,2,2-trifluoroethanol/H2O.	Dimethyl Sulfoxide	121-138	NLR family pyrin domain containing 3	Homo sapiens	54-57
12119188-10	2002	In different in vitro models of cell cultures, Lp A-I:A-II induce either a lower or a similar cellular cholesterol efflux (the first step of reverse cholesterol transport) than Lp A-I.	Cholesterol	103-114	NLR family pyrin domain containing 3	Homo sapiens	54-58
12752436-2	2003	Conformational analysis of angiotensin I (AI) and II (AII) peptides has been performed through 2D 1H-NMR spectroscopy in dimethylsulfoxide and 2,2,2-trifluoroethanol/H2O.	Trifluoroethanol	143-165	NLR family pyrin domain containing 3	Homo sapiens	54-57
12752436-2	2003	Conformational analysis of angiotensin I (AI) and II (AII) peptides has been performed through 2D 1H-NMR spectroscopy in dimethylsulfoxide and 2,2,2-trifluoroethanol/H2O.	Water	166-169	NLR family pyrin domain containing 3	Homo sapiens	54-57
12752436-3	2003	The solution structural models of AI and AII have been determined in dimethylsulfoxide using NOE distance and 3JHNHalpha coupling constants.	Dimethyl Sulfoxide	69-86	NLR family pyrin domain containing 3	Homo sapiens	41-44
12752436-8	2003	Detailed analysis of the peptide structural features attempts to elucidate the conformational role of the C-terminal dipeptide to the different binding affinity of AI and AII towards the AT1 receptor and sets the basis for understanding the factors that might govern free- or bound-depended AII structural differentiation.	Dipeptides	117-126	NLR family pyrin domain containing 3	Homo sapiens	171-174
12752436-8	2003	Detailed analysis of the peptide structural features attempts to elucidate the conformational role of the C-terminal dipeptide to the different binding affinity of AI and AII towards the AT1 receptor and sets the basis for understanding the factors that might govern free- or bound-depended AII structural differentiation.	Dipeptides	117-126	NLR family pyrin domain containing 3	Homo sapiens	291-294
12373782-12	2002	The glycine-IR population consists mainly of AII amacrine cell types, but clearly another non-AII type is involved.	Glycine	4-11	NLR family pyrin domain containing 3	Homo sapiens	45-48
12373782-13	2002	The non-AII glycine-IR population resembles a small- to medium-field diffuse type.	Glycine	12-19	NLR family pyrin domain containing 3	Homo sapiens	8-11
12119188-10	2002	In different in vitro models of cell cultures, Lp A-I:A-II induce either a lower or a similar cellular cholesterol efflux (the first step of reverse cholesterol transport) than Lp A-I.	Cholesterol	149-160	NLR family pyrin domain containing 3	Homo sapiens	54-58
11869839-5	2002	METHODS: Vascular AI/AII conversion was studied in patients with chronic heart failure (CHF) taking chronic lisinopril therapy by the differential infusion of AI and AII into the brachial artery.	Lisinopril	108-118	NLR family pyrin domain containing 3	Homo sapiens	18-24
12210236-7	2002	Our CE-MS results suggest that the multiple components observed in the acetonitrile-containing CE separation appear to be oxidized forms of the proteins in addition to native forms of the apolipoprotein A-I and A-II.	acetonitrile	71-83	NLR family pyrin domain containing 3	Homo sapiens	211-215
12034692-13	2002	Losartan (1 microM) significantly blocked the AII induced BK channel activation (p=0.0131), the Ca(2+)(I) response (p&lt;10(-4)), and the AII induced volume effect (p=0.0046).	Losartan	0-8	NLR family pyrin domain containing 3	Homo sapiens	46-49
12034692-13	2002	Losartan (1 microM) significantly blocked the AII induced BK channel activation (p=0.0131), the Ca(2+)(I) response (p&lt;10(-4)), and the AII induced volume effect (p=0.0046).	Losartan	0-8	NLR family pyrin domain containing 3	Homo sapiens	138-141
11912549-0	2002	Serum testosterone associates with lower high-density lipoprotein cholesterol in black and white males, 10 to 15 years of age, through lowered apolipoprotein AI and AII concentrations.	Testosterone	6-18	NLR family pyrin domain containing 3	Homo sapiens	165-168
11869839-5	2002	METHODS: Vascular AI/AII conversion was studied in patients with chronic heart failure (CHF) taking chronic lisinopril therapy by the differential infusion of AI and AII into the brachial artery.	Lisinopril	108-118	NLR family pyrin domain containing 3	Homo sapiens	21-24
12481201-2	2002	Its active metabolite, fenofibric acid, is responsible for the primary pharmacodynamic effects of the drug: reductions in total plasma cholesterol, low density lipoprotein cholesterol, triglycerides, and very low-density lipoprotein concentrations and increases in high-density lipoprotein cholesterol and apolipoproteins AI and AII concentrations.	fenofibric acid	23-38	NLR family pyrin domain containing 3	Homo sapiens	329-332
11802744-1	2002	Annexin II tetramer (AII(t)) is a member of the Ca(2+)- and phospholipid-binding protein family and is implicated in membrane fusion during surfactant secretion.	Phospholipids	60-72	NLR family pyrin domain containing 3	Homo sapiens	21-24
11802744-4	2002	It is therefore hypothesized that nitration of AII(t) by ONOO(-) may be a mechanism for the NO inhibition of regulated exocytosis.	onoo	57-61	NLR family pyrin domain containing 3	Homo sapiens	47-50
11802744-5	2002	We therefore performed in vitro studies to test effects of ONOO(-) on AII(t).	onoo	59-63	NLR family pyrin domain containing 3	Homo sapiens	70-73
11802744-6	2002	Western blot analysis using anti-nitrotyrosine antibodies showed a dose-dependent nitration of tyrosine residues in AII(t) treated with ONOO(-).	3-nitrotyrosine	33-46	NLR family pyrin domain containing 3	Homo sapiens	116-119
11802744-6	2002	Western blot analysis using anti-nitrotyrosine antibodies showed a dose-dependent nitration of tyrosine residues in AII(t) treated with ONOO(-).	Tyrosine	38-46	NLR family pyrin domain containing 3	Homo sapiens	116-119
11802744-6	2002	Western blot analysis using anti-nitrotyrosine antibodies showed a dose-dependent nitration of tyrosine residues in AII(t) treated with ONOO(-).	onoo	136-140	NLR family pyrin domain containing 3	Homo sapiens	116-119
11802744-9	2002	AII(t)-mediated liposome aggregation was inhibited by ONOO(-) with an IC(50) of approximately 30 microM.	onoo	54-58	NLR family pyrin domain containing 3	Homo sapiens	0-3
11802744-10	2002	The inhibition was abolished by urate (a scavenger of ONOO(-) and *OH), but not by mannitol (a scavenger of *OH) or superoxide dismutase (a scavenger of O(2)(-)) and appeared to be specific to AII(t), since ONOO(-) only slightly influenced annexin I-mediated liposome aggregation.	Uric Acid	32-37	NLR family pyrin domain containing 3	Homo sapiens	193-196
11802744-12	2002	Furthermore, ONOO(-) only partially inhibited the binding of AII(t) to membranes.	onoo(-)	13-20	NLR family pyrin domain containing 3	Homo sapiens	61-64
11802744-13	2002	Nitration of AII(t) also occurred in intact A549 cells, a lung epithelial cell line, treated with ONOO(-).	onoo	98-102	NLR family pyrin domain containing 3	Homo sapiens	13-16
11829529-6	2002	Transfection with pcDNA-AII increased AII expression and activity but had little effect on nitrite production even if no l-arginine was added.	Arginine	121-131	NLR family pyrin domain containing 3	Homo sapiens	18-27
11829529-6	2002	Transfection with pcDNA-AII increased AII expression and activity but had little effect on nitrite production even if no l-arginine was added.	Arginine	121-131	NLR family pyrin domain containing 3	Homo sapiens	24-27
11701466-11	2001	The uptake of [(3)H]cholesterol ester was approximately 75% greater from LP-AI versus LP-AI+AII particles, but neither niacin nor gemfibrozil affected cholesterol ester uptake.	[(3)h]cholesterol ester	14-37	NLR family pyrin domain containing 3	Homo sapiens	86-95
11773507-8	2002	Moreover, a significant dietary oil by cholesterol level interaction was found for Apo AII and the HDL cholesterol/Apo AII ratio.	Oils	32-35	NLR family pyrin domain containing 3	Homo sapiens	87-90
11773507-8	2002	Moreover, a significant dietary oil by cholesterol level interaction was found for Apo AII and the HDL cholesterol/Apo AII ratio.	Cholesterol	39-50	NLR family pyrin domain containing 3	Homo sapiens	87-90
12030443-1	2001	Plasma glutathione peroxidase (PGPx) and apolipoproteins A-I, A-II, and B-100 reduce phosphatidylcholine hydroperoxide (PC-OOH) to its hydroxide (PC-OH).	phosphatidylcholine hydroperoxide	85-118	NLR family pyrin domain containing 3	Homo sapiens	41-77
12030443-1	2001	Plasma glutathione peroxidase (PGPx) and apolipoproteins A-I, A-II, and B-100 reduce phosphatidylcholine hydroperoxide (PC-OOH) to its hydroxide (PC-OH).	phosphatidylcholine hydroperoxide	120-126	NLR family pyrin domain containing 3	Homo sapiens	41-77
12030443-1	2001	Plasma glutathione peroxidase (PGPx) and apolipoproteins A-I, A-II, and B-100 reduce phosphatidylcholine hydroperoxide (PC-OOH) to its hydroxide (PC-OH).	hydroxide ion	135-144	NLR family pyrin domain containing 3	Homo sapiens	41-77
12030443-1	2001	Plasma glutathione peroxidase (PGPx) and apolipoproteins A-I, A-II, and B-100 reduce phosphatidylcholine hydroperoxide (PC-OOH) to its hydroxide (PC-OH).	pc-oh	146-151	NLR family pyrin domain containing 3	Homo sapiens	41-77
11701466-11	2001	The uptake of [(3)H]cholesterol ester was approximately 75% greater from LP-AI versus LP-AI+AII particles, but neither niacin nor gemfibrozil affected cholesterol ester uptake.	Cholesterol Esters	20-37	NLR family pyrin domain containing 3	Homo sapiens	86-95
12733354-0	2001	[Effects of retinoic acid on secretion of apolipoproteins A I, A II, B100, C III and E by cultured HepG2 cells].	Tretinoin	12-25	NLR family pyrin domain containing 3	Homo sapiens	42-80
11687797-7	2001	This gene, called CIAS1, is expressed in peripheral blood leukocytes and encodes a protein with a pyrin domain, a nucleotide-binding site (NBS, NACHT subfamily) domain and a leucine-rich repeat (LRR) motif region, suggesting a role in the regulation of inflammation and apoptosis.	Leucine	174-181	NLR family pyrin domain containing 3	Homo sapiens	18-23
12733354-2	2001	METHODS: We observed the effect of retinoic acid on the secretion of apolipoproteins A I, A II, C III, B100 and E by cultured HepG2 cells.	Tretinoin	35-48	NLR family pyrin domain containing 3	Homo sapiens	69-107
12733354-5	2001	RESULTS: Retinoic acid increased the secretion of apoA I, B100, C III and A II, and it inhibited the secretion of apoE.	Tretinoin	9-22	NLR family pyrin domain containing 3	Homo sapiens	64-78
12733354-7	2001	When the concentration of retinoic acid in cultured media was 2 x 10(-4) mol/l, the secretion of apoA I, A II, B100 and C III increased by 14.3% (P &lt; 0.01), 23.8% (P &lt; 0.05), 16.1% (P &lt; 0.01) and 47.6% (P &lt; 0.01) respectively, and the secretion of apoE decreased by 37.2% (P &lt; 0.01).	Tretinoin	26-39	NLR family pyrin domain containing 3	Homo sapiens	105-109
10998468-9	2000	These results suggest that the mechanisms of LpAI and LpAI:AII modulations differ according to each environmental factor, some dependent on the lipid content of lipoproteins and others not, but LpAI and LpAI:AII levels seem independent of triglyceride concentration.	Triglycerides	239-251	NLR family pyrin domain containing 3	Homo sapiens	59-62
10971280-7	2000	RESULTS: The potency of AII was similar in child and adult detrusor strips, with mean (SEM) pD2 values of 6.9 (1.0) (n = 25) and 6.7 (0.2) (n = 9) respectively, and the maximum responses (to 10 micromol/L AII) rather low (39% and 49%, respectively, P &gt; 0.05), compared with carbachol (100 micromol/L).	Carbachol	277-286	NLR family pyrin domain containing 3	Homo sapiens	24-27
10998468-8	2000	Conversely, after adjustment for HDL-cholesterol, the significant association between LpAI:AII and BMI disappeared, while the associations between LpAI:AII and alcohol consumption, cigarette smoking and physical activity remained significant.	Alcohols	160-167	NLR family pyrin domain containing 3	Homo sapiens	152-155
10971280-9	2000	Responses to AII in strips from children under 3 years old were antagonized by the AT1 receptor antagonist losartan (1 micromol/L) but not by the AT2 receptor antagonist PD 123319 (1 micromol/L), indicating interaction with the AT1 receptor.	Losartan	107-115	NLR family pyrin domain containing 3	Homo sapiens	13-16
11026543-3	2000	The conformations of compounds with a good binding activity are quite similar to that of DuP753, a prototype of AII antagonist, suggesting that these compounds also bind to the same site of AII receptor.	Losartan	89-95	NLR family pyrin domain containing 3	Homo sapiens	112-115
11026543-3	2000	The conformations of compounds with a good binding activity are quite similar to that of DuP753, a prototype of AII antagonist, suggesting that these compounds also bind to the same site of AII receptor.	Losartan	89-95	NLR family pyrin domain containing 3	Homo sapiens	190-193
12147952-0	2000	Differential effects of direct antagonism of AII compared to ACE inhibitors on serum potassium levels and azotemia in patients with severe congestive heart failure.	Potassium	85-94	NLR family pyrin domain containing 3	Homo sapiens	45-48
10913291-0	2000	8-Substituted cAMP analogues reveal marked differences in adaptability, hydrogen bonding, and charge accommodation between homologous binding sites (AI/AII and BI/BII) in cAMP kinase I and II.	Cyclic AMP	14-18	NLR family pyrin domain containing 3	Homo sapiens	152-155
10843787-3	2000	The administration of the mu-antagonist naloxonazine and the kappa-antagonist nor-Binaltorphimine further elevated plasma levels of AVT stimulated by hypertonic NaCl or AII.	naloxonazine	40-52	NLR family pyrin domain containing 3	Homo sapiens	161-172
10843787-3	2000	The administration of the mu-antagonist naloxonazine and the kappa-antagonist nor-Binaltorphimine further elevated plasma levels of AVT stimulated by hypertonic NaCl or AII.	norbinaltorphimine	78-97	NLR family pyrin domain containing 3	Homo sapiens	161-172
10404104-2	1999	In this report, it is shown that commercially available antibodies to the calcium binding protein calretinin may be used to label the population of AII amacrine cells selectively.	Calcium	74-81	NLR family pyrin domain containing 3	Homo sapiens	148-151
10718754-11	2000	Application of the ionotropic glutamate receptor antagonists CNQX or DNQX enhanced the on-centre responses of AII cells but attenuated the off-surround responses.	6-Cyano-7-nitroquinoxaline-2,3-dione	61-65	NLR family pyrin domain containing 3	Homo sapiens	110-113
10718754-11	2000	Application of the ionotropic glutamate receptor antagonists CNQX or DNQX enhanced the on-centre responses of AII cells but attenuated the off-surround responses.	FG 9041	69-73	NLR family pyrin domain containing 3	Homo sapiens	110-113
10718754-14	2000	Application of the glycine antagonist, strychnine, had only minor and variable effects on AII cell responses.	Strychnine	39-49	NLR family pyrin domain containing 3	Homo sapiens	90-93
10718754-15	2000	However, the GABA antagonists picrotoxin and bicuculline enhanced the on-centre response but attenuated or completely blocked the off-surround response of AII cells.	gamma-Aminobutyric Acid	13-17	NLR family pyrin domain containing 3	Homo sapiens	155-158
10718754-15	2000	However, the GABA antagonists picrotoxin and bicuculline enhanced the on-centre response but attenuated or completely blocked the off-surround response of AII cells.	Picrotoxin	30-40	NLR family pyrin domain containing 3	Homo sapiens	155-158
10718754-15	2000	However, the GABA antagonists picrotoxin and bicuculline enhanced the on-centre response but attenuated or completely blocked the off-surround response of AII cells.	Bicuculline	45-56	NLR family pyrin domain containing 3	Homo sapiens	155-158
10718754-16	2000	The GABA antagonists had no effect on the responses of horizontal cells indicating that their effects on AII cell responses reflected actions on inner retinal circuitry rather than feedback circuitry in the outer plexiform layer.	gamma-Aminobutyric Acid	4-8	NLR family pyrin domain containing 3	Homo sapiens	105-108
10718754-18	2000	Application of the voltage-gated sodium channel blocker TTX enhanced the on-centre responses of AII cells but attenuated or abolished their off-surround responses.	Tetrodotoxin	56-59	NLR family pyrin domain containing 3	Homo sapiens	96-99
10480081-2	1999	Three novel ACE inhibitory peptides, A-II, B-II and C, were isolated and their amino acid sequences identified as Tyr-Pro-Glu-Arg (residues 8-11), Tyr-Tyr-Pro-Gln-Ile-Met-Gln-Tyr (residues 136-143) and Asn-Asn-Val-Met-Leu-Gln-Trp (residues 164-170) respectively.	tyr-pro-glu-arg	114-129	NLR family pyrin domain containing 3	Homo sapiens	37-53
10480081-2	1999	Three novel ACE inhibitory peptides, A-II, B-II and C, were isolated and their amino acid sequences identified as Tyr-Pro-Glu-Arg (residues 8-11), Tyr-Tyr-Pro-Gln-Ile-Met-Gln-Tyr (residues 136-143) and Asn-Asn-Val-Met-Leu-Gln-Trp (residues 164-170) respectively.	Tyr-Tyr-Pro-Gln-Ile-Met-Gln-Tyr	147-178	NLR family pyrin domain containing 3	Homo sapiens	37-53
10480081-2	1999	Three novel ACE inhibitory peptides, A-II, B-II and C, were isolated and their amino acid sequences identified as Tyr-Pro-Glu-Arg (residues 8-11), Tyr-Tyr-Pro-Gln-Ile-Met-Gln-Tyr (residues 136-143) and Asn-Asn-Val-Met-Leu-Gln-Trp (residues 164-170) respectively.	Asn-Asn-Val-Met-Leu-Gln-Trp	202-229	NLR family pyrin domain containing 3	Homo sapiens	37-53
10432222-3	1999	This differential aldosterone responsiveness could be related to the levels of type 1 AII receptors (AT1R) in the APA.	Aldosterone	18-29	NLR family pyrin domain containing 3	Homo sapiens	86-89
9792814-4	1998	AII treatment of VSMC increased the levels of Gialpha-2 and Gialpha-3 proteins and actinomycin D, an inhibitor of RNA synthesis attenuated the AII-evoked enhanced expression of Gialpha-2 and Gialpha-3 proteins.	vsmc	17-21	NLR family pyrin domain containing 3	Homo sapiens	0-3
10354195-8	1999	LpAI:AII increased from 73.8 to 101.6 mg dL-1 (+32%) (P &lt; 0.05), whereas alcohol had no effect on the concentration of LpAI.	lpai	0-4	NLR family pyrin domain containing 3	Homo sapiens	5-8
10354195-11	1999	CONCLUSION: The decrease in the fractional catabolic rate of apoAII could lead to an accumulation of apoAII-containing lipoproteins in plasma and account for the dramatic increase in LpAI:AII observed in the plasma of subjects consuming alcohol.	Alcohols	237-244	NLR family pyrin domain containing 3	Homo sapiens	64-67
10361451-2	1999	Although angiotensin receptor antagonists (AII-A) share the common property with ACE-I with regard to blockade of angiotensin activity via angiotensin type 1 receptors (AT1), AII-A is also reported to stimulate AT2 that plausibly activates nitric oxide production within renal medulla and augments synthesis of vasodilatory P450-metabolites in renal afferent arterioles.	Nitric Oxide	240-252	NLR family pyrin domain containing 3	Homo sapiens	43-46
10361451-2	1999	Although angiotensin receptor antagonists (AII-A) share the common property with ACE-I with regard to blockade of angiotensin activity via angiotensin type 1 receptors (AT1), AII-A is also reported to stimulate AT2 that plausibly activates nitric oxide production within renal medulla and augments synthesis of vasodilatory P450-metabolites in renal afferent arterioles.	Nitric Oxide	240-252	NLR family pyrin domain containing 3	Homo sapiens	175-178
9920290-4	1999	MCF-7, MCF-7/LY2, and MDA-MB-231 cells all showed nuclear fragmentation in response to 100 microM A(II) when stained with Hoechst 33342 and examined by fluorescence microscopy.	bisbenzimide ethoxide trihydrochloride	122-135	NLR family pyrin domain containing 3	Homo sapiens	98-103
9920290-8	1999	A previous study by single-color (propidium) flow cytometry demonstrated that A(II) blocks MDA-MB-231 cells in G2/M of the cell cycle.	Propidium	34-43	NLR family pyrin domain containing 3	Homo sapiens	78-83
9920290-13	1999	Cycloheximide inhibited A(II)-induced cell death, indicating that its toxicity requires de novo protein synthesis.	Cycloheximide	0-13	NLR family pyrin domain containing 3	Homo sapiens	24-29
9792814-4	1998	AII treatment of VSMC increased the levels of Gialpha-2 and Gialpha-3 proteins and actinomycin D, an inhibitor of RNA synthesis attenuated the AII-evoked enhanced expression of Gialpha-2 and Gialpha-3 proteins.	vsmc	17-21	NLR family pyrin domain containing 3	Homo sapiens	143-146
9792814-4	1998	AII treatment of VSMC increased the levels of Gialpha-2 and Gialpha-3 proteins and actinomycin D, an inhibitor of RNA synthesis attenuated the AII-evoked enhanced expression of Gialpha-2 and Gialpha-3 proteins.	Dactinomycin	83-96	NLR family pyrin domain containing 3	Homo sapiens	0-3
9765239-8	1998	Kinetic analysis showed that HL had a greater affinity for the phospholipids in (A-II/CE)rHDL (Km(app) = 0.2 mM) than in (A-I/CE)rHDL (Km(app) = 3.1 mM).	Phospholipids	63-76	NLR family pyrin domain containing 3	Homo sapiens	81-85
9765239-10	1998	HL also had a greater affinity for the phospholipids and triacylglycerol in (A-II/TG)rHDL than in (A-I/TG)rHDL.	Phospholipids	39-52	NLR family pyrin domain containing 3	Homo sapiens	77-81
9792814-4	1998	AII treatment of VSMC increased the levels of Gialpha-2 and Gialpha-3 proteins and actinomycin D, an inhibitor of RNA synthesis attenuated the AII-evoked enhanced expression of Gialpha-2 and Gialpha-3 proteins.	Dactinomycin	83-96	NLR family pyrin domain containing 3	Homo sapiens	143-146
9765239-10	1998	HL also had a greater affinity for the phospholipids and triacylglycerol in (A-II/TG)rHDL than in (A-I/TG)rHDL.	Triglycerides	57-72	NLR family pyrin domain containing 3	Homo sapiens	77-81
9765239-11	1998	The Vmax for phospholipid hydrolysis was, by contrast, greater for (A-I/CE)rHDL than for (A-II/CE)rHDL: 309.3 versus 49.1 nmol of NEFA formed/ml of HL/h.	Phospholipids	13-25	NLR family pyrin domain containing 3	Homo sapiens	90-94
9765239-12	1998	Comparable Vmax values were obtained for the hydrolysis of the phospholipids in (A-II/TG)rHDL and (A-I/TG)rHDL.	Phospholipids	63-76	NLR family pyrin domain containing 3	Homo sapiens	81-85
10322661-6	1998	However, the addition of HDL, and apoA I, A II, C I and C II before incubation with LDL inhibited the cellular injury induced by LDL as demonstrated by lowered LDH release, increased level of PGF1 alpha and prevention of morphological changes.	prostaglandin F1	192-196	NLR family pyrin domain containing 3	Homo sapiens	42-46
9765239-13	1998	In the case of triacylglycerol hydrolysis, the respective Vmax values for (A-I/TG)rHDL and (A-II/TG)rHDL were 1154.8 and 240.2 nmol of NEFA formed/ml of HL/h.	Triglycerides	15-30	NLR family pyrin domain containing 3	Homo sapiens	92-96
9765239-13	1998	In the case of triacylglycerol hydrolysis, the respective Vmax values for (A-I/TG)rHDL and (A-II/TG)rHDL were 1154.8 and 240.2 nmol of NEFA formed/ml of HL/h.	Fatty Acids, Nonesterified	135-139	NLR family pyrin domain containing 3	Homo sapiens	92-96
9665867-2	1998	The homologous coupling of both horizontal cells and rod (AII) amacrine cells is reduced by dopamine, but there appear to be cell and species differences in how the ambient illumination interacts with the dopaminergic system to modulate the coupling.	Dopamine	92-100	NLR family pyrin domain containing 3	Homo sapiens	58-61
9665867-3	1998	Both the homologous coupling of horizontal cells and the heterologous coupling between AII amacrine cells and cone bipolar cells are reduced by nitric oxide, but it is not known if changes in illumination modulate coupling through an endogenous nitrergic mechanism.	Nitric Oxide	144-156	NLR family pyrin domain containing 3	Homo sapiens	87-90
9568641-2	1998	In the present study we examined the effects of antiestrogens [Analog II (1,1-dichloro-cis-2,3-diphenyl cyclopropane) (AII), ICI-182,780 (ICI) and tamoxifen (TAM)], on the in vitro release of uPA from estrogen receptor (ER)-positive MCF-7 (MCF) and ER-negative MDA-MB-231 (MDA) human breast cancer cell lines.	1,1-dichloro-cis-2,3-diphenyl cyclopropane	74-116	NLR family pyrin domain containing 3	Homo sapiens	119-122
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	ESS	35-38	NLR family pyrin domain containing 3	Homo sapiens	49-52
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	ESS	35-38	NLR family pyrin domain containing 3	Homo sapiens	49-52
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	Cholesterol	216-227	NLR family pyrin domain containing 3	Homo sapiens	27-30
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	ESS	278-281	NLR family pyrin domain containing 3	Homo sapiens	27-30
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	ESS	278-281	NLR family pyrin domain containing 3	Homo sapiens	49-52
9535417-4	1998	In normal adults, lower LV MWS and ESS-corrected MWS, an index of LV contractility, were related independently to high total peripheral resistance, high heart rate, and male gender (all P&lt;.00001), lower serum HDL cholesterol (P=.001) and diastolic pressure (P=.003), and for ESS-corrected MWS only, arterial relative wall thickness (RWT, P=.03).	ESS	278-281	NLR family pyrin domain containing 3	Homo sapiens	49-52
9535417-7	1998	Lower ESS-corrected MWS in the entire population was independently associated with higher peripheral resistance and heart rate (both P&lt;.00001), body mass index (P=.0006), arterial RWT (P=.004); male gender; and lower diastolic pressure (both P&lt;.00001), age (P&lt;.00005), arterial expansion in systole (P=.006), and serum HDL cholesterol levels (P=.04).	Cholesterol	332-343	NLR family pyrin domain containing 3	Homo sapiens	20-23
9535417-8	1998	Among a subset (n=60), ESS-corrected MWS was positively related to apolipoprotein A1 (P=.004) and negatively to hemoglobin A1c (P&lt;.01).	ESS	23-26	NLR family pyrin domain containing 3	Homo sapiens	37-40
9497326-2	1998	Evidence for direct reduction of lipid hydroperoxides by methionine residues of apolipoproteins AI and AII.	Lipid Peroxides	33-53	NLR family pyrin domain containing 3	Homo sapiens	80-106
9497326-2	1998	Evidence for direct reduction of lipid hydroperoxides by methionine residues of apolipoproteins AI and AII.	Methionine	57-67	NLR family pyrin domain containing 3	Homo sapiens	80-106
9513926-3	1997	Ouabain itself at high concentration (10(-5) M) in Mg++ buffer blocks AII action on aldosterone secretion on rat ZG cells and at 1000-fold lower concentrations inhibits AII-action in human cells as previously reported by us.	Magnesium	51-55	NLR family pyrin domain containing 3	Homo sapiens	70-73
9686347-10	1998	The evidence for the role of AII in nitric oxide and polyamine metabolism is presented and this appears consonant with the data on the tissue distribution.	Nitric Oxide	36-48	NLR family pyrin domain containing 3	Homo sapiens	29-32
9686347-10	1998	The evidence for the role of AII in nitric oxide and polyamine metabolism is presented and this appears consonant with the data on the tissue distribution.	Polyamines	53-62	NLR family pyrin domain containing 3	Homo sapiens	29-32
9513926-5	1997	High Mg++ buffer had this effect at both 10(-8) and 10(-7) M concentrations of ouabain (control 8.6 +/- 0.4, AII [10(-9) M] 13.9 +/- 0.7, AII + Ouabain [5 x 10(-8) M] 10.9 +/- 0.6, AII + ouabain [10(-7) M] 7.8 +/- 0.3 ng/10(6) cells/h, both p &lt; 0.01 vs. AII).	Magnesium	5-9	NLR family pyrin domain containing 3	Homo sapiens	109-112
9513926-5	1997	High Mg++ buffer had this effect at both 10(-8) and 10(-7) M concentrations of ouabain (control 8.6 +/- 0.4, AII [10(-9) M] 13.9 +/- 0.7, AII + Ouabain [5 x 10(-8) M] 10.9 +/- 0.6, AII + ouabain [10(-7) M] 7.8 +/- 0.3 ng/10(6) cells/h, both p &lt; 0.01 vs. AII).	Magnesium	5-9	NLR family pyrin domain containing 3	Homo sapiens	138-141
9513926-5	1997	High Mg++ buffer had this effect at both 10(-8) and 10(-7) M concentrations of ouabain (control 8.6 +/- 0.4, AII [10(-9) M] 13.9 +/- 0.7, AII + Ouabain [5 x 10(-8) M] 10.9 +/- 0.6, AII + ouabain [10(-7) M] 7.8 +/- 0.3 ng/10(6) cells/h, both p &lt; 0.01 vs. AII).	Magnesium	5-9	NLR family pyrin domain containing 3	Homo sapiens	138-141
9513926-4	1997	When buffer Mg++ is higher (4mM) than normal (0.7 mM) in cultured human adrenal cells it decreases both basal aldosterone secretion (8.6 +/- 0.4 vs. 6.8 +/- 0.2, p &lt; 0.001) and AII action on aldosterone (13.9 +/- 0.6 vs. 9.7 +/- 0.7 ng/10(6) cells/h, p &lt; 0.01).	Magnesium	12-16	NLR family pyrin domain containing 3	Homo sapiens	180-183
9513926-5	1997	High Mg++ buffer had this effect at both 10(-8) and 10(-7) M concentrations of ouabain (control 8.6 +/- 0.4, AII [10(-9) M] 13.9 +/- 0.7, AII + Ouabain [5 x 10(-8) M] 10.9 +/- 0.6, AII + ouabain [10(-7) M] 7.8 +/- 0.3 ng/10(6) cells/h, both p &lt; 0.01 vs. AII).	Magnesium	5-9	NLR family pyrin domain containing 3	Homo sapiens	138-141
9513926-6	1997	In contrast, a low Mg++ buffer stimulated both basal (6.9 +/- 0.2 vs. 8.3 +/- 0.4 ng/10(6) cells/h, p &lt; 0.01) and AII stimulation of aldosterone secretion (8.4 +/- 0.2 vs. 9.8 +/- 0.4 ng/10(6) cells/h, p &lt; 0.01).	Magnesium	19-23	NLR family pyrin domain containing 3	Homo sapiens	117-120
9438215-6	1997	The levels of PRA, AI, AII, and Aldo were also clearly decreased in women with TPH, whereas those values in normotensive women were not altered from nonpregnant levels.	tph	79-82	NLR family pyrin domain containing 3	Homo sapiens	23-26
9513926-6	1997	In contrast, a low Mg++ buffer stimulated both basal (6.9 +/- 0.2 vs. 8.3 +/- 0.4 ng/10(6) cells/h, p &lt; 0.01) and AII stimulation of aldosterone secretion (8.4 +/- 0.2 vs. 9.8 +/- 0.4 ng/10(6) cells/h, p &lt; 0.01).	Aldosterone	136-147	NLR family pyrin domain containing 3	Homo sapiens	117-120
9513926-7	1997	When ouabain was added to low Mg++ buffer there was further inhibition of AII induced aldosterone secretion than with normal Mg++ buffer.	Ouabain	5-12	NLR family pyrin domain containing 3	Homo sapiens	74-77
9513926-7	1997	When ouabain was added to low Mg++ buffer there was further inhibition of AII induced aldosterone secretion than with normal Mg++ buffer.	Magnesium	30-34	NLR family pyrin domain containing 3	Homo sapiens	74-77
9513926-9	1997	We conclude that ouabain actions and the effect of angiotensin II on aldosterone is inhibited by an increased level of Mg++ while low levels of Mg++ are stimulatory to both basal and AII action on aldosterone.	Magnesium	144-148	NLR family pyrin domain containing 3	Homo sapiens	183-186
9219896-1	1997	The complexes of individual human plasma apolipoproteins (apo) A-I, E and A-II with dipalmitoylphosphatidylcholine (DPPC) in the absence or in the presence of cholesterol (Chol) were prepared with initial DPPC/Chol/protein weight ratio as 3:0.15:1.	1,2-Dipalmitoylphosphatidylcholine	116-120	NLR family pyrin domain containing 3	Homo sapiens	74-78
9249242-16	1997	In the presence of enalaprilat (100 microM), carboxypeptidase inhibitor CPI (10 microg ml(-1)) and aprotinin (15 microM), CH 5450 (10 nM-1 microM) caused a concentration-dependent inhibition of AII formation.	Enalaprilat	19-30	NLR family pyrin domain containing 3	Homo sapiens	194-197
9219896-1	1997	The complexes of individual human plasma apolipoproteins (apo) A-I, E and A-II with dipalmitoylphosphatidylcholine (DPPC) in the absence or in the presence of cholesterol (Chol) were prepared with initial DPPC/Chol/protein weight ratio as 3:0.15:1.	1,2-Dipalmitoylphosphatidylcholine	84-114	NLR family pyrin domain containing 3	Homo sapiens	74-78
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-oxidanyl-4-phosphonooxy-oxolan-2-yl]methoxy-oxidanyl-phosphoryl] [(2R,3S,4R,5S)-3,4,5-tris(oxidanyl)oxolan-2-yl]methyl hydrogen phosphate	21-24	NLR family pyrin domain containing 3	Homo sapiens	39-42
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-oxidanyl-4-phosphonooxy-oxolan-2-yl]methoxy-oxidanyl-phosphoryl] [(2R,3S,4R,5S)-3,4,5-tris(oxidanyl)oxolan-2-yl]methyl hydrogen phosphate	21-24	NLR family pyrin domain containing 3	Homo sapiens	130-133
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-oxidanyl-4-phosphonooxy-oxolan-2-yl]methoxy-oxidanyl-phosphoryl] [(2R,3S,4R,5S)-3,4,5-tris(oxidanyl)oxolan-2-yl]methyl hydrogen phosphate	69-72	NLR family pyrin domain containing 3	Homo sapiens	39-42
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-oxidanyl-4-phosphonooxy-oxolan-2-yl]methoxy-oxidanyl-phosphoryl] [(2R,3S,4R,5S)-3,4,5-tris(oxidanyl)oxolan-2-yl]methyl hydrogen phosphate	69-72	NLR family pyrin domain containing 3	Homo sapiens	130-133
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	Losartan	96-104	NLR family pyrin domain containing 3	Homo sapiens	39-42
9406969-4	1997	All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT1) receptor antagonist.	Losartan	96-104	NLR family pyrin domain containing 3	Homo sapiens	130-133
9219896-15	1997	Based on these results, the degree of Chol exclusion from the boundary lipid region for complexes with different apo"s increasing in the order A-II &gt; E &gt; A-I can be suggested.	Cholesterol	38-42	NLR family pyrin domain containing 3	Homo sapiens	143-147
9219896-5	1997	Chol seems to be excluded partially in the following manner for isolated complexes with different apo"s: A-II &gt; E &gt; A-I.	Cholesterol	0-4	NLR family pyrin domain containing 3	Homo sapiens	105-109
9192192-5	1997	RESULTS: Both LpA-I and LpA-I:A-II were significantly higher in men drinking more than 30 g a day of alcohol than in non-drinkers (LpA-I: difference between means 6.5 mg/dL, 95% C.I.	Alcohols	101-108	NLR family pyrin domain containing 3	Homo sapiens	30-34
9192192-8	1997	The association of alcohol consumption with LpA-I and LpA-I:A-II levels was independent from age, body mass index, physical activity, serum triglycerides and diet composition.	Alcohols	19-26	NLR family pyrin domain containing 3	Homo sapiens	60-64
9192192-9	1997	CONCLUSIONS: Alcohol consumption is associated with an increase of serum levels of both LpA-I and LpA-I:A-II particles and this may, at least in part, explain the reduced cardiovascular morbidity observed in subjects drinking moderate amounts of alcoholic beverages.	Alcohols	13-20	NLR family pyrin domain containing 3	Homo sapiens	104-108
9125302-8	1996	In conclusion, reduced HDL cholesterol levels found in NIDDM are, principally, due to reduced concentrations of apo A-I and apo A-II-containing particles (LpAI/AII).	Cholesterol	27-38	NLR family pyrin domain containing 3	Homo sapiens	128-132
9216636-3	1997	We have recently shown that AII and its major metabolite Z-alpha-chlorochalcone (ZCC) inhibit proliferation of both estrogen-responsive and -nonresponsive human breast cancer cells, suggesting its mechanism is not mediated by the type I estrogen receptor (ER).	2-chloro-1,3-diphenyl-2-propen-1-one	57-79	NLR family pyrin domain containing 3	Homo sapiens	28-31
9216636-3	1997	We have recently shown that AII and its major metabolite Z-alpha-chlorochalcone (ZCC) inhibit proliferation of both estrogen-responsive and -nonresponsive human breast cancer cells, suggesting its mechanism is not mediated by the type I estrogen receptor (ER).	2-chloro-1,3-diphenyl-2-propen-1-one	81-84	NLR family pyrin domain containing 3	Homo sapiens	28-31
9389149-4	1996	It was also found that the high concentration of A II may stimulate the adrenal gland secreting glucosteroid, and increase of tissue A II may be faciliated by the activation of beta adrenergic receptors.	glucosteroid	96-108	NLR family pyrin domain containing 3	Homo sapiens	49-53
8816069-6	1996	Decreases in LpAI levels were more slightly in patients with hepatic or renal diseases than those in LpAI:AII levels.	lpai	101-105	NLR family pyrin domain containing 3	Homo sapiens	106-109
8694526-6	1996	In this study an increased [Gly]/[Cr + PCr] ratio was observed in GM with respect to AII and AA.	Glycine	28-31	NLR family pyrin domain containing 3	Homo sapiens	85-88
8702221-6	1996	AII underwent slow solvolysis in culture medium to Z-2-chloro-1,3-diphenyl-2-propen-1-ol and its oxidized form Z-alpha-chlorochalcone (ZCC).	z-2-chloro-1,3-diphenyl-2-propen-1-ol	51-88	NLR family pyrin domain containing 3	Homo sapiens	0-3
8702221-6	1996	AII underwent slow solvolysis in culture medium to Z-2-chloro-1,3-diphenyl-2-propen-1-ol and its oxidized form Z-alpha-chlorochalcone (ZCC).	2-chloro-1,3-diphenyl-2-propen-1-one	111-133	NLR family pyrin domain containing 3	Homo sapiens	0-3
8702221-6	1996	AII underwent slow solvolysis in culture medium to Z-2-chloro-1,3-diphenyl-2-propen-1-ol and its oxidized form Z-alpha-chlorochalcone (ZCC).	2-chloro-1,3-diphenyl-2-propen-1-one	135-138	NLR family pyrin domain containing 3	Homo sapiens	0-3
8702221-7	1996	ZCC was the major metabolite of AII in all three cell lines.	2-chloro-1,3-diphenyl-2-propen-1-one	0-3	NLR family pyrin domain containing 3	Homo sapiens	32-35
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	0-13	NLR family pyrin domain containing 3	Homo sapiens	67-71
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	0-13	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	0-13	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	15-17	NLR family pyrin domain containing 3	Homo sapiens	67-71
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	15-17	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	15-17	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	105-107	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-2	1996	Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes.	Tretinoin	105-107	NLR family pyrin domain containing 3	Homo sapiens	120-124
8668150-11	1996	In conclusion, retinoids induce hepatic apo A-II production at the transcriptional level via the interaction of RXR with an element in the J site containing two imperfect half-sites spaced by 1 oligonucleotide, thereby demonstrating an important role of RXR in controlling human lipoprotein metabolism.	Retinoids	15-24	NLR family pyrin domain containing 3	Homo sapiens	44-48
8668150-12	1996	Since the J site also confers responsiveness of the apo A-II gene to fibrates and fatty acids via the activation of peroxisome proliferator-activated receptor-RXR heterodimers, this site can be considered a plurimetabolic response element.	Fatty Acids	82-93	NLR family pyrin domain containing 3	Homo sapiens	56-60
9125302-8	1996	In conclusion, reduced HDL cholesterol levels found in NIDDM are, principally, due to reduced concentrations of apo A-I and apo A-II-containing particles (LpAI/AII).	Cholesterol	27-38	NLR family pyrin domain containing 3	Homo sapiens	155-163
7477263-5	1995	We found that neurobiotin (relative molecular mass, 286) passed easily through both types of gap junctions, but that biotin-X cadaverine (relative molecular mass, 442) passed through AII/bipolar cell gap junctions poorly compared to AII/AII gap junctions.	biotin-x cadaverine	117-136	NLR family pyrin domain containing 3	Homo sapiens	183-186
8829821-5	1996	The subsequent addition of nifedipine, nicardipine, and amlodipine reversed the afferent arteriolar vasoconstriction in a dose-dependent manner, and elicited complete vasodilation at 10(-6) M. In contrast, efferent arteriolar vasoconstriction was relatively refractory to the dilator action of these calcium antagonists; maximal dilation observed at 10(-6) M was 21 +/- 1% (A-II) and 22 +/- 3% (NE) for nifedipine, 25 +/- 3% (A-II) and 20 +/- 6% (NE) for nicardipine, and 39 +/- 6% (A-II) and 37 +/- 3% (NE) for amlodipine.	Nifedipine	27-37	NLR family pyrin domain containing 3	Homo sapiens	426-438
8829821-5	1996	The subsequent addition of nifedipine, nicardipine, and amlodipine reversed the afferent arteriolar vasoconstriction in a dose-dependent manner, and elicited complete vasodilation at 10(-6) M. In contrast, efferent arteriolar vasoconstriction was relatively refractory to the dilator action of these calcium antagonists; maximal dilation observed at 10(-6) M was 21 +/- 1% (A-II) and 22 +/- 3% (NE) for nifedipine, 25 +/- 3% (A-II) and 20 +/- 6% (NE) for nicardipine, and 39 +/- 6% (A-II) and 37 +/- 3% (NE) for amlodipine.	Nicardipine	39-50	NLR family pyrin domain containing 3	Homo sapiens	426-438
8829821-5	1996	The subsequent addition of nifedipine, nicardipine, and amlodipine reversed the afferent arteriolar vasoconstriction in a dose-dependent manner, and elicited complete vasodilation at 10(-6) M. In contrast, efferent arteriolar vasoconstriction was relatively refractory to the dilator action of these calcium antagonists; maximal dilation observed at 10(-6) M was 21 +/- 1% (A-II) and 22 +/- 3% (NE) for nifedipine, 25 +/- 3% (A-II) and 20 +/- 6% (NE) for nicardipine, and 39 +/- 6% (A-II) and 37 +/- 3% (NE) for amlodipine.	Amlodipine	56-66	NLR family pyrin domain containing 3	Homo sapiens	426-438
8829821-7	1996	At 10(-6) M, efonidipine completely inhibited the afferent (A-II, 89 +/- 7% reversal; NE, 99 +/- 8% reversal) and efferent arteriolar vasoconstriction (A-II, 93 +/- 4% reversal; NE, 87 +/- 9% reversal).	efonidipine	13-24	NLR family pyrin domain containing 3	Homo sapiens	152-160
8740244-7	1996	A decrease in the plasma level of apolipoprotein B and of LDL-apo B, but not of VLDL-apo B, was observed during pravastatin therapy; the plasma apolipoprotein AI and AII levels, as well as HDL2- and HDL3-apo AI and apo AII levels, however, remained unchanged.	Pravastatin	112-123	NLR family pyrin domain containing 3	Homo sapiens	166-169
8550898-3	1995	AII cells of the monkey retina were stained immunocytochemically with antibodies against the calcium-binding protein calretinin.	Calcium	93-100	NLR family pyrin domain containing 3	Homo sapiens	0-3
7670941-13	1995	Our data are consistent with the concept that a low HDL cholesterol level in subjects heterozygous for the apoA-IHelsinki mutation (Lys107-->0) having normal LCAT activity is a consequence of decreased concentration of LpA-I:A-II particles and of a smaller size and reduced cholesterol content of HDL particles.	Cholesterol	56-67	NLR family pyrin domain containing 3	Homo sapiens	225-229
7635967-3	1995	This increase in plasma apo A-II was due to a direct effect on hepatic apo A-II production, since fenofibric acid induced apo A-II mRNA levels to 450 and 250% of control levels in primary cultures of human hepatocytes and in human hepatoblastoma HepG2 cells respectively.	fenofibric acid	98-113	NLR family pyrin domain containing 3	Homo sapiens	75-79
8566314-0	1995	Tyrosine phosphorylation, MAPK and PLD in AII stimulated mitogenesis.	Tyrosine	0-8	NLR family pyrin domain containing 3	Homo sapiens	42-45
7635967-2	1995	Administration of fenofibrate (300 mg/d) to 16 patients with coronary artery disease resulted in a marked increase in plasma apo A-II concentrations (0.34 +/- 0.11 to 0.45 +/- 0.17 grams/liter; P &lt; 0.01).	Fenofibrate	18-29	NLR family pyrin domain containing 3	Homo sapiens	129-133
7635967-5	1995	Transient transfection experiments of a reporter construct driven by the human apo A-II gene promoter indicated that fenofibrate induced apo A-II gene expression at the transcriptional level.	Fenofibrate	117-128	NLR family pyrin domain containing 3	Homo sapiens	83-87
7619858-7	1995	However, when apo A-I or apo A-IV protein concentration was kept constant and supplemented with apo A-II, a lower [3H]FC efflux was found only at 1:3 M/M of apo A-I/A-II.	Tritium	115-117	NLR family pyrin domain containing 3	Homo sapiens	100-104
7635967-3	1995	This increase in plasma apo A-II was due to a direct effect on hepatic apo A-II production, since fenofibric acid induced apo A-II mRNA levels to 450 and 250% of control levels in primary cultures of human hepatocytes and in human hepatoblastoma HepG2 cells respectively.	fenofibric acid	98-113	NLR family pyrin domain containing 3	Homo sapiens	28-32
7619858-11	1995	The cellular uptake of [3H]FC was higher when apo A-II had been added to apo A-I or apo A-IV than when the apolipoproteins were added alone.	Tritium	24-26	NLR family pyrin domain containing 3	Homo sapiens	50-54
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Tritium	6-8	NLR family pyrin domain containing 3	Homo sapiens	93-97
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Tritium	6-8	NLR family pyrin domain containing 3	Homo sapiens	162-166
7619858-12	1995	In conclusion, apo A-II was found to be less effective in cholesterol efflux and to interfere with the action of A-I only when the cholesterol donors were macrophages and when the relative amount of apo A-I to apo A-II was low.	Cholesterol	58-69	NLR family pyrin domain containing 3	Homo sapiens	19-23
7619858-12	1995	In conclusion, apo A-II was found to be less effective in cholesterol efflux and to interfere with the action of A-I only when the cholesterol donors were macrophages and when the relative amount of apo A-I to apo A-II was low.	Cholesterol	131-142	NLR family pyrin domain containing 3	Homo sapiens	19-23
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Fc(alpha) receptor	9-11	NLR family pyrin domain containing 3	Homo sapiens	93-97
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Fc(alpha) receptor	9-11	NLR family pyrin domain containing 3	Homo sapiens	162-166
7588378-3	1995	Treatment of H295R cells with forskolin or dbcAMP to activate the protein kinase A pathway caused a rapid (maximal by 3 h) and sustained decrease in AT1-R mRNA levels which in turn preceded a time-dependent (maximal by 12 h) and dose-dependent loss of [125I]AII binding and phosphoinositidase C activation on subsequent AII challenge.	Colforsin	30-39	NLR family pyrin domain containing 3	Homo sapiens	258-261
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Tritium	122-124	NLR family pyrin domain containing 3	Homo sapiens	93-97
7619858-5	1995	When [3H]FC labeled MP were incubated for 2 or 4 h with equimolar concentrations of apo A-I, A-II, A-IV or E, the lowest [3H]cholesterol efflux occurred with apo A-II.	Cholesterol	125-136	NLR family pyrin domain containing 3	Homo sapiens	93-97
7619858-6	1995	Exposure of [3H]FC MP to liposomes containing apo A-I/A-II at 1:2 M/M (keeping the total protein concentration at 50 micrograms/ml), resulted in a lower [3H]FC efflux as compared to apo A-I alone.	Tritium	13-15	NLR family pyrin domain containing 3	Homo sapiens	54-58
7619858-6	1995	Exposure of [3H]FC MP to liposomes containing apo A-I/A-II at 1:2 M/M (keeping the total protein concentration at 50 micrograms/ml), resulted in a lower [3H]FC efflux as compared to apo A-I alone.	Tritium	154-156	NLR family pyrin domain containing 3	Homo sapiens	54-58
7562885-6	1995	A decrease in the plasma level of apolipoprotein B and of LDL-apo B, but not of VLDL-apo B, was observed during pravastatin therapy; the plasma apolipoprotein AI and AII levels as well as HDL2- and HDL3-apo AI and apo AII levels remained, however, unchanged.	Pravastatin	112-123	NLR family pyrin domain containing 3	Homo sapiens	166-169
7562885-6	1995	A decrease in the plasma level of apolipoprotein B and of LDL-apo B, but not of VLDL-apo B, was observed during pravastatin therapy; the plasma apolipoprotein AI and AII levels as well as HDL2- and HDL3-apo AI and apo AII levels remained, however, unchanged.	Pravastatin	112-123	NLR family pyrin domain containing 3	Homo sapiens	218-221
7652193-1	1995	The presence of specific AII receptors in 6 different human neuroblastoma cell lines was investigated using binding, cAMP and [Ca2+]i studies.	Cyclic AMP	117-121	NLR family pyrin domain containing 3	Homo sapiens	25-28
7652193-4	1995	The presence of AT1 receptors was further substantiated by AII-induced inhibition of VIP-stimulated cAMP levels and by AII-evoked [Ca2+]i transient.	Cyclic AMP	100-104	NLR family pyrin domain containing 3	Homo sapiens	59-62
7629811-7	1995	Finally, various novel AII antagonists having dibenzo[a,d]cycloheptene or dibenzo[b,f]oxepin were designed and synthesized.	5H-Dibenzo[a,d]cycloheptene	46-70	NLR family pyrin domain containing 3	Homo sapiens	23-26
7629811-7	1995	Finally, various novel AII antagonists having dibenzo[a,d]cycloheptene or dibenzo[b,f]oxepin were designed and synthesized.	dibenzo[b,f]oxepin	74-92	NLR family pyrin domain containing 3	Homo sapiens	23-26
8582103-10	1995	Slightly but significantly reduced plasma cortisol levels observed in the AII-R APA group may reflect secretion by AII-R APA of a cortisol-like substance that is capable of suppressing ACTH and thus adrenal cortisol production.	Hydrocortisone	42-50	NLR family pyrin domain containing 3	Homo sapiens	74-77
8582103-10	1995	Slightly but significantly reduced plasma cortisol levels observed in the AII-R APA group may reflect secretion by AII-R APA of a cortisol-like substance that is capable of suppressing ACTH and thus adrenal cortisol production.	Hydrocortisone	42-50	NLR family pyrin domain containing 3	Homo sapiens	115-118
8582103-12	1995	The tendency of aldosterone to follow the diurnal rhythm of ACTH in AII-U APA may thus represent an unmasking of the normal ability of ACTH to regulate aldosterone, secondary to the loss of AII responsiveness, rather than an enhancement of ACTH effect.	Aldosterone	16-27	NLR family pyrin domain containing 3	Homo sapiens	68-71
7588378-3	1995	Treatment of H295R cells with forskolin or dbcAMP to activate the protein kinase A pathway caused a rapid (maximal by 3 h) and sustained decrease in AT1-R mRNA levels which in turn preceded a time-dependent (maximal by 12 h) and dose-dependent loss of [125I]AII binding and phosphoinositidase C activation on subsequent AII challenge.	Colforsin	30-39	NLR family pyrin domain containing 3	Homo sapiens	320-323
7588378-3	1995	Treatment of H295R cells with forskolin or dbcAMP to activate the protein kinase A pathway caused a rapid (maximal by 3 h) and sustained decrease in AT1-R mRNA levels which in turn preceded a time-dependent (maximal by 12 h) and dose-dependent loss of [125I]AII binding and phosphoinositidase C activation on subsequent AII challenge.	Bucladesine	43-49	NLR family pyrin domain containing 3	Homo sapiens	258-261
7588378-3	1995	Treatment of H295R cells with forskolin or dbcAMP to activate the protein kinase A pathway caused a rapid (maximal by 3 h) and sustained decrease in AT1-R mRNA levels which in turn preceded a time-dependent (maximal by 12 h) and dose-dependent loss of [125I]AII binding and phosphoinositidase C activation on subsequent AII challenge.	Bucladesine	43-49	NLR family pyrin domain containing 3	Homo sapiens	320-323
7588378-5	1995	The effect of AII, but not forskolin, was blocked by the presence of cycloheximide.	Cycloheximide	69-82	NLR family pyrin domain containing 3	Homo sapiens	14-17
7588378-6	1995	The action of AII on AT1-R mRNA was probably mediated through both protein kinase C and Ca(2+)-sensitive protein kinases as the effect at 4 h was not completely reproduced by phorbol ester alone, but was fully reproduced by a combination of phorbol ester and Ca2+ ionophore.	Phorbol Esters	175-188	NLR family pyrin domain containing 3	Homo sapiens	14-17
7588378-6	1995	The action of AII on AT1-R mRNA was probably mediated through both protein kinase C and Ca(2+)-sensitive protein kinases as the effect at 4 h was not completely reproduced by phorbol ester alone, but was fully reproduced by a combination of phorbol ester and Ca2+ ionophore.	Phorbol Esters	241-254	NLR family pyrin domain containing 3	Homo sapiens	14-17
7484424-6	1995	Other potential important cellular effects of AII in these systems include: 1) stimulation of growth factors, cytokines, and arachidonic acid products that could have autocrine or paracrine effects, 2) regulation of cell migration and adhesion, 3) alteration of responses to neurohormones, 4) development and maintenance of a differentiated phenotype, and others.	Arachidonic Acid	125-141	NLR family pyrin domain containing 3	Homo sapiens	46-49
7813085-3	1995	There is evidence for an antagonizing role of apo AII in reverse cholesterol transport.	Cholesterol	65-76	NLR family pyrin domain containing 3	Homo sapiens	50-53
8882516-7	1995	In a subsequent test, injections of synthetic AII and AII-amide (peptide recently isolated from an achaete (Salzet et al (1995) J Biol Chem 270, 1575-1582) enhanced the increase in body weight and, therefore, strengthened the hypothesis of the neuroendocrine control of Nereis osmoregulation.	Amides	58-63	NLR family pyrin domain containing 3	Homo sapiens	54-57
7721047-2	1994	AI and AII induced contractions in cat femoral arteries, which were inhibited by saralasin.	Saralasin	81-90	NLR family pyrin domain containing 3	Homo sapiens	7-10
7721047-6	1994	AII contractions were increased by indomethacin, L-NAME and endothelium removal.	Indomethacin	35-47	NLR family pyrin domain containing 3	Homo sapiens	0-3
7721047-6	1994	AII contractions were increased by indomethacin, L-NAME and endothelium removal.	NG-Nitroarginine Methyl Ester	49-55	NLR family pyrin domain containing 3	Homo sapiens	0-3
7721047-11	1994	These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.	Epoprostenol	214-218	NLR family pyrin domain containing 3	Homo sapiens	129-132
7721047-11	1994	These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.	Epoprostenol	214-218	NLR family pyrin domain containing 3	Homo sapiens	129-132
7721047-11	1994	These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.	Epoprostenol	214-218	NLR family pyrin domain containing 3	Homo sapiens	129-132
7721047-11	1994	These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.	Epoprostenol	214-218	NLR family pyrin domain containing 3	Homo sapiens	129-132
7806972-8	1994	Stepwise regression analysis revealed a significant correlation between postprandial lipemia and the increase in triglyceride concentration only of LpAI,AII within HDL3.	Triglycerides	113-125	NLR family pyrin domain containing 3	Homo sapiens	153-156
7869853-13	1994	The apo A-II content of fraction B was related to the mobilization of cholesteryl esters.	Cholesterol Esters	70-88	NLR family pyrin domain containing 3	Homo sapiens	8-12
8172070-6	1994	The discovery of simple benzyl-substituted imidazoles, which possess weak but highly selective A-II receptor antagonistic properties, led to the development of losartan (DuP 753).	benzyl-substituted imidazoles	24-53	NLR family pyrin domain containing 3	Homo sapiens	95-99
8194473-3	1994	This preceded a time-dependent (maximal, 70% within 12 h) and dose-dependent (IC50, 2 microM forskolin) loss of [125I]AII binding together with decreased phosphoinositidase-C activation (72% decrease) on subsequent AII challenge.	Colforsin	93-102	NLR family pyrin domain containing 3	Homo sapiens	118-121
8194473-3	1994	This preceded a time-dependent (maximal, 70% within 12 h) and dose-dependent (IC50, 2 microM forskolin) loss of [125I]AII binding together with decreased phosphoinositidase-C activation (72% decrease) on subsequent AII challenge.	Colforsin	93-102	NLR family pyrin domain containing 3	Homo sapiens	215-218
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Calcium	82-89	NLR family pyrin domain containing 3	Homo sapiens	14-17
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Calcimycin	101-107	NLR family pyrin domain containing 3	Homo sapiens	14-17
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Calcimycin	101-107	NLR family pyrin domain containing 3	Homo sapiens	183-186
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Phorbol Esters	113-126	NLR family pyrin domain containing 3	Homo sapiens	14-17
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Tetradecanoylphorbol Acetate	128-164	NLR family pyrin domain containing 3	Homo sapiens	14-17
8194473-6	1994	The effect of AII on AT1-R mRNA levels was fully reproduced by the combination of calcium ionophore (A23187) and phorbol ester (12-O-tetradecanoylphorbol 13-acetate), suggesting that AII action was through protein kinase-C and possibly other Ca(2+)-sensitive protein kinases.	Tetradecanoylphorbol Acetate	128-164	NLR family pyrin domain containing 3	Homo sapiens	183-186
8194473-7	1994	The effect of AII, but not forskolin, was reversed by treatment in the presence of cycloheximide.	Cycloheximide	83-96	NLR family pyrin domain containing 3	Homo sapiens	14-17
8077854-2	1994	It appeared that the ability of apoA-I, A-II, and A-IV to modulate the CETP-mediated transfer of radiolabeled cholesteryl esters between low density lipoproteins (LDL) and high density lipoproteins (HDL) was markedly influenced by the final apolipoprotein:lipoprotein ratio in incubation mixtures.	Cholesterol Esters	110-128	NLR family pyrin domain containing 3	Homo sapiens	40-44
8077854-13	1994	In conclusion, data from the present study indicate that apolipoproteins A-I, A-II, and A-IV could be potent modulators of the CETP-mediated transfer of cholesteryl esters between HDL and LDL fractions.	Cholesterol Esters	153-171	NLR family pyrin domain containing 3	Homo sapiens	78-82
8172070-6	1994	The discovery of simple benzyl-substituted imidazoles, which possess weak but highly selective A-II receptor antagonistic properties, led to the development of losartan (DuP 753).	Losartan	160-168	NLR family pyrin domain containing 3	Homo sapiens	95-99
8172070-6	1994	The discovery of simple benzyl-substituted imidazoles, which possess weak but highly selective A-II receptor antagonistic properties, led to the development of losartan (DuP 753).	Losartan	170-177	NLR family pyrin domain containing 3	Homo sapiens	95-99
8172070-7	1994	Losartan is a potent, orally active, specific, competitive nonpeptide A-II receptor antagonist that appears to be an effective antihypertensive agent both in animal studies and in preliminary clinical trials.	Losartan	0-8	NLR family pyrin domain containing 3	Homo sapiens	70-74
8172070-10	1994	Furthermore, losartan, a selective A-II type 1 (AT1) receptor antagonist, has also been a valuable pharmacologic probe for studying the mechanism of A-II stimulation of its receptors.	Losartan	13-21	NLR family pyrin domain containing 3	Homo sapiens	35-39
8172070-10	1994	Furthermore, losartan, a selective A-II type 1 (AT1) receptor antagonist, has also been a valuable pharmacologic probe for studying the mechanism of A-II stimulation of its receptors.	Losartan	13-21	NLR family pyrin domain containing 3	Homo sapiens	149-153
1464753-8	1992	The concentrations of apoA-I, A-II, A-IV, E, and Cs that promoted half-maximal efflux of phospholipid from cholesterol-enriched fibroblasts were 53, 30, 68, 137, and 594 nM, respectively.	Phospholipids	89-101	NLR family pyrin domain containing 3	Homo sapiens	30-34
8069242-1	1994	The relative binding affinities of non-peptide antagonists, and the sensitivity of 125I-angiotensin II (125I-AII) binding to the reducing agent, dithiothreitol, indicated the presence of AT1 angiotensin receptors on RIE-1 rat intestinal epithelial cells.	Dithiothreitol	145-159	NLR family pyrin domain containing 3	Homo sapiens	109-112
8245722-4	1993	Of particular interest was the demonstration of the existence of the disulfide-linked species apolipoprotein B-100:A-II and B-100:C-IIToronto in the very low density and low density lipoproteins in subjects who were carriers of apoC-IIToronto.	Disulfides	69-78	NLR family pyrin domain containing 3	Homo sapiens	115-119
8477848-4	1993	These AT1 receptors are functional since A-II was able to increase cortisol production after 48 h of treatment.	Hydrocortisone	67-75	NLR family pyrin domain containing 3	Homo sapiens	41-45
8515427-6	1993	Analysis of the conformational constraints imposed in these active analogs suggests that AII agonists bind to their receptor with different backbone conformations in the region of the central tyrosine residue.	Tyrosine	192-200	NLR family pyrin domain containing 3	Homo sapiens	89-92
8432861-0	1993	Characterization of apolipoprotein A-I- and A-II-containing lipoproteins in a new case of high density lipoprotein deficiency resembling Tangier disease and their effects on intracellular cholesterol efflux.	Cholesterol	188-199	NLR family pyrin domain containing 3	Homo sapiens	44-48
8432861-11	1993	Despite these unusual physicochemical characteristics, the apo A-I-containing particles and Lp(AII) were effective suppressors of intracellular cholesterol esterification in cholesterol-loaded human skin fibroblast.	Cholesterol	144-155	NLR family pyrin domain containing 3	Homo sapiens	95-98
8432861-11	1993	Despite these unusual physicochemical characteristics, the apo A-I-containing particles and Lp(AII) were effective suppressors of intracellular cholesterol esterification in cholesterol-loaded human skin fibroblast.	Cholesterol	174-185	NLR family pyrin domain containing 3	Homo sapiens	95-98
1337459-6	1992	We found that enalapril blocked the plasma angiotensin converting enzyme (ACE) with a secondary increment in plasma renin activity (PRA) and reductions in angiotensin II (AII) and aldosterone.	Enalapril	14-23	NLR family pyrin domain containing 3	Homo sapiens	171-174
1337459-8	1992	Hydrochlorothiazide increased PRA, AII, and aldosterone, and lowered blood pressure mainly through a reduction in cardiac output.	Hydrochlorothiazide	0-19	NLR family pyrin domain containing 3	Homo sapiens	35-38
1292582-4	1992	Plasma concentrations of HDL cholesterol and of the apolipoproteins AI and AII were increased by simvastatin.	Simvastatin	97-108	NLR family pyrin domain containing 3	Homo sapiens	52-78
1487127-7	1992	Indomethacin (10 microM) and endothelium removal increased the responses to AII, whereas those induced by AI were barely affected.	Indomethacin	0-12	NLR family pyrin domain containing 3	Homo sapiens	76-79
1464753-8	1992	The concentrations of apoA-I, A-II, A-IV, E, and Cs that promoted half-maximal efflux of phospholipid from cholesterol-enriched fibroblasts were 53, 30, 68, 137, and 594 nM, respectively.	Cholesterol	107-118	NLR family pyrin domain containing 3	Homo sapiens	30-34
1402396-11	1992	Lipolysis of triglycerides by hepatic lipase was 60% higher in postprandial A-I/A-II-HDL2 than in postprandial A-I-HDL2.	Triglycerides	13-26	NLR family pyrin domain containing 3	Homo sapiens	80-89
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	29-33
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	158-162
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	158-162
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	158-162
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	224-227
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	45-56	NLR family pyrin domain containing 3	Homo sapiens	242-245
1420297-11	1992	The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII).	Cholesterol	107-118	NLR family pyrin domain containing 3	Homo sapiens	29-33
1517206-3	1992	From FB and MP, the maximum efflux rates with apoA-I and A-II per 24 h were as much as 30% of the apparent maximum efflux rate of prelabeled cellular cholesterol to human HDL.	Cholesterol	150-161	NLR family pyrin domain containing 3	Homo sapiens	57-61
1517206-6	1992	When standardized for the initial cellular unesterified cholesterol pool size, the maximum efflux rates/24 h were 5.4 and 5.0% for apoA-I and A-II from rat SMC and even less from monkey and rabbit SMC in contrast to 42.4 and 39.7% from FB, and 53.0 and 45.5% from MP, respectively.	Cholesterol	56-67	NLR family pyrin domain containing 3	Homo sapiens	142-146
1418160-7	1992	Magnesium sulfate alone had no significant effect on MAP but attenuated the pressor response to both NE (delta MAP, 16 +/- 1.5 mmHg) and A II (delta MAP, 12 +/- 2.5 mmHg).	Magnesium Sulfate	0-17	NLR family pyrin domain containing 3	Homo sapiens	137-141
1418160-8	1992	After discontinuation of the magnesium sulfate infusion, the control pressor responses to NE and A II were again seen (delta MAP, 39 +/- 3.5 mmHg and delta MAP, 28 +/- 4.2 mmHg, respectively).	Magnesium Sulfate	29-46	NLR family pyrin domain containing 3	Homo sapiens	90-101
1639815-1	1992	Apolipoproteins B, CIII, and AII are synthesized primarily in the liver and intestine and play an important role in lipid and cholesterol metabolism.	Cholesterol	126-137	NLR family pyrin domain containing 3	Homo sapiens	29-32
1421601-8	1992	In patients with cirrhosis and ascites, there is an overall activation of the renal prostaglandin system, which probably acts to maintain renal haemodynamics and GFR by counteracting the vasoconstricting effects of AII and noradrenaline on renal circulation.	Prostaglandins	84-97	NLR family pyrin domain containing 3	Homo sapiens	215-218
1352575-7	1992	We have described a new variety of aldosterone-producing adenoma which is responsive to angiotensin II (AII-responsive APA), consists of at least 20% zona glomerulosa-like cells, and does not make "hybrid steroids" in excess.	Steroids	205-213	NLR family pyrin domain containing 3	Homo sapiens	104-107
1640863-4	1992	Alcohol caused apolipoprotein (apo) AI and apo AII concentrations to increase in all controls by 12% and 16% (P less than .05), but not in obese subjects.	Alcohols	0-7	NLR family pyrin domain containing 3	Homo sapiens	47-50
1795436-2	1991	Probucol caused significant decreases of HDL-cholesterol, plasma apo A-I/apo A-II ratio and particles larger in diameter than 10.4 nm.	Probucol	0-8	NLR family pyrin domain containing 3	Homo sapiens	77-81
1627616-10	1992	The effect of myristic acid on CETP-induced HDL3 redistribution was mainly due to a redistribution of HDL3 (AI w/o AII) particles.	Myristic Acid	14-27	NLR family pyrin domain containing 3	Homo sapiens	115-118
1597929-0	1992	Dinucleotide repeat polymorphism at the apolipoprotein AII locus--phenotyping from peripheral blood and hair.	Dinucleoside Phosphates	0-12	NLR family pyrin domain containing 3	Homo sapiens	55-58
1597929-2	1992	We report here dinucleotide repeat polymorphism at the apolipoprotein AII locus in Japanese subjects.	Dinucleoside Phosphates	15-27	NLR family pyrin domain containing 3	Homo sapiens	70-73
1816327-0	1991	Cholesterol efflux from cells to immunopurified subfractions of human high density lipoprotein: LP-AI and LP-AI/AII.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	70-115
1816327-4	1991	When these cells were prepared to contain normal physiological quantities of cholesterol (20-35 micrograms/mg protein), LP-AI and LP-AI/AII were nearly equally efficient in promoting efflux of both whole-cell and lysosomal cholesterol.	Cholesterol	77-88	NLR family pyrin domain containing 3	Homo sapiens	120-139
1816327-4	1991	When these cells were prepared to contain normal physiological quantities of cholesterol (20-35 micrograms/mg protein), LP-AI and LP-AI/AII were nearly equally efficient in promoting efflux of both whole-cell and lysosomal cholesterol.	Cholesterol	223-234	NLR family pyrin domain containing 3	Homo sapiens	120-139
1816327-5	1991	For whole-cell cholesterol, the rate constants for efflux to LP-AI and LP-AI/AII were: 0.050/h and 0.053/h, respectively, with Fu5AH cells; 0.0063/h and 0.0074/h with GM3468 human skin fibroblasts; and 0.0076/h and 0.0079/h with rabbit aortic smooth muscle cells.	Cholesterol	15-26	NLR family pyrin domain containing 3	Homo sapiens	71-80
1816327-7	1991	In longterm incubations, the net depletion of cholesterol mass from cholesterol-enriched cells was either identical with the two HDL subfractions, or somewhat greater with LP-AI/AII.	Cholesterol	46-57	NLR family pyrin domain containing 3	Homo sapiens	178-181
1816327-7	1991	In longterm incubations, the net depletion of cholesterol mass from cholesterol-enriched cells was either identical with the two HDL subfractions, or somewhat greater with LP-AI/AII.	Cholesterol	68-79	NLR family pyrin domain containing 3	Homo sapiens	178-181
1403348-1	1992	Polymorphism of apolipoproteins AI and AII (apo AI and apo AII) can be easily investigated in plasma by a simple method involving a 30-min incubation of EDTA plasma in the presence of urea, dithiothreitol, and Nonidet P-40 followed by subsequent isoelectric focusing (IEF).	Edetic Acid	153-157	NLR family pyrin domain containing 3	Homo sapiens	16-42
1403348-1	1992	Polymorphism of apolipoproteins AI and AII (apo AI and apo AII) can be easily investigated in plasma by a simple method involving a 30-min incubation of EDTA plasma in the presence of urea, dithiothreitol, and Nonidet P-40 followed by subsequent isoelectric focusing (IEF).	Urea	184-188	NLR family pyrin domain containing 3	Homo sapiens	16-42
1403348-1	1992	Polymorphism of apolipoproteins AI and AII (apo AI and apo AII) can be easily investigated in plasma by a simple method involving a 30-min incubation of EDTA plasma in the presence of urea, dithiothreitol, and Nonidet P-40 followed by subsequent isoelectric focusing (IEF).	Dithiothreitol	190-204	NLR family pyrin domain containing 3	Homo sapiens	16-42
1795436-3	1991	Comparing Lp A-I and A-I/A-II ratios with those in normolipidemic controls and the ratios before and after administration of probucol, the decrease of LpA-I ratio was found to be remarkable after prolonged administration of probucol, and it was presumed that the decrease of HDL cholesterol by prolonged administration reflects the decrease of LpA-I particles more than the decrease of LpA-I/A-II.	Probucol	224-232	NLR family pyrin domain containing 3	Homo sapiens	25-29
1795436-3	1991	Comparing Lp A-I and A-I/A-II ratios with those in normolipidemic controls and the ratios before and after administration of probucol, the decrease of LpA-I ratio was found to be remarkable after prolonged administration of probucol, and it was presumed that the decrease of HDL cholesterol by prolonged administration reflects the decrease of LpA-I particles more than the decrease of LpA-I/A-II.	Probucol	224-232	NLR family pyrin domain containing 3	Homo sapiens	392-396
1873917-5	1991	During furosemide infusion, PAI, PAII, PRA, as well as UV-AI and UV-AII increased.	Furosemide	7-17	NLR family pyrin domain containing 3	Homo sapiens	34-37
1873917-6	1991	During indomethacin treatment, PAI, PAII, and PRA decreased, whereas UV-AI and UV-AII did not change consistently.	Indomethacin	7-19	NLR family pyrin domain containing 3	Homo sapiens	37-40
1873917-7	1991	Sodium restriction increased PAI, PAII, and PRA, but did not alter UV-AI and UV-AII.	Sodium	0-6	NLR family pyrin domain containing 3	Homo sapiens	35-38
1680084-2	1991	After aspirin administration there was a significant decrease in AII sensitivity in sensitive patients with no change in nonsensitive patients.	Aspirin	6-13	NLR family pyrin domain containing 3	Homo sapiens	65-68
1680084-3	1991	Low-dose aspirin favorably affects sensitivity to AII in sensitive patients, thus indicating a reduced vascular reactivity as a consequence of this regimen.	Aspirin	9-16	NLR family pyrin domain containing 3	Homo sapiens	50-53
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	lpai	40-44	NLR family pyrin domain containing 3	Homo sapiens	45-48
2036455-1	1991	The effect of apolipoproteins A-I, A-II, C-II, C-III and E on the hydrolysis of phosphatidylcholine and triacylglycerol by hepatic lipase was studied.	Phosphatidylcholines	80-99	NLR family pyrin domain containing 3	Homo sapiens	14-39
1906713-2	1991	Exposure to particles containing apo AII (LpAI) and particles containing apo AI and apo AII (LpAI:AII) isolated from native human plasma, and from HDL2 or HDL3, showed that only LpAI were able to promote cholesterol efflux, despite the fact that both kinds of particles were able to bind to receptor sites within the same range of concentrations (apparent Kd values between 10 and 25 micrograms/ml).	Cholesterol	204-215	NLR family pyrin domain containing 3	Homo sapiens	93-101
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	lpai	40-44	NLR family pyrin domain containing 3	Homo sapiens	276-279
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	lpai	32-36	NLR family pyrin domain containing 3	Homo sapiens	37-40
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	Cholesterol	154-165	NLR family pyrin domain containing 3	Homo sapiens	40-48
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	lpai	32-36	NLR family pyrin domain containing 3	Homo sapiens	191-199
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	Cholesterol	130-141	NLR family pyrin domain containing 3	Homo sapiens	32-40
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	Cholesterol	154-165	NLR family pyrin domain containing 3	Homo sapiens	45-48
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	Cholesterol	130-141	NLR family pyrin domain containing 3	Homo sapiens	37-40
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	lpai	94-98	NLR family pyrin domain containing 3	Homo sapiens	40-48
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	Cholesterol	216-227	NLR family pyrin domain containing 3	Homo sapiens	32-40
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	Cholesterol	216-227	NLR family pyrin domain containing 3	Homo sapiens	37-40
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	lpai	94-98	NLR family pyrin domain containing 3	Homo sapiens	45-48
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	lpai	116-120	NLR family pyrin domain containing 3	Homo sapiens	32-40
1906713-3	1991	During this long-term exposure, LpAI:AII demonstrated a concentration-dependent inhibition (10-60 micrograms/ml) of LpAI-mediated cholesterol efflux from adipose cells under conditions where LpAI:AII did not deliver cholesterol to the cells and where no net change in the distribution of apo AI between LpAI and LpAI:AII was observed.	lpai	116-120	NLR family pyrin domain containing 3	Homo sapiens	37-40
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	lpai	94-98	NLR family pyrin domain containing 3	Homo sapiens	276-279
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	Cholesterol	63-74	NLR family pyrin domain containing 3	Homo sapiens	40-48
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	Cholesterol	63-74	NLR family pyrin domain containing 3	Homo sapiens	45-48
2242564-3	1990	Concentrations of LpAI and LpAI:AII in the bypass patients were significantly lower (P less than 0.001) than those in the controls.	lpai	27-31	NLR family pyrin domain containing 3	Homo sapiens	32-35
1906713-4	1991	The antagonizing and modulating role of LpAI:AII in preventing cholesterol efflux mediated by LpAI appears not to be related to the lipid composition and cholesterol content of the particles but, rather, appears dependent upon the presence of apo AI in LpAI particles and apo AII in LpAI:AII particles.	Cholesterol	63-74	NLR family pyrin domain containing 3	Homo sapiens	276-279
1901225-3	1991	When human apolipoproteins A-I or A-II are present in the reaction mixture enough to saturate the surface of the emulsion, the enhancement of the pyrene-cholesteryl ester transfer reaction by the transfer protein was 7.5-times more than in the absence of the apolipoproteins while the rate of spontaneous transfer was not affected significantly by the apolipoproteins.	pyrene	146-152	NLR family pyrin domain containing 3	Homo sapiens	11-38
1901225-3	1991	When human apolipoproteins A-I or A-II are present in the reaction mixture enough to saturate the surface of the emulsion, the enhancement of the pyrene-cholesteryl ester transfer reaction by the transfer protein was 7.5-times more than in the absence of the apolipoproteins while the rate of spontaneous transfer was not affected significantly by the apolipoproteins.	Cholesterol Esters	153-170	NLR family pyrin domain containing 3	Homo sapiens	11-38
1998741-1	1991	The kinetics and mechanism of transfer of 14C-labeled human apolipoproteins A-I, A-II and C-III1 between small unilamellar vesicles (SUV) have been investigated.	Carbon-14	42-45	NLR family pyrin domain containing 3	Homo sapiens	60-85
2002032-10	1991	At a high surface pressure of 25 mN/m all apolipoproteins tested (apolipoproteins A-I, A-II, C-I, C-II, C-III, and E) inhibited the penetration into and HL activity on phosphatidylethanolamine At 18.5 mN/m all apolipoproteins except apolipoprotein E inhibited the hydrolysis of triacylglycerol in the triacylglycerol:phosphatidylcholine mixed film.	phosphatidylethanolamine	168-192	NLR family pyrin domain containing 3	Homo sapiens	42-96
2002032-10	1991	At a high surface pressure of 25 mN/m all apolipoproteins tested (apolipoproteins A-I, A-II, C-I, C-II, C-III, and E) inhibited the penetration into and HL activity on phosphatidylethanolamine At 18.5 mN/m all apolipoproteins except apolipoprotein E inhibited the hydrolysis of triacylglycerol in the triacylglycerol:phosphatidylcholine mixed film.	Triglycerides	278-293	NLR family pyrin domain containing 3	Homo sapiens	42-96
2002032-10	1991	At a high surface pressure of 25 mN/m all apolipoproteins tested (apolipoproteins A-I, A-II, C-I, C-II, C-III, and E) inhibited the penetration into and HL activity on phosphatidylethanolamine At 18.5 mN/m all apolipoproteins except apolipoprotein E inhibited the hydrolysis of triacylglycerol in the triacylglycerol:phosphatidylcholine mixed film.	Triglycerides	301-316	NLR family pyrin domain containing 3	Homo sapiens	42-96
2002032-10	1991	At a high surface pressure of 25 mN/m all apolipoproteins tested (apolipoproteins A-I, A-II, C-I, C-II, C-III, and E) inhibited the penetration into and HL activity on phosphatidylethanolamine At 18.5 mN/m all apolipoproteins except apolipoprotein E inhibited the hydrolysis of triacylglycerol in the triacylglycerol:phosphatidylcholine mixed film.	Phosphatidylcholines	317-336	NLR family pyrin domain containing 3	Homo sapiens	42-96
1899429-0	1991	Increased apo A-I and apo A-II fractional catabolic rate in patients with low high density lipoprotein-cholesterol levels with or without hypertriglyceridemia.	Cholesterol	103-114	NLR family pyrin domain containing 3	Homo sapiens	26-30
2268337-9	1990	Stimulation by apo A-I/DMPC complexes or native HDL3 of cells prelabelled with (2-palmitoyl 9,10[3H])phosphatidylcholine induced also the formation of labelled diacylglycerol whereas apo A-II/DMPC complexes and HDL3 treated with tetranitromethane showed no effect.	Dimyristoylphosphatidylcholine	23-27	NLR family pyrin domain containing 3	Homo sapiens	187-191
2268337-9	1990	Stimulation by apo A-I/DMPC complexes or native HDL3 of cells prelabelled with (2-palmitoyl 9,10[3H])phosphatidylcholine induced also the formation of labelled diacylglycerol whereas apo A-II/DMPC complexes and HDL3 treated with tetranitromethane showed no effect.	(2-palmitoyl 9,10[3h])phosphatidylcholine	79-120	NLR family pyrin domain containing 3	Homo sapiens	187-191
2268337-9	1990	Stimulation by apo A-I/DMPC complexes or native HDL3 of cells prelabelled with (2-palmitoyl 9,10[3H])phosphatidylcholine induced also the formation of labelled diacylglycerol whereas apo A-II/DMPC complexes and HDL3 treated with tetranitromethane showed no effect.	Diglycerides	160-174	NLR family pyrin domain containing 3	Homo sapiens	187-191
2193493-9	1990	Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins.	Clonidine	0-9	NLR family pyrin domain containing 3	Homo sapiens	81-107
2292036-2	1990	These data contrast with results obtained using the AII-type 2 antagonist PD123177.	PD 123177	74-82	NLR family pyrin domain containing 3	Homo sapiens	52-55
2227802-1	1990	The effects of peptide inhibitors (bestatin and amastatin) and divalent cations (Ca2+ and Co2+) on the velocity of Asp1 liberation from angiotensin II (A-II) by human placental membrane fractions and binding of 125I A-II to human placental membranes were tested at 22 degrees C and 4 degrees C. Asp1 liberation was measured by high performance liquid chromatography.	ubenimex	35-43	NLR family pyrin domain containing 3	Homo sapiens	136-156
2227802-1	1990	The effects of peptide inhibitors (bestatin and amastatin) and divalent cations (Ca2+ and Co2+) on the velocity of Asp1 liberation from angiotensin II (A-II) by human placental membrane fractions and binding of 125I A-II to human placental membranes were tested at 22 degrees C and 4 degrees C. Asp1 liberation was measured by high performance liquid chromatography.	amastatin	48-57	NLR family pyrin domain containing 3	Homo sapiens	136-156
2227802-1	1990	The effects of peptide inhibitors (bestatin and amastatin) and divalent cations (Ca2+ and Co2+) on the velocity of Asp1 liberation from angiotensin II (A-II) by human placental membrane fractions and binding of 125I A-II to human placental membranes were tested at 22 degrees C and 4 degrees C. Asp1 liberation was measured by high performance liquid chromatography.	Cobalt(2+)	90-94	NLR family pyrin domain containing 3	Homo sapiens	136-156
2373138-3	1990	Phenobarbital enhanced antipyrine elimination and increased the apolipoprotein A-I/A-II ratio.	Phenobarbital	0-13	NLR family pyrin domain containing 3	Homo sapiens	83-87
2117929-8	1990	It suggests that metabolic activities giving rise to both HDL-2(LpAI) and HDL-2(LpAI,AII) determine plasma HDL cholesterol concentrations.	Cholesterol	111-122	NLR family pyrin domain containing 3	Homo sapiens	80-88
2324684-2	1990	In this study of 23 young healthy subjects, high levels of serum lipid peroxides were associated with low serum HDL2 cholesterol concentrations and low HDL2/HDL3 cholesterol and apolipoprotein A-I/A-II ratios.	Peroxides	71-80	NLR family pyrin domain containing 3	Homo sapiens	197-201
2384994-3	1990	Alcohol consumption, apolipoprotein AI and AII levels were inversely correlated to CS.	Cesium	83-85	NLR family pyrin domain containing 3	Homo sapiens	43-46
2153592-4	1990	In lipoprotein-free medium, apolipoproteins A-I, A-II, B, C, and E accumulate in the medium together with cholesterol, cholesteryl ester, triglyceride, and all the primary bile acids.	Cholesterol	106-117	NLR family pyrin domain containing 3	Homo sapiens	28-56
2153592-4	1990	In lipoprotein-free medium, apolipoproteins A-I, A-II, B, C, and E accumulate in the medium together with cholesterol, cholesteryl ester, triglyceride, and all the primary bile acids.	Cholesterol Esters	119-136	NLR family pyrin domain containing 3	Homo sapiens	28-56
2153592-4	1990	In lipoprotein-free medium, apolipoproteins A-I, A-II, B, C, and E accumulate in the medium together with cholesterol, cholesteryl ester, triglyceride, and all the primary bile acids.	Triglycerides	138-150	NLR family pyrin domain containing 3	Homo sapiens	28-56
2295765-3	1990	Probucol treatment for this period caused significant reductions in the serum levels of total cholesterol, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol, and apoprotein AI, AII, B, and CIII in both groups.	Probucol	0-8	NLR family pyrin domain containing 3	Homo sapiens	209-212
33798500-4	2021	Activation of the NLRP3 inflammasome by monosodium urate crystals with release of IL-1beta plays a major role in the initiation of the gout flare; aggregated neutrophil extracellular traps are important in the resolution phase.	Uric Acid	40-56	NLR family pyrin domain containing 3	Homo sapiens	18-23
33765556-0	2021	CY-09 attenuates the progression of osteoarthritis via inhibiting NLRP3 inflammasome-mediated pyroptosis.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	66-71
33765556-3	2021	This research was conducted to confirm whether NLRP3 expression and activity are impacted in the development of OA and to detect the role of CY-09, a selective and direct inhibitor of NLRP3 in the in vitro and in vivo models of OA.	CY5.5 cyanine dye	141-146	NLR family pyrin domain containing 3	Homo sapiens	184-189
33765556-5	2021	CY-09 can maintain extracellular matrix (ECM) homeostasis and regulate inflammation in TNF-alpha treated chondrocytes via inhibition of NLRP3 inflammasome-mediated pyroptosis.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	136-141
33765556-7	2021	In conclusion, our research indicates that experimental OA activated the NLRP3 activity, and pharmacological inhibition of NLRP3 inflammasome activation by CY-09 protects chondrocytes against inflammation and attenuates OA development.	CY5.5 cyanine dye	156-161	NLR family pyrin domain containing 3	Homo sapiens	123-128
33767434-6	2021	Herein, we found that Mn2+ strongly promoted immune responses by facilitating antigen uptake, presentation, and germinal center formation via both cGAS-STING and NLRP3 activation.	Manganese(2+)	22-26	NLR family pyrin domain containing 3	Homo sapiens	162-167
33971816-0	2021	Correction to: Dexmedetomidine attenuates myocardial ischemia-reperfusion injury in vitro by inhibiting NLRP3 Inflammasome activation.	Dexmedetomidine	15-30	NLR family pyrin domain containing 3	Homo sapiens	104-109
33805302-4	2021	Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1beta secretion, and improvements in the levels of antioxidant molecules.	icaritin	165-173	NLR family pyrin domain containing 3	Homo sapiens	209-267
33763153-0	2021	Regulatory effect of mitoQ on the mtROS-NLRP3 inflammasome pathway in leptin-pretreated BEAS-2 cells.	mitoquinone	21-26	NLR family pyrin domain containing 3	Homo sapiens	40-45
33763153-3	2021	NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been previously demonstrated to serve a role in obese asthma mediated by mitochondrial reactive oxygen species (mtROS).	Reactive Oxygen Species	161-184	NLR family pyrin domain containing 3	Homo sapiens	0-48
33763153-3	2021	NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been previously demonstrated to serve a role in obese asthma mediated by mitochondrial reactive oxygen species (mtROS).	Reactive Oxygen Species	161-184	NLR family pyrin domain containing 3	Homo sapiens	50-55
33821820-6	2021	RESULTS: The NLRP3 inflammasome activation in response to common PAMPs (LPS, ss-glucan) resulted higher in B lymphocytes of PWH than in HD.	ss-glucan	77-86	NLR family pyrin domain containing 3	Homo sapiens	13-18
33805302-4	2021	Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1beta secretion, and improvements in the levels of antioxidant molecules.	icaritin	165-173	NLR family pyrin domain containing 3	Homo sapiens	269-274
33805302-4	2021	Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1beta secretion, and improvements in the levels of antioxidant molecules.	icaritin	165-173	NLR family pyrin domain containing 3	Homo sapiens	396-401
33805302-4	2021	Using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1beta secretion, and improvements in the levels of antioxidant molecules.	icaritin	165-173	NLR family pyrin domain containing 3	Homo sapiens	396-401
33805302-6	2021	By employing molecular docking, we also discovered that icaritin can interact with NLRP3, VDAC, ATP5B, and several blood-brain barrier (BBB)-related proteins.	icaritin	56-64	NLR family pyrin domain containing 3	Homo sapiens	83-88
33817415-0	2021	Protective effects of sirtuin 3 on titanium particle-induced osteogenic inhibition by regulating the NLRP3 inflammasome via the GSK-3beta/beta-catenin signalling pathway.	Titanium	35-43	NLR family pyrin domain containing 3	Homo sapiens	101-106
33806797-3	2021	Currently, there is limited evidence that supports the pathological role of NLRP3 inflammasome activation in glucose handling in the skeletal muscle of obese individuals.	Glucose	109-116	NLR family pyrin domain containing 3	Homo sapiens	76-81
31736980-3	2019	OLT1177  (Dapansutrile) is a newly developed drug that is safe in humans and inhibits specifically the NLRP3 inflammasome.	nesosteine	0-7	NLR family pyrin domain containing 3	Homo sapiens	103-108
33235030-0	2020	A Phase IB, Randomized, Double-Blinded, Dose Escalation, Single Center, Repeat-Dose Safety and Pharmacodynamics Study of the Oral NLRP3 Inhibitor Dapansutrile in Subjects with NYHA II-III Systolic Heart Failure.	dapansutrile	146-158	NLR family pyrin domain containing 3	Homo sapiens	130-135
33235030-2	2020	The aim of this study was to determine the safety of an oral inhibitor of the NLRP3 inflammasome, dapansutrile (OLT1177), in patients with HF and reduced ejection fraction (HFrEF).	dapansutrile	98-110	NLR family pyrin domain containing 3	Homo sapiens	78-83
31412862-0	2019	Berberine inhibits NLRP3 Inflammasome pathway in human triple-negative breast cancer MDA-MB-231 cell.	Berberine	0-9	NLR family pyrin domain containing 3	Homo sapiens	19-24
34906776-3	2022	Flavocoxid is a mixed extract containing baicalin and catechin showing antioxidant effects and anti-inflammatory activity mainly due to a dual inhibition of inducible cyclooxygenase (COX-2), 5-lipoxygenase (5-LOX) and NLRP3 pathway.	flavocoxid	0-10	NLR family pyrin domain containing 3	Homo sapiens	218-223
31427442-3	2019	In this study, we explored how NAD+ affects TLR4 and NOD-like receptor with a PYD-domain 3 (NLRP3) inflammasome activation, two key innate immune responses.	NAD	31-35	NLR family pyrin domain containing 3	Homo sapiens	92-97
34862106-8	2022	The inflammatory factor was only activated (33 cytokines) by noncytotoxic concentration of PSMPs (3 ng/mL); however, the cytotoxic concentration (300 ng/mL) of PSMPs induced autophagy, which might further reduce NLRP3 expression, thus contributing to dampening inflammation (35 cytokines) in HEK293 cells.	psmps	91-96	NLR family pyrin domain containing 3	Homo sapiens	212-217
34862106-8	2022	The inflammatory factor was only activated (33 cytokines) by noncytotoxic concentration of PSMPs (3 ng/mL); however, the cytotoxic concentration (300 ng/mL) of PSMPs induced autophagy, which might further reduce NLRP3 expression, thus contributing to dampening inflammation (35 cytokines) in HEK293 cells.	psmps	160-165	NLR family pyrin domain containing 3	Homo sapiens	212-217
34766707-3	2022	We isolated primary AEC from three healthy adults and treated them with silica particles at different concentrations for 48 h. We found evidence for silica-induced inflammasome activation by the co-localization of Caspase-1 and NLRP3, as well as increased levels of IL-1beta and IL-18.	Silicon Dioxide	72-78	NLR family pyrin domain containing 3	Homo sapiens	228-233
34766707-3	2022	We isolated primary AEC from three healthy adults and treated them with silica particles at different concentrations for 48 h. We found evidence for silica-induced inflammasome activation by the co-localization of Caspase-1 and NLRP3, as well as increased levels of IL-1beta and IL-18.	Silicon Dioxide	149-155	NLR family pyrin domain containing 3	Homo sapiens	228-233
34766707-8	2022	These data suggest that microcrystalline silica can induce significant inflammation and pyroptosis in human primary AEC through NLRP3 inflammasome pathway and NF-kappaB signaling pathway at both the gene and protein levels, and the possible mechanism could be miR-455-3p mediated ceRNA hypothesis.	Silicon Dioxide	41-47	NLR family pyrin domain containing 3	Homo sapiens	128-133
34688696-10	2022	KEY FINDINGS: Our results showed that quercetin prevented THP-1 macrophage pyroptosis by reducing the expression of NLRP3 and cleaved-caspase1, as well as IL-1beta and N-GSDMD in a concentration dependent manner.	Quercetin	38-47	NLR family pyrin domain containing 3	Homo sapiens	116-121
34688696-11	2022	Quercetin suppressed NLRP3 inflammasome activation by inhibiting ROS overproduction.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	21-26
34688696-11	2022	Quercetin suppressed NLRP3 inflammasome activation by inhibiting ROS overproduction.	Reactive Oxygen Species	65-68	NLR family pyrin domain containing 3	Homo sapiens	21-26
34688696-13	2022	In addition, we found that quercetin suppressed the increase of TLR2/Myd88 and p-AMPK induced by LPS/ATP, while both TLR2 and AMPK agonist weakened the inhibitory effect of quercetin on the activity of NLRP3 inflammasome and alleviated the protective effect on macrophages pyroptosis.	Quercetin	27-36	NLR family pyrin domain containing 3	Homo sapiens	202-207
34688696-13	2022	In addition, we found that quercetin suppressed the increase of TLR2/Myd88 and p-AMPK induced by LPS/ATP, while both TLR2 and AMPK agonist weakened the inhibitory effect of quercetin on the activity of NLRP3 inflammasome and alleviated the protective effect on macrophages pyroptosis.	Quercetin	173-182	NLR family pyrin domain containing 3	Homo sapiens	202-207
34863712-7	2022	The current reporter assay not only provides a specific NLRP3PYD-NLRP3PYD assay to study the PYD-PYD interaction in vitro, but also provides a suitable system for screening chemicals and drugs to identify activators and inhibitors of NLRP3.	pyd-pyd	93-100	NLR family pyrin domain containing 3	Homo sapiens	56-61
34863712-7	2022	The current reporter assay not only provides a specific NLRP3PYD-NLRP3PYD assay to study the PYD-PYD interaction in vitro, but also provides a suitable system for screening chemicals and drugs to identify activators and inhibitors of NLRP3.	pyd-pyd	93-100	NLR family pyrin domain containing 3	Homo sapiens	65-70
34863712-7	2022	The current reporter assay not only provides a specific NLRP3PYD-NLRP3PYD assay to study the PYD-PYD interaction in vitro, but also provides a suitable system for screening chemicals and drugs to identify activators and inhibitors of NLRP3.	pyd-pyd	93-100	NLR family pyrin domain containing 3	Homo sapiens	234-239
27343554-4	2016	Knockdown of NLRP3 with siRNA suppresses UVB-induced production of not only IL-1beta, but also other inflammatory mediators, including IL-1alpha, IL-6, TNF-alpha, and PGE2.	Dinoprostone	167-171	NLR family pyrin domain containing 3	Homo sapiens	13-18
34730058-10	2022	MiR-144-3p knockdown inhibited IL-1beta-induced pyroptosis in N1511 cells, and the expressions of NOD-like receptor family pyrin domain containing 3 (NLRP3), Cleaved caspase-1, Gasdermin D (GSDMD), and Cleaved caspase-3 in IL-1beta-stimulated N1511 cells were increased.	mir-144-3p	0-10	NLR family pyrin domain containing 3	Homo sapiens	150-155
34906776-3	2022	Flavocoxid is a mixed extract containing baicalin and catechin showing antioxidant effects and anti-inflammatory activity mainly due to a dual inhibition of inducible cyclooxygenase (COX-2), 5-lipoxygenase (5-LOX) and NLRP3 pathway.	Catechin	54-62	NLR family pyrin domain containing 3	Homo sapiens	218-223
34906776-8	2022	These results suggest a correlation between oxidative stress and NLRP3 activation and indicate that flavocoxid suppresses the inflammatory storm that accompanies oral mucositis.	flavocoxid	100-110	NLR family pyrin domain containing 3	Homo sapiens	65-70
34610469-0	2022	Elaidic acid induced NLRP3 inflammasome activation via ERS-MAPK signaling pathways in Kupffer cells.	elaidic acid	0-12	NLR family pyrin domain containing 3	Homo sapiens	21-26
34959186-0	2022	Disulfiram attenuates MCMV-Induced pneumonia by inhibition of NF-kappaB/NLRP3 signaling pathway in immunocompromised mice.	Disulfiram	0-10	NLR family pyrin domain containing 3	Homo sapiens	72-77
34970856-2	2022	The NLRP3 inhibitor, colchicine, therefore, appears to be promising for the treatment of COVID-19.	Colchicine	21-31	NLR family pyrin domain containing 3	Homo sapiens	4-9
34970856-9	2022	DISCUSSION AND CONCLUSION: The ability of colchicine to reduce the length of stay in hospitalized patients with COVID-19 is consistent with its potential to prevent clinical deterioration via inhibition of NLRP3 inflammasome.	Colchicine	42-52	NLR family pyrin domain containing 3	Homo sapiens	206-211
34415562-0	2022	Retinoic acid attenuates nuclear factor kappaB mediated induction of NLRP3 inflammasome.	Tretinoin	0-13	NLR family pyrin domain containing 3	Homo sapiens	69-74
34415562-10	2022	RESULTS: We found that carbachol increased the expression of NLRP3 inflammasome (NLRP3, ASC, cleaved caspase-1, IL-1beta, and IL-18).	Carbachol	23-32	NLR family pyrin domain containing 3	Homo sapiens	61-66
34415562-10	2022	RESULTS: We found that carbachol increased the expression of NLRP3 inflammasome (NLRP3, ASC, cleaved caspase-1, IL-1beta, and IL-18).	Carbachol	23-32	NLR family pyrin domain containing 3	Homo sapiens	81-86
34415562-13	2022	The addition of RA also significantly reduced the effect of carbachol on NLRP3 inflammasomes.	Tretinoin	16-18	NLR family pyrin domain containing 3	Homo sapiens	73-78
34415562-13	2022	The addition of RA also significantly reduced the effect of carbachol on NLRP3 inflammasomes.	Carbachol	60-69	NLR family pyrin domain containing 3	Homo sapiens	73-78
34415562-14	2022	CONCLUSIONS: Our current study suggests that carbachol induces NLRP3 inflammasome activation through mAChR and NF-kB, and that RA abolishes the inflammatory response.	Carbachol	45-54	NLR family pyrin domain containing 3	Homo sapiens	63-68
34415562-14	2022	CONCLUSIONS: Our current study suggests that carbachol induces NLRP3 inflammasome activation through mAChR and NF-kB, and that RA abolishes the inflammatory response.	Tretinoin	127-129	NLR family pyrin domain containing 3	Homo sapiens	63-68
34883112-0	2022	MF-094, a potent and selective USP30 inhibitor, accelerates diabetic wound healing by inhibiting the NLRP3 inflammasome.	MF-094	0-6	NLR family pyrin domain containing 3	Homo sapiens	101-106
34875574-0	2022	Human fetal membrane IL-1beta production in response to bacterial components is mediated by uric-acid induced NLRP3 inflammasome activation.	Uric Acid	92-101	NLR family pyrin domain containing 3	Homo sapiens	110-115
34875574-8	2022	LPS, PGN, and MDP induced FM IL-1beta and IL-18 secretion in a non-pyroptotic manner through activation of the NLRP3 inflammasome with contributions from ATP release through Pannexin-1, and ROS signaling.	Acetylmuramyl-Alanyl-Isoglutamine	14-17	NLR family pyrin domain containing 3	Homo sapiens	111-116
34904823-5	2022	PA treatment suppresses the nuclear translocation of NF-kappaB, enhances PARKIN translocation into the mitochondria, and maintains cellular redox homeostasis in both mouse and human microglial cells that limit NLRP3 inflammasome activation along with processing of active caspase-1, IL-1beta, and IL-18.	perillyl alcohol	0-2	NLR family pyrin domain containing 3	Homo sapiens	210-215
34904823-6	2022	To further correlate the in vitro study with the in vivo MPTP model, treatment with PA also inhibited the nuclear translocation of NF-kappaB and downregulated the NLRP3 inflammasome activation.	perillyl alcohol	84-86	NLR family pyrin domain containing 3	Homo sapiens	163-168
34610469-6	2022	Our research indicated that EA induced the endoplasmic reticulum stress (ERS) response in Kupffer cells (KCs), accompanied by the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, which resulted in NLRP3 inflammasome formation, and eventually increased the release of inflammatory factors.	elaidic acid	28-30	NLR family pyrin domain containing 3	Homo sapiens	225-230
34843717-0	2022	Luxeptinib Disables NLRP3 Inflammasome-Mediated IL-1beta release and Pathways Required for Secretion of Inflammatory Cytokines IL-6 and TNFalpha.	Luxeptinib	0-10	NLR family pyrin domain containing 3	Homo sapiens	20-25
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	15-19	NLR family pyrin domain containing 3	Homo sapiens	69-74
34843717-6	2022	The aim of this study was to determine the extent to which luxeptinib interferes with the release of IL-1beta, IL-6 and TNFalpha from THP-1 monocytes and bone marrow-derived macrophages following endotoxin exposure and priming of the NLRP3 inflammasome.	Luxeptinib	59-69	NLR family pyrin domain containing 3	Homo sapiens	234-239
34843717-10	2022	Implications: The ability of luxeptinib to inhibit the NLRP3-mediated release of IL-1beta and pathways involved in the release of IL-6 and TNFalpha at concentrations which are well-tolerated in patients makes it a candidate for the treatment of inflammatory diseases and inflammation-associated resistance in cancer.	Luxeptinib	29-39	NLR family pyrin domain containing 3	Homo sapiens	55-60
34643941-10	2022	Supporting its anti-IIR effects, amitriptyline downregulated basal and induced expression of NLR family pyrin domain containing 3 (NLRP3), an inflammasome member from IL1R signalling linked to OA & gout pathologies.	Amitriptyline	33-46	NLR family pyrin domain containing 3	Homo sapiens	93-129
34643941-10	2022	Supporting its anti-IIR effects, amitriptyline downregulated basal and induced expression of NLR family pyrin domain containing 3 (NLRP3), an inflammasome member from IL1R signalling linked to OA & gout pathologies.	Amitriptyline	33-46	NLR family pyrin domain containing 3	Homo sapiens	131-136
34696918-0	2022	Vitamin D decreases expression of NLRP1 and NLRP3 ninflammasomes in placental explants from women with preeclampsia cultured with hydrogen peroxide.	Vitamin D	0-9	NLR family pyrin domain containing 3	Homo sapiens	44-49
34696918-0	2022	Vitamin D decreases expression of NLRP1 and NLRP3 ninflammasomes in placental explants from women with preeclampsia cultured with hydrogen peroxide.	Hydrogen Peroxide	130-147	NLR family pyrin domain containing 3	Homo sapiens	44-49
34696918-1	2022	This study aimed to evaluate the immunomodulatory effect of vitamin D (VD) on the NLRP1 and NLRP3 inflammasomes in placental explants from preeclamptic (PE) and normotensive (NT) pregnant women.	Vitamin D	60-69	NLR family pyrin domain containing 3	Homo sapiens	92-97
34696918-6	2022	Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1beta, TNF-alpha and HMGB1, while H2O2 was also able to increase TNF-alpha and caspase-1 gene expression in PE.	Hydrogen Peroxide	41-45	NLR family pyrin domain containing 3	Homo sapiens	101-106
34643941-12	2022	CONCLUSION: We demonstrate amitriptyline"s ability to block TLR4-, IL1R- & NLRP3-dependent IIRs.	Amitriptyline	27-40	NLR family pyrin domain containing 3	Homo sapiens	75-80
34976136-0	2022	NLRP3 inflammasome activation in gestational diabetes mellitus placentas is associated with hydrogen sulfide synthetase deficiency.	Hydrogen	92-100	NLR family pyrin domain containing 3	Homo sapiens	0-5
34976136-8	2022	Pearson"s correlation analysis was performed to assess the correlation between NLRP3 inflammasome and H2S synthetase.	Deuterium	102-105	NLR family pyrin domain containing 3	Homo sapiens	79-84
34976136-13	2022	Notably, NaHS and L-cysteine significantly suppressed the expression levels of NLRP3 and cleaved caspase-1, and the production of IL-1 and IL-18 in human placental cells.	sodium bisulfide	9-13	NLR family pyrin domain containing 3	Homo sapiens	79-84
34976136-13	2022	Notably, NaHS and L-cysteine significantly suppressed the expression levels of NLRP3 and cleaved caspase-1, and the production of IL-1 and IL-18 in human placental cells.	Cysteine	18-28	NLR family pyrin domain containing 3	Homo sapiens	79-84
34976136-14	2022	Taken together, the results of the present study suggest that H2S synthetase deficiency in placenta may contribute to excessive activation of NLRP3 inflammasome in GDM.	Deuterium	62-65	NLR family pyrin domain containing 3	Homo sapiens	142-147
34854954-8	2022	Moreover, we found that ROS inhibition via NAC effectively blocks NLRP3 activation and pyroptosis.	ros	24-27	NLR family pyrin domain containing 3	Homo sapiens	66-71
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	151-155	NLR family pyrin domain containing 3	Homo sapiens	69-74
34747550-5	2022	Numerous NCs exerted their therapeutic effects on DOX-mediated cardiac damage via targeting different signaling pathways, including SIRT1/LKB1/AMPK, SIRT1/PGC-1alpha, SIRT1/NLRP3, and SIRT3/FoxO.	Doxorubicin	50-53	NLR family pyrin domain containing 3	Homo sapiens	173-178
34883226-3	2022	Through cell culture, virus infection, and RT-qPCR, we found that LiCl could down-regulate the apoptosis-related genes Caspase-3 and Bax, up-regulate Bcl-2, and down-regulate the inflammatory-related genes (NF-kappaB, NLRP3, TNF-alpha, and IL-1beta) via inhibiting virus replication.	Lithium Chloride	66-70	NLR family pyrin domain containing 3	Homo sapiens	218-223
34864055-7	2022	We report that the lysosomal cysteine protease cathepsin Z potentiates the development of inflammation associated with respiratory silicosis by augmenting NLRP3 inflammasome-derived IL-1beta expression in response to silica.	Silicon Dioxide	217-223	NLR family pyrin domain containing 3	Homo sapiens	155-160
34826552-0	2022	Norfloxacin suppresses Leptospira-induced inflammation through inhibiting p65 and ERK phosphorylation and NLRP3 inflammasome activation.	Norfloxacin	0-11	NLR family pyrin domain containing 3	Homo sapiens	106-111
34826552-8	2022	Norfloxacin also inhibited the Leptospira-induced NLRP3 inflammasome activation with the increased level of Na/K-ATPase Pump beta1 subunit and decreased level of Kcnk6.	Norfloxacin	0-11	NLR family pyrin domain containing 3	Homo sapiens	50-55
34856474-10	2022	RESULTS: In thiram-induced TD, Bax/Bak activation persuade a parallel pathway, mediated by the NLRP3 base inflammasome.	Thiram	12-18	NLR family pyrin domain containing 3	Homo sapiens	95-100
34826552-8	2022	Norfloxacin also inhibited the Leptospira-induced NLRP3 inflammasome activation with the increased level of Na/K-ATPase Pump beta1 subunit and decreased level of Kcnk6.	kcnk6	162-167	NLR family pyrin domain containing 3	Homo sapiens	50-55
34826552-9	2022	These results indicated that norfloxacin suppressed Leptospira-induced inflammation through inhibiting p65 and ERK phosphorylation and NLRP3 inflammasome activation.	Norfloxacin	29-40	NLR family pyrin domain containing 3	Homo sapiens	135-140
34856474-0	2022	Chlorogenic acid suppresses mitochondrial apoptotic effectors Bax/Bak to counteract Nod-like receptor pyrin domain 3 (NLRP3) inflammasome in thiram exposed chondrocytes.	Chlorogenic Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	84-116
34856474-14	2022	CONCLUSION: Chondrocytes have ability to undergo Bax/Bak-mediated apoptosis and generate pro-inflammatory signals, e.g., NLRP3 in thiram-induced TD.	Thiram	130-136	NLR family pyrin domain containing 3	Homo sapiens	121-126
34856474-0	2022	Chlorogenic acid suppresses mitochondrial apoptotic effectors Bax/Bak to counteract Nod-like receptor pyrin domain 3 (NLRP3) inflammasome in thiram exposed chondrocytes.	Chlorogenic Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	118-123
34856474-0	2022	Chlorogenic acid suppresses mitochondrial apoptotic effectors Bax/Bak to counteract Nod-like receptor pyrin domain 3 (NLRP3) inflammasome in thiram exposed chondrocytes.	Thiram	141-147	NLR family pyrin domain containing 3	Homo sapiens	84-116
34856476-6	2022	RESULTS: Different classes of phytopigments such as carotenoids, xanthophylls, flavonoids, anthocyanins, anthraquinones alleviate major CVDs (e.g., cardiac hypertrophy, atherosclerosis, hypertension, cardiotoxicities) via acting on signaling pathways related to AMPK, NF-kappaB, NRF2, PPARs, AKT, TLRs, MAPK, JAK/STAT, NLRP3, TNF-alpha, and RA.	Carotenoids	52-63	NLR family pyrin domain containing 3	Homo sapiens	319-324
34856474-0	2022	Chlorogenic acid suppresses mitochondrial apoptotic effectors Bax/Bak to counteract Nod-like receptor pyrin domain 3 (NLRP3) inflammasome in thiram exposed chondrocytes.	Thiram	141-147	NLR family pyrin domain containing 3	Homo sapiens	118-123
34856476-6	2022	RESULTS: Different classes of phytopigments such as carotenoids, xanthophylls, flavonoids, anthocyanins, anthraquinones alleviate major CVDs (e.g., cardiac hypertrophy, atherosclerosis, hypertension, cardiotoxicities) via acting on signaling pathways related to AMPK, NF-kappaB, NRF2, PPARs, AKT, TLRs, MAPK, JAK/STAT, NLRP3, TNF-alpha, and RA.	Flavonoids	79-89	NLR family pyrin domain containing 3	Homo sapiens	319-324
34856476-6	2022	RESULTS: Different classes of phytopigments such as carotenoids, xanthophylls, flavonoids, anthocyanins, anthraquinones alleviate major CVDs (e.g., cardiac hypertrophy, atherosclerosis, hypertension, cardiotoxicities) via acting on signaling pathways related to AMPK, NF-kappaB, NRF2, PPARs, AKT, TLRs, MAPK, JAK/STAT, NLRP3, TNF-alpha, and RA.	Anthocyanins	91-103	NLR family pyrin domain containing 3	Homo sapiens	319-324
34856476-6	2022	RESULTS: Different classes of phytopigments such as carotenoids, xanthophylls, flavonoids, anthocyanins, anthraquinones alleviate major CVDs (e.g., cardiac hypertrophy, atherosclerosis, hypertension, cardiotoxicities) via acting on signaling pathways related to AMPK, NF-kappaB, NRF2, PPARs, AKT, TLRs, MAPK, JAK/STAT, NLRP3, TNF-alpha, and RA.	Anthraquinones	105-119	NLR family pyrin domain containing 3	Homo sapiens	319-324
34969174-0	2022	The interplay between ASMase signaling pathway and NLRP3 in the epithelial to mesenchymal transition of HBE cells induced by silica.	Silicon Dioxide	125-131	NLR family pyrin domain containing 3	Homo sapiens	51-56
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	121-126
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	148-153
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	92-119
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	121-126
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	148-153
34969174-4	2022	However, whether ASMase and NLRP3 are involved in regulating SiO2 -induced EMT has not been confirmed.	Silicon Dioxide	61-65	NLR family pyrin domain containing 3	Homo sapiens	28-33
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	92-119
34969174-7	2022	The ASMase inhibitor desipramine decreased the level of S1P and the expression of alpha-smooth muscle actin (alpha-SMA) and NLRP3 in SiO2 dust-stained HBE cells, whereas the expression of E-cadherin (E-cad) increased.	Desipramine	21-32	NLR family pyrin domain containing 3	Homo sapiens	124-129
34969174-7	2022	The ASMase inhibitor desipramine decreased the level of S1P and the expression of alpha-smooth muscle actin (alpha-SMA) and NLRP3 in SiO2 dust-stained HBE cells, whereas the expression of E-cadherin (E-cad) increased.	Silicon Dioxide	133-137	NLR family pyrin domain containing 3	Homo sapiens	124-129
34965405-0	2022	Melatonin counteracts oxidative damage in lens by regulation of Nrf2 and NLRP3 inflammasome activity.	Melatonin	0-9	NLR family pyrin domain containing 3	Homo sapiens	73-78
34969174-8	2022	The NLRP3 inhibitor MCC950 inhibited the secretion of interleukin-1beta (IL-1beta) and decreased the expression of NLRP3, Caspase-1, and alpha-SMA in SiO2 dust-stained HBE cells, whereas E-cad expression increased and ASMase activity and S1P levels decreased.	Silicon Dioxide	150-154	NLR family pyrin domain containing 3	Homo sapiens	4-9
34969174-10	2022	Inhibition of ASMase activity or NLRP3 expression reduced the SiO2 dust-induced cell inflammatory response and slowed the occurrence of EMT in HBE cells.	Silicon Dioxide	62-66	NLR family pyrin domain containing 3	Homo sapiens	33-38
34969174-11	2022	Therefore, NLRP3 and ASMase may interact in SiO2 dust-induced EMT in HBE cells.	Silicon Dioxide	44-48	NLR family pyrin domain containing 3	Homo sapiens	11-16
34965405-2	2022	ROS generation is known to activate NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain-cointaining 3) inflammasome, and is believed to be an important link between oxidative stress and inflammation, that is also related to cataract development.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	36-41
34965405-6	2022	Particularly, the modulation of Nrf2 (nuclear erythroid 2-related factor)/Keap 1 (Kelch-like ECH-associated protein 1), an essential oxidative stress regulator, and NLRP3 activity by melatonin was evaluated in lens epithelial cells.	Melatonin	183-192	NLR family pyrin domain containing 3	Homo sapiens	165-170
34965405-9	2022	NLRP3, caspase-1 and IL1-beta expression significantly increased in human lens cells exposed to H2O2 or irradiated with white LED light.	Hydrogen Peroxide	96-100	NLR family pyrin domain containing 3	Homo sapiens	0-5
34965405-10	2022	Activation of NLRP3 inflammasome triggered by oxidative stressors was also abrogated by melatonin.	Melatonin	88-97	NLR family pyrin domain containing 3	Homo sapiens	14-19
34955407-0	2022	Corrigendum to "Antcin A alleviates pyroptosis and inflammatory response in Kupffercells of non-alcoholic fatty liver disease by targeting NLRP3" (Int.	antcin A	16-24	NLR family pyrin domain containing 3	Homo sapiens	139-144
34903138-6	2021	For the molecular mechanism research, SS-31 stabilized mitochondrial morphology and inhibited the activation of the NF-kappaB pathway and the activation of the NLRP3 inflammasome.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	38-43	NLR family pyrin domain containing 3	Homo sapiens	160-165
34903138-7	2021	To evaluate whether the inhibition of NLRP3 inflammasome activation by SS-31 is dependent on the clearance of mitochondrial ROS, we comparatively analyzed the activation of NLRP3 inflammasome in NP cells pretreated with SS-31 and the ROS scavenger N-acetyl-L-cysteine (NAC).	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	71-76	NLR family pyrin domain containing 3	Homo sapiens	38-43
34903138-2	2021	Damaged mitochondria release dangerous molecules such as reactive oxygen species (ROS), activating the NLRP3 inflammasome.	Reactive Oxygen Species	57-80	NLR family pyrin domain containing 3	Homo sapiens	103-108
34903138-2	2021	Damaged mitochondria release dangerous molecules such as reactive oxygen species (ROS), activating the NLRP3 inflammasome.	Reactive Oxygen Species	82-85	NLR family pyrin domain containing 3	Homo sapiens	103-108
34903138-8	2021	The results indicate that SS-31 could inhibit NLRP3 inflammasome activation by limiting the production of mitochondrial ROS.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	26-31	NLR family pyrin domain containing 3	Homo sapiens	46-51
34903138-8	2021	The results indicate that SS-31 could inhibit NLRP3 inflammasome activation by limiting the production of mitochondrial ROS.	Reactive Oxygen Species	120-123	NLR family pyrin domain containing 3	Homo sapiens	46-51
34930938-8	2021	Functionally, using CCK-8, TUNEL, and Transwell migration assays, these results showed that activation of NLRP3/caspase-1 inflammasome by LPS + ATP could enhance the ability of proliferation and migration; and decrease the apoptosis of LNCaP and PC3 cell lines.	Adenosine Triphosphate	144-147	NLR family pyrin domain containing 3	Homo sapiens	106-111
34992411-3	2021	Emerging evidence suggests that activation of the NOD-like receptor (NLR) family and the pyridine-containing domain 3 (NLRP3) inflammasome is instrumental in inflammation and may result in AS.	pyridine	89-97	NLR family pyrin domain containing 3	Homo sapiens	119-124
34930938-9	2021	Western blotting assay showed that the activation of caspase-1 would increase after the stimulation of NLRP3 inflammasome by LPS + ATP.	Adenosine Triphosphate	131-134	NLR family pyrin domain containing 3	Homo sapiens	103-108
34988126-2	2021	Aging is linked to chronic sterile inflammation and high burden of reactive oxygen species (ROS), leading to activation of pattern recognition receptors (PRRs) such as Nlrp3 in vascular cells.	Reactive Oxygen Species	67-90	NLR family pyrin domain containing 3	Homo sapiens	168-173
34987391-5	2021	Moreover, in vitro models of lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs) and human peripheral blood mononuclear cells (PBMCs) were established to explore the mechanism of methyl gallate on NLRP3 inflammasome activation.	methyl gallate	203-217	NLR family pyrin domain containing 3	Homo sapiens	221-226
34987391-6	2021	The results showed that methyl gallate significantly ameliorated HN by inhibiting uric acid production and promoting uric acid excretion as well as ameliorating renal injury induced by NLRP3 activation.	methyl gallate	24-38	NLR family pyrin domain containing 3	Homo sapiens	185-190
34987391-7	2021	Mechanistically, methyl gallate is a direct NLRP3 inhibitor that inhibits NLRP3 inflammasome activation but has no effect on the activation of AIM2 or NLRC4 inflammasomes in macrophages.	methyl gallate	17-31	NLR family pyrin domain containing 3	Homo sapiens	44-49
34988126-2	2021	Aging is linked to chronic sterile inflammation and high burden of reactive oxygen species (ROS), leading to activation of pattern recognition receptors (PRRs) such as Nlrp3 in vascular cells.	Reactive Oxygen Species	92-95	NLR family pyrin domain containing 3	Homo sapiens	168-173
34987391-7	2021	Mechanistically, methyl gallate is a direct NLRP3 inhibitor that inhibits NLRP3 inflammasome activation but has no effect on the activation of AIM2 or NLRC4 inflammasomes in macrophages.	methyl gallate	17-31	NLR family pyrin domain containing 3	Homo sapiens	74-79
34987391-8	2021	Furthermore, methyl gallate inhibited the assembly of NLRP3 inflammasomes by blocking the ROS over-generation and oligomerization of NLRP3.	methyl gallate	13-27	NLR family pyrin domain containing 3	Homo sapiens	54-59
34987391-8	2021	Furthermore, methyl gallate inhibited the assembly of NLRP3 inflammasomes by blocking the ROS over-generation and oligomerization of NLRP3.	methyl gallate	13-27	NLR family pyrin domain containing 3	Homo sapiens	133-138
34987391-8	2021	Furthermore, methyl gallate inhibited the assembly of NLRP3 inflammasomes by blocking the ROS over-generation and oligomerization of NLRP3.	ros	90-93	NLR family pyrin domain containing 3	Homo sapiens	54-59
34987391-10	2021	In conclusion, methyl gallate has a nephroprotective effect against PO-induced HN through blocking the oligomerization of NLRP3 and then exerting anti-inflammatory activity in the NLRP3-driven diseases.	methyl gallate	15-29	NLR family pyrin domain containing 3	Homo sapiens	122-127
34916479-0	2021	Galangin Enhances Anticancer Efficacy of 5-Fluorouracil in Esophageal Cancer Cells and Xenografts Through NLR Family Pyrin Domain Containing 3 (NLRP3) Downregulation.	galangin	0-8	NLR family pyrin domain containing 3	Homo sapiens	106-142
34987391-10	2021	In conclusion, methyl gallate has a nephroprotective effect against PO-induced HN through blocking the oligomerization of NLRP3 and then exerting anti-inflammatory activity in the NLRP3-driven diseases.	methyl gallate	15-29	NLR family pyrin domain containing 3	Homo sapiens	180-185
34860497-0	2021	Attenuation of NLRP3 Inflammasome Activation by Indirubin-Derived PROTAC Targeting HDAC6.	indirubin	48-57	NLR family pyrin domain containing 3	Homo sapiens	15-20
34916479-0	2021	Galangin Enhances Anticancer Efficacy of 5-Fluorouracil in Esophageal Cancer Cells and Xenografts Through NLR Family Pyrin Domain Containing 3 (NLRP3) Downregulation.	galangin	0-8	NLR family pyrin domain containing 3	Homo sapiens	144-149
34916479-0	2021	Galangin Enhances Anticancer Efficacy of 5-Fluorouracil in Esophageal Cancer Cells and Xenografts Through NLR Family Pyrin Domain Containing 3 (NLRP3) Downregulation.	Fluorouracil	41-55	NLR family pyrin domain containing 3	Homo sapiens	106-142
34916479-1	2021	BACKGROUND Galangin is believed to exert antioxidant effects by inhibition of the NLR family pyrin domain containing 3 (NLRP3) inflammasome, which has been linked to chemotherapy sensitivity in cancers.	galangin	11-19	NLR family pyrin domain containing 3	Homo sapiens	82-118
34916479-1	2021	BACKGROUND Galangin is believed to exert antioxidant effects by inhibition of the NLR family pyrin domain containing 3 (NLRP3) inflammasome, which has been linked to chemotherapy sensitivity in cancers.	galangin	11-19	NLR family pyrin domain containing 3	Homo sapiens	120-125
34916479-8	2021	NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels.	Fluorouracil	57-61	NLR family pyrin domain containing 3	Homo sapiens	0-5
34916479-8	2021	NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels.	Fluorouracil	57-61	NLR family pyrin domain containing 3	Homo sapiens	120-125
34916479-8	2021	NLRP3 was identified as being significantly activated by 5-FU, but galangin treatment reversed the effect and inhibited NLRP3 expression, which was accompanied by downregulated interleukin-1b levels.	galangin	67-75	NLR family pyrin domain containing 3	Homo sapiens	120-125
34956386-7	2021	What is more, upregulated protein expression of p-IKKalpha/beta, p-NF-kappaB p65, NLRP3, cleaved caspase 1, and mature IL-1beta occurred in HepG2 cells in response to PA stress while rescued with the PCB2 intervention.	Protactinium	167-169	NLR family pyrin domain containing 3	Homo sapiens	82-87
34956386-8	2021	In conclusion, our study demonstrated that PA induces ERS in HepG2 cells and subsequently activates downstream NLRP3 inflammasome-mediated cellular injury, while PCB2 inhibits NLRP3/caspase 1/IL-1beta pathway, inflammation, and apoptosis with the presence of ERS, thereby promoting cell survival, which may provide pharmacological evidence for clinical approaches on NAFLD.	Protactinium	43-45	NLR family pyrin domain containing 3	Homo sapiens	111-116
34922061-0	2021	Upregulated NLRP3 inflammasome activation is attenuated by anthocyanins in patients with nonalcoholic fatty liver disease: A case-control and an intervention study.	Anthocyanins	59-71	NLR family pyrin domain containing 3	Homo sapiens	12-17
34922061-9	2021	After anthocyanin administration, both mRNA expression of NLRP3 inflammasome components (caspase-1, IL-1beta, and IL-18) in PBMCs and plasma levels of IL-1beta and IL-18 decreased dramatically in NAFLD patients compared with controls.	Anthocyanins	6-17	NLR family pyrin domain containing 3	Homo sapiens	58-63
34801560-10	2021	Further experiments showed that iRFA treatment induced upregulation of HSP70, which inhibited the cisplatin-induced NLRP3 inflammasome activation, leading to inhibition of pyroptosis.	irfa	32-36	NLR family pyrin domain containing 3	Homo sapiens	116-121
34801560-10	2021	Further experiments showed that iRFA treatment induced upregulation of HSP70, which inhibited the cisplatin-induced NLRP3 inflammasome activation, leading to inhibition of pyroptosis.	Cisplatin	98-107	NLR family pyrin domain containing 3	Homo sapiens	116-121
34922061-10	2021	CONCLUSIONS: This study has demonstrated that the activation of NLRP3 inflammasome is highly increased in NAFLD patients, but it can be markedly suppressed by anthocyanins, which provides a rationale for the development of anti-inflammatory therapies in NAFLD.	Anthocyanins	159-171	NLR family pyrin domain containing 3	Homo sapiens	64-69
34801560-11	2021	HSP70 knockdown or NLRP3 overexpression could reverse the effect of iRFA treatment in vitro.	irfa	68-72	NLR family pyrin domain containing 3	Homo sapiens	19-24
34787067-0	2021	Zafirlukast ameliorates Docetaxel-induced activation of NOD-like receptor protein 3 (NLRP3) inflammasome, mediated by Sirtuin1 (SIRT1) in hepatocytes.	zafirlukast	0-11	NLR family pyrin domain containing 3	Homo sapiens	56-83
34966742-0	2021	5-Hydroxymethylfurfural Alleviates Inflammatory Lung Injury by Inhibiting Endoplasmic Reticulum Stress and NLRP3 Inflammasome Activation.	5-hydroxymethylfurfural	0-23	NLR family pyrin domain containing 3	Homo sapiens	107-112
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	25-30	NLR family pyrin domain containing 3	Homo sapiens	34-39
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	25-30	NLR family pyrin domain containing 3	Homo sapiens	177-182
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	168-173	NLR family pyrin domain containing 3	Homo sapiens	34-39
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	168-173	NLR family pyrin domain containing 3	Homo sapiens	177-182
34966742-7	2021	In conclusion, our findings elucidate the anti-inflammatory and protective efficacy of 5-HMF in LPS-induced acute lung injury, and also demonstrate the key mechanism of its action against NLRP3 inflammasome-related inflammatory disorders via the inhibition of ER stress.	5-hydroxymethylfurfural	87-92	NLR family pyrin domain containing 3	Homo sapiens	188-193
34906598-7	2021	Furthermore, the non-selective NLRP3 inhibitor colchicine has been recently shown to significantly reduce cardiovascular events in patients with chronic coronary disease.	Colchicine	47-57	NLR family pyrin domain containing 3	Homo sapiens	31-36
34858005-0	2021	Activation of NLRP3 Inflammasome by Palmitic Acid in Human Sebocytes.	Palmitic Acid	36-49	NLR family pyrin domain containing 3	Homo sapiens	14-19
34858005-9	2021	In addition, NLRP3 knockdown attenuated IL-1beta production by sebocytes stimulated with PA.	Palmitic Acid	89-91	NLR family pyrin domain containing 3	Homo sapiens	13-18
34858005-11	2021	Conclusion: These findings indicate that PA activates the NLRP3 inflammasome before induction of an inflammatory response in sebocytes.	Palmitic Acid	41-43	NLR family pyrin domain containing 3	Homo sapiens	58-63
34955826-1	2021	Background: In this study, we mainly aimed to explore the correlation between galloflavin and NLRP3 and its effect on colorectal cancer.	galloflavin	78-89	NLR family pyrin domain containing 3	Homo sapiens	94-99
34955826-6	2021	Small molecule-protein docking and pull-down assay were performed to confirm the targeting relationship between galloflavin and NLRP3.	galloflavin	112-123	NLR family pyrin domain containing 3	Homo sapiens	128-133
34955826-11	2021	The knockout of NLRP3 inhibited the effect of galloflavin, which did not significantly change the migration and invasion abilities.	galloflavin	46-57	NLR family pyrin domain containing 3	Homo sapiens	16-21
34955826-12	2021	Molecular docking and pull-down assay revealed a targeted binding relationship between galloflavin and NLRP3 and that galloflavin is bound to NLRP3 not ASC protein.	galloflavin	87-98	NLR family pyrin domain containing 3	Homo sapiens	103-108
34955826-12	2021	Molecular docking and pull-down assay revealed a targeted binding relationship between galloflavin and NLRP3 and that galloflavin is bound to NLRP3 not ASC protein.	galloflavin	118-129	NLR family pyrin domain containing 3	Homo sapiens	103-108
34955826-12	2021	Molecular docking and pull-down assay revealed a targeted binding relationship between galloflavin and NLRP3 and that galloflavin is bound to NLRP3 not ASC protein.	galloflavin	118-129	NLR family pyrin domain containing 3	Homo sapiens	142-147
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	0-16	NLR family pyrin domain containing 3	Homo sapiens	80-85
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	18-21	NLR family pyrin domain containing 3	Homo sapiens	80-85
34899969-11	2021	Conclusion: NAC could effectively inhibit the production of IL-18 by suppressing NLRP3 expression in macrophages to reduce the production of IFN-gamma in NK cells.	Acetylcysteine	12-15	NLR family pyrin domain containing 3	Homo sapiens	81-86
34226664-8	2021	Moreover, darapladib substantially reduced the Ang II infusion-induced expression of nucleotide-binding oligomerization domain-like receptor with pyrin domain 3 (NLRP3) and interleukin (IL)-1beta and markedly attenuated caspase-1 activation in cardiac tissues.	darapladib	10-20	NLR family pyrin domain containing 3	Homo sapiens	85-160
34226664-8	2021	Moreover, darapladib substantially reduced the Ang II infusion-induced expression of nucleotide-binding oligomerization domain-like receptor with pyrin domain 3 (NLRP3) and interleukin (IL)-1beta and markedly attenuated caspase-1 activation in cardiac tissues.	darapladib	10-20	NLR family pyrin domain containing 3	Homo sapiens	162-167
34226664-9	2021	Furthermore, darapladib ameliorated Ang II-stimulated macrophage migration and IL-1beta secretion in macrophages by blocking NLRP3 inflammasome activation.	darapladib	13-23	NLR family pyrin domain containing 3	Homo sapiens	125-130
34226664-10	2021	Darapladib also effectively blocked macrophage-mediated transformation of fibroblasts into myofibroblasts by inhibiting the activation of the NLRP3 inflammasome in macrophages.	darapladib	0-10	NLR family pyrin domain containing 3	Homo sapiens	142-147
34226664-11	2021	Overall, our study identifies a novel anti-inflammatory and anti-cardiac fibrosis role of darapladib in Lp-PLA2 inhibition, elucidating the protective effects of suppressing NLRP3 inflammasome activation.	darapladib	90-100	NLR family pyrin domain containing 3	Homo sapiens	174-179
34787067-0	2021	Zafirlukast ameliorates Docetaxel-induced activation of NOD-like receptor protein 3 (NLRP3) inflammasome, mediated by Sirtuin1 (SIRT1) in hepatocytes.	zafirlukast	0-11	NLR family pyrin domain containing 3	Homo sapiens	85-90
34787067-0	2021	Zafirlukast ameliorates Docetaxel-induced activation of NOD-like receptor protein 3 (NLRP3) inflammasome, mediated by Sirtuin1 (SIRT1) in hepatocytes.	Docetaxel	24-33	NLR family pyrin domain containing 3	Homo sapiens	56-83
34787067-0	2021	Zafirlukast ameliorates Docetaxel-induced activation of NOD-like receptor protein 3 (NLRP3) inflammasome, mediated by Sirtuin1 (SIRT1) in hepatocytes.	Docetaxel	24-33	NLR family pyrin domain containing 3	Homo sapiens	85-90
34787067-9	2021	Mechanistically, our results demonstrate that Zafirlukast inhibited the activation of NOD-like receptor protein 3 (NLRP3), mediated by SIRT1.	zafirlukast	46-57	NLR family pyrin domain containing 3	Homo sapiens	86-113
34338149-0	2021	Omarigliptin ameliorated high glucose-induced nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation through activating adenosine monophosphate-activated protein kinase alpha (AMPKalpha) in renal glomerular endothelial cells.	2-(2,5-difluorophenyl)-5-(2-(methylsulfonyl)-2,6-dihydropyrrolo(3,4-c)pyrazol-5(4H)-yl)tetrahydro-2H-pyran-3-amine	0-12	NLR family pyrin domain containing 3	Homo sapiens	105-110
34338149-0	2021	Omarigliptin ameliorated high glucose-induced nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation through activating adenosine monophosphate-activated protein kinase alpha (AMPKalpha) in renal glomerular endothelial cells.	Glucose	30-37	NLR family pyrin domain containing 3	Homo sapiens	105-110
34787067-9	2021	Mechanistically, our results demonstrate that Zafirlukast inhibited the activation of NOD-like receptor protein 3 (NLRP3), mediated by SIRT1.	zafirlukast	46-57	NLR family pyrin domain containing 3	Homo sapiens	115-120
34338149-0	2021	Omarigliptin ameliorated high glucose-induced nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation through activating adenosine monophosphate-activated protein kinase alpha (AMPKalpha) in renal glomerular endothelial cells.	Adenosine	155-164	NLR family pyrin domain containing 3	Homo sapiens	105-110
34488537-4	2021	Interestingly, miR-556-5p ablation triggered pyroptotic cell death in cisplatin-treated CR-NSCLC cells via upregulating NLRP3, and the promoting effects of miR-556-5p silence on cisplatin-sensitivity in CR-NSCLC cells were abrogated by both cell pyroptosis inhibitor NSA and NLRP3 downregulation.	Cisplatin	70-79	NLR family pyrin domain containing 3	Homo sapiens	120-125
34338149-7	2021	Furthermore, the activated NLRP3 inflammasome and the excessive production of interleukin 18 (IL-18) and interleukin 1beta (IL-1beta) in HrGECs induced by incubation with HG were pronouncedly reversed by the introduction of Omarigliptin, accompanied by the activation of the AMPK/mTOR signaling pathway.	2-(2,5-difluorophenyl)-5-(2-(methylsulfonyl)-2,6-dihydropyrrolo(3,4-c)pyrazol-5(4H)-yl)tetrahydro-2H-pyran-3-amine	224-236	NLR family pyrin domain containing 3	Homo sapiens	27-32
34338149-8	2021	After the co-administration of the adenosine monophosphate-activated protein kinase alpha (AMPKalpha) inhibitor, compound C, the protective effects of Omarigliptin against HG-induced NLRP3 inflammasome activation and production of pro-inflammatory factors were dramatically abolished.	Adenosine	35-44	NLR family pyrin domain containing 3	Homo sapiens	183-188
34338149-8	2021	After the co-administration of the adenosine monophosphate-activated protein kinase alpha (AMPKalpha) inhibitor, compound C, the protective effects of Omarigliptin against HG-induced NLRP3 inflammasome activation and production of pro-inflammatory factors were dramatically abolished.	2-(2,5-difluorophenyl)-5-(2-(methylsulfonyl)-2,6-dihydropyrrolo(3,4-c)pyrazol-5(4H)-yl)tetrahydro-2H-pyran-3-amine	151-163	NLR family pyrin domain containing 3	Homo sapiens	183-188
34338149-9	2021	Taken together, our data revealed that Omarigliptin ameliorated HG-induced inflammation in renal glomerular endothelial cells through suppressing NLRP3 inflammasome activation mediated by AMPKalpha.	2-(2,5-difluorophenyl)-5-(2-(methylsulfonyl)-2,6-dihydropyrrolo(3,4-c)pyrazol-5(4H)-yl)tetrahydro-2H-pyran-3-amine	39-51	NLR family pyrin domain containing 3	Homo sapiens	146-151
34338149-9	2021	Taken together, our data revealed that Omarigliptin ameliorated HG-induced inflammation in renal glomerular endothelial cells through suppressing NLRP3 inflammasome activation mediated by AMPKalpha.	ampkalpha	188-197	NLR family pyrin domain containing 3	Homo sapiens	146-151
34488537-0	2021	Knock-down of microRNA miR-556-5p increases cisplatin-sensitivity in non-small cell lung cancer (NSCLC) via activating NLR family pyrin domain containing 3 (NLRP3)-mediated pyroptotic cell death.	Cisplatin	44-53	NLR family pyrin domain containing 3	Homo sapiens	119-155
34488537-0	2021	Knock-down of microRNA miR-556-5p increases cisplatin-sensitivity in non-small cell lung cancer (NSCLC) via activating NLR family pyrin domain containing 3 (NLRP3)-mediated pyroptotic cell death.	Cisplatin	44-53	NLR family pyrin domain containing 3	Homo sapiens	157-162
34488537-4	2021	Interestingly, miR-556-5p ablation triggered pyroptotic cell death in cisplatin-treated CR-NSCLC cells via upregulating NLRP3, and the promoting effects of miR-556-5p silence on cisplatin-sensitivity in CR-NSCLC cells were abrogated by both cell pyroptosis inhibitor NSA and NLRP3 downregulation.	Cisplatin	70-79	NLR family pyrin domain containing 3	Homo sapiens	275-280
34488537-4	2021	Interestingly, miR-556-5p ablation triggered pyroptotic cell death in cisplatin-treated CR-NSCLC cells via upregulating NLRP3, and the promoting effects of miR-556-5p silence on cisplatin-sensitivity in CR-NSCLC cells were abrogated by both cell pyroptosis inhibitor NSA and NLRP3 downregulation.	Cisplatin	178-187	NLR family pyrin domain containing 3	Homo sapiens	275-280
34488537-5	2021	Taken together, this study firstly evidenced that induction of NLRP3-mediated cell pyroptosis by miR-556-5p downregulation was effective to increase cisplatin-sensitivity in NSCLC, which provided new therapy strategies to overcome chemo-resistance for NSCLC patients in clinic.	Cisplatin	149-158	NLR family pyrin domain containing 3	Homo sapiens	63-68
34496682-5	2021	RESULTS: High cobalt chloride exposure mediated significant increase in caspase-1 activity, cytokine levels, and IL1B and NLRP3 expression with a corresponding regulatory decrease for CASP1 and PYCARD expression.	cobaltous chloride	14-29	NLR family pyrin domain containing 3	Homo sapiens	122-127
34925366-1	2021	Gout flares require monosodium urate (MSU) to activate the NLRP3 inflammasome and secrete sufficient IL-1beta.	Uric Acid	20-36	NLR family pyrin domain containing 3	Homo sapiens	59-64
34925366-1	2021	Gout flares require monosodium urate (MSU) to activate the NLRP3 inflammasome and secrete sufficient IL-1beta.	Uric Acid	38-41	NLR family pyrin domain containing 3	Homo sapiens	59-64
34925366-5	2021	Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1beta secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare.	purine	0-6	NLR family pyrin domain containing 3	Homo sapiens	70-75
34925366-5	2021	Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1beta secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare.	Adenosine	27-36	NLR family pyrin domain containing 3	Homo sapiens	70-75
34925366-5	2021	Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1beta secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare.	purine	196-202	NLR family pyrin domain containing 3	Homo sapiens	70-75
34925366-5	2021	Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1beta secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare.	Adenosine	223-232	NLR family pyrin domain containing 3	Homo sapiens	70-75
34925366-5	2021	Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1beta secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare.	Adenosine	249-258	NLR family pyrin domain containing 3	Homo sapiens	70-75
34768128-10	2021	RESULTS: CS resulted in shrinkage of endothelial cells, impaired aorta relaxation, reduced eNOS expression, and induced expression of iNOS, NLRP3, caspase-1p20 and IL-1beta, which could be prevented by knockdown of iNOS and NLRP3.	Cesium	9-11	NLR family pyrin domain containing 3	Homo sapiens	140-145
34509315-0	2021	Dopamine promotes the progression of AML via activating NLRP3 inflammasome and IL-1beta.	Dopamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	56-61
34509315-4	2021	Here, we investigated the effects and mechanisms of dopamine in NLRP3 inflammasome activation and cellular viability of acute myeloid leukemia U937 cells.	Dopamine	52-60	NLR family pyrin domain containing 3	Homo sapiens	64-69
34509315-5	2021	Our results showed that dopamine enhanced the viability of U937 cells and activated the NLRP3 inflammasome in U937 cells.	Dopamine	24-32	NLR family pyrin domain containing 3	Homo sapiens	88-93
34509315-8	2021	Furthermore, we treated U937 cells with DR1/2/3/5 antagonist before dopamine, and it manifestly reversed the NLRP3 inflammasome activation and the viability-enhancing effect in U937 cells induced by dopamine.	Dopamine	68-76	NLR family pyrin domain containing 3	Homo sapiens	109-114
34509315-8	2021	Furthermore, we treated U937 cells with DR1/2/3/5 antagonist before dopamine, and it manifestly reversed the NLRP3 inflammasome activation and the viability-enhancing effect in U937 cells induced by dopamine.	Dopamine	199-207	NLR family pyrin domain containing 3	Homo sapiens	109-114
34509315-10	2021	We concluded that dopamine could enhance the viability of U937 cells through DR1/5 receptor pathway and activate NLRP3 inflammasome.	Dopamine	18-26	NLR family pyrin domain containing 3	Homo sapiens	113-118
34768128-10	2021	RESULTS: CS resulted in shrinkage of endothelial cells, impaired aorta relaxation, reduced eNOS expression, and induced expression of iNOS, NLRP3, caspase-1p20 and IL-1beta, which could be prevented by knockdown of iNOS and NLRP3.	Cesium	9-11	NLR family pyrin domain containing 3	Homo sapiens	224-229
34794890-1	2021	OBJECTIVE: To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-kappaB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-kappaB/NLRP3/GSDMD signals.	isoliquiritigenin	242-259	NLR family pyrin domain containing 3	Homo sapiens	315-320
34768128-12	2021	Altogether, activation of the NLRP3 inflammasome by iNOS in CS-exposed HAECs may be mediated by the sGC/cGMP/PKG/TACE/TNF- alpha pathway.	Cesium	60-62	NLR family pyrin domain containing 3	Homo sapiens	30-35
34794890-6	2021	RESULTS: P. gingivalis-LPS/ATP stimulation significantly promoted expression of NF-kappaB, the NLRP3 inflammasome, GSDMD, and IL-1beta at gene and protein levels.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	95-100
34794890-0	2021	Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-kappaB/ NLRP3/GSDMD signals in human gingival fibroblasts.	isoliquiritigenin	0-17	NLR family pyrin domain containing 3	Homo sapiens	95-100
34794890-0	2021	Isoliquiritigenin alleviates P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting NF-kappaB/ NLRP3/GSDMD signals in human gingival fibroblasts.	Adenosine Triphosphate	47-50	NLR family pyrin domain containing 3	Homo sapiens	95-100
34794890-9	2021	CONCLUSIONS: P. gingivalis-LPS/ATP induced pyroptosis in HGFs by activating NF-kappaB/NLRP3/GSDMD signals and ISL attenuated P. gingivalis-LPS/ATP-induced pyroptosis by inhibiting these signals.	Adenosine Triphosphate	31-34	NLR family pyrin domain containing 3	Homo sapiens	86-91
34768128-14	2021	The findings identify a mechanism through which iNOS and NLRP3 contribute to the pathogenesis of CS-induced pyroptosis and impaired aorta relaxation in HAECs.	Cesium	97-99	NLR family pyrin domain containing 3	Homo sapiens	57-62
34794890-1	2021	OBJECTIVE: To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-kappaB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-kappaB/NLRP3/GSDMD signals.	Adenosine	124-133	NLR family pyrin domain containing 3	Homo sapiens	171-176
34794890-1	2021	OBJECTIVE: To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-kappaB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-kappaB/NLRP3/GSDMD signals.	Adenosine	124-133	NLR family pyrin domain containing 3	Homo sapiens	315-320
34794890-1	2021	OBJECTIVE: To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-kappaB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-kappaB/NLRP3/GSDMD signals.	Adenosine Triphosphate	148-151	NLR family pyrin domain containing 3	Homo sapiens	171-176
34794890-1	2021	OBJECTIVE: To investigate whether pyroptosis is induced by Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)/ adenosine triphosphate (ATP) through NF-kappaB/NLRP3/GSDMD signaling in human gingival fibroblasts (HGFs) and whether isoliquiritigenin (ISL) alleviates pyroptosis by inhibition of NF-kappaB/NLRP3/GSDMD signals.	Adenosine Triphosphate	148-151	NLR family pyrin domain containing 3	Homo sapiens	315-320
34643253-8	2021	Similar in HPDE6C7 cells, CAE treatment caused supernatant IL-1beta level, NLRP3 and caspase-1 mRNA expression levels to significantly increase.	Ceruletide	26-29	NLR family pyrin domain containing 3	Homo sapiens	75-80
34600073-5	2021	And, it was found that Parkin could exert neuroprotective effects on RGCs by inhibiting nucleotide-binding domain leucine-rich repeat containing family pyrin domain containing 3 (NLRP3) inflammasome.	Leucine	114-121	NLR family pyrin domain containing 3	Homo sapiens	179-184
34481870-0	2021	Genkwanin suppresses MPP+-induced cytotoxicity by inhibiting TLR4/MyD88/NLRP3 inflammasome pathway in a cellular model of Parkinson"s disease.	genkwanin	0-9	NLR family pyrin domain containing 3	Homo sapiens	72-77
34481870-12	2021	Genkwanin suppressed MPP+-induced activation of TLR4/MyD88/NLRP3 inflammasome pathway in SH-SY5Y cells.	genkwanin	0-9	NLR family pyrin domain containing 3	Homo sapiens	59-64
34481870-14	2021	In conclusion, genkwanin attenuated neuroinflammation and neurotoxicity by inhibiting TLR4/MyD88/NLRP3 inflammasome pathway in MPP+-induced cellular model of PD.	genkwanin	15-24	NLR family pyrin domain containing 3	Homo sapiens	97-102
34717147-0	2021	Inhibitory effects of sulforaphane on NLRP3 inflammasome activation.	sulforaphane	22-34	NLR family pyrin domain containing 3	Homo sapiens	38-43
34600073-6	2021	Moreover, the genetic and pharmacological downregulation of NLRP3 improved survival of RGCs against glutamate excitotoxicity.	Glutamic Acid	100-109	NLR family pyrin domain containing 3	Homo sapiens	60-65
34739715-0	2021	Resveratrol Inhibits NLRP3 Inflammasome-Induced Pyroptosis and miR-155 Expression in Microglia Through Sirt1/AMPK Pathway.	Resveratrol	0-11	NLR family pyrin domain containing 3	Homo sapiens	21-26
34600073-7	2021	In the end, knockdown of Parkin exacerbated glutamate induced RGCs damage via triggering NLRP3 inflammasome activation.	Glutamic Acid	44-53	NLR family pyrin domain containing 3	Homo sapiens	89-94
34739715-6	2021	Our results demonstrated that resveratrol inhibits LPS- and ATP-activated NLRP3 inflammasome and protects microglial cells upon oxidative stress, proinflammatory cytokine production, and pyroptotic cell death resulting from inflammasome activation.	Resveratrol	30-41	NLR family pyrin domain containing 3	Homo sapiens	74-79
34739715-10	2021	To sum up, our results suggest that resveratrol suppresses the NLRP3 inflammasome and miR-155 expression through AMPK and Sirt1 pathways in microglia.	Resveratrol	36-47	NLR family pyrin domain containing 3	Homo sapiens	63-68
34663173-0	2021	Genistein alleviates H2O2-induced senescence of human umbilical vein endothelial cells via regulating the TXNIP/NLRP3 axis.	Genistein	0-9	NLR family pyrin domain containing 3	Homo sapiens	112-117
34663173-0	2021	Genistein alleviates H2O2-induced senescence of human umbilical vein endothelial cells via regulating the TXNIP/NLRP3 axis.	Hydrogen Peroxide	21-25	NLR family pyrin domain containing 3	Homo sapiens	112-117
34663173-9	2021	Expressions of TXNIP and NLRP3 in HUVECs were up-regulated by H2O2 but down-regulated by Gen. Overexpressed TXNIP partially reversed the suppressive effect of Gen on H2O2-induced senescence and apoptosis of HUVECs.	Hydrogen Peroxide	62-66	NLR family pyrin domain containing 3	Homo sapiens	25-30
34663173-8	2021	H2O2-induced HUVEC senescence and the expression of TXNIP and NLRP3 in HUVECs were down-regulated by Gen (40 and 80 microg/mL).	Hydrogen Peroxide	0-4	NLR family pyrin domain containing 3	Homo sapiens	62-67
34663173-9	2021	Expressions of TXNIP and NLRP3 in HUVECs were up-regulated by H2O2 but down-regulated by Gen. Overexpressed TXNIP partially reversed the suppressive effect of Gen on H2O2-induced senescence and apoptosis of HUVECs.	Hydrogen Peroxide	166-170	NLR family pyrin domain containing 3	Homo sapiens	25-30
34663173-8	2021	H2O2-induced HUVEC senescence and the expression of TXNIP and NLRP3 in HUVECs were down-regulated by Gen (40 and 80 microg/mL).	Genistein	101-104	NLR family pyrin domain containing 3	Homo sapiens	62-67
34663173-10	2021	Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H2O2-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP.	Genistein	120-123	NLR family pyrin domain containing 3	Homo sapiens	32-37
34663173-11	2021	DISCUSSION AND CONCLUSIONS: H2O2-induced HUVEC senescence was alleviated by Gen via suppressing the TXNIP/NLRP3 axis, which may offer a potential therapeutic approach for improving HUVEC senescence and provide a new direction for the treatment of cardiovascular disease.	Hydrogen Peroxide	28-32	NLR family pyrin domain containing 3	Homo sapiens	106-111
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	NLR family pyrin domain containing 3	Homo sapiens	123-128
34663173-11	2021	DISCUSSION AND CONCLUSIONS: H2O2-induced HUVEC senescence was alleviated by Gen via suppressing the TXNIP/NLRP3 axis, which may offer a potential therapeutic approach for improving HUVEC senescence and provide a new direction for the treatment of cardiovascular disease.	Genistein	76-79	NLR family pyrin domain containing 3	Homo sapiens	106-111
34293432-0	2021	Lysophosphatidylcholine induces apoptosis and inflammatory damage in brain microvascular endothelial cells via GPR4-mediated NLRP3 inflammasome activation.	Lysophosphatidylcholines	0-23	NLR family pyrin domain containing 3	Homo sapiens	125-130
34872043-2	2021	Several studies have shown that 1,25-dihydroxyvitamin D3 (1,25(OH)2VD3) inhibits the priming step required for NLRP3 inflammasome activation in immune cells.	Calcitriol	32-56	NLR family pyrin domain containing 3	Homo sapiens	111-116
34293432-5	2021	Our results showed that LPC significantly increased the levels of inflammatory cytokines (IL-1beta, IL-18, and IL-33) and markedly induced apoptosis and NLRP3 inflammasome activation in BMECs.	Lysophosphatidylcholines	24-27	NLR family pyrin domain containing 3	Homo sapiens	153-158
34293432-7	2021	Above all, we also proved that LPC induced apoptosis and inflammatory injury in BMECs by causing GPR4 to activate NLRP3 inflammasomes.	Lysophosphatidylcholines	31-34	NLR family pyrin domain containing 3	Homo sapiens	114-119
34866924-9	2021	Thus, melatonin has shown regulatory effects against the TBI-induced autophagic dysfunction, regulation of mitogen-activated protein kinases, such as ERK, activation of the NLRP-3 inflammasome, and release of the inflammatory cytokines.	Melatonin	6-15	NLR family pyrin domain containing 3	Homo sapiens	173-179
34844623-0	2021	Honokiol alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via Nrf2 activation in vitro and in vivo.	honokiol	0-8	NLR family pyrin domain containing 3	Homo sapiens	64-69
34782454-7	2021	Decreased desmosterol accumulation in mitochondria promotes macrophage mitochondrial reactive oxygen species production and NLR family pyrin domain containing 3 (NLRP3)-dependent inflammasome activation.	Desmosterol	10-21	NLR family pyrin domain containing 3	Homo sapiens	124-160
34899720-0	2021	SIRT1 Promotes M2 Microglia Polarization via Reducing ROS-Mediated NLRP3 Inflammasome Signaling After Subarachnoid Hemorrhage.	Reactive Oxygen Species	54-57	NLR family pyrin domain containing 3	Homo sapiens	67-72
34899720-8	2021	In contrast, EX527 abated the upregulation of SIRT1 and reversed the inhibitory effects of SRT1720 on ROS-NLRP3 inflammasome activation and EBI.	SRT1720	91-98	NLR family pyrin domain containing 3	Homo sapiens	106-111
34899720-8	2021	In contrast, EX527 abated the upregulation of SIRT1 and reversed the inhibitory effects of SRT1720 on ROS-NLRP3 inflammasome activation and EBI.	Reactive Oxygen Species	102-105	NLR family pyrin domain containing 3	Homo sapiens	106-111
34899720-11	2021	Altogether, these findings indicate that SRT1720, an SIRT1 agonist, can ameliorate EBI after SAH by shifting the microglial phenotype toward M2 via modulation of ROS-mediated NLRP3 inflammasome signaling.	Reactive Oxygen Species	162-165	NLR family pyrin domain containing 3	Homo sapiens	175-180
34933712-6	2021	Therefore, in the current study, the effect of borage oil was considered on the signaling pathway of the NLRP3 inflammasome complex, TLR4, and serum levels of inflammatory cytokines (IL-1? and IL-18) in type II diabetic patients with ARDS.	borage oil	47-57	NLR family pyrin domain containing 3	Homo sapiens	105-110
34933712-9	2021	The expression of NLRP3 and TLR4 genes (by Real-time PCR technique) and serum levels of IL-1? and IL-18 (by ELISA test) were evaluated before and after treatment with borage oil through blood samples taken from patients.	borage oil	167-177	NLR family pyrin domain containing 3	Homo sapiens	18-23
34933712-10	2021	The results showed that serum levels of inflammatory cytokines (IL-1? and IL-18), NLRP3 gene, and TLR4 gene were significantly decreased in diabetic type II patients with mild ARDS by treating with borage oil.	borage oil	198-208	NLR family pyrin domain containing 3	Homo sapiens	82-87
34782454-7	2021	Decreased desmosterol accumulation in mitochondria promotes macrophage mitochondrial reactive oxygen species production and NLR family pyrin domain containing 3 (NLRP3)-dependent inflammasome activation.	Desmosterol	10-21	NLR family pyrin domain containing 3	Homo sapiens	162-167
34782454-8	2021	Deficiency of NLRP3 or apoptosis-associated speck-like protein containing a CARD (ASC) rescues the increased inflammasome activity and atherogenesis observed in desmosterol-depleted macrophages.	Desmosterol	161-172	NLR family pyrin domain containing 3	Homo sapiens	14-19
34782457-3	2021	However, retinal lipofuscin also presents biological and physicochemical characteristics indistinguishable from conventional granules, including indigestibility, tendency to cause lysosome swelling that results in rupture or defective functions, and ability to trigger NLRP3 inflammation, a symptom of low-level disruption of lysosomes.	Lipofuscin	17-27	NLR family pyrin domain containing 3	Homo sapiens	269-274
34867542-12	2021	NLRP3 levels were irrelevant to monthly alcohol assumption as well as to the MoCA, PSQI, GAD-7, PHQ-9, and Fazekas scale scores and WMV.	Alcohols	40-47	NLR family pyrin domain containing 3	Homo sapiens	0-5
34832969-4	2021	Because Stavudine (D4T), an antiretroviral drug, was recently shown to reduce inflammasome activation, we verified whether its effect is mediated by miR-7-5p, miR-22-3p, miR-30e-5p and miR-223-3p: miRNAs that bind the NLRP3-mRNA-UTR region and interfere with protein translation, reducing NLRP3 activation.	Stavudine	8-17	NLR family pyrin domain containing 3	Homo sapiens	218-223
34832969-4	2021	Because Stavudine (D4T), an antiretroviral drug, was recently shown to reduce inflammasome activation, we verified whether its effect is mediated by miR-7-5p, miR-22-3p, miR-30e-5p and miR-223-3p: miRNAs that bind the NLRP3-mRNA-UTR region and interfere with protein translation, reducing NLRP3 activation.	Stavudine	8-17	NLR family pyrin domain containing 3	Homo sapiens	289-294
34791735-6	2022	Results showed that quercetin could reduce LPS-induced C28/I2 cell apoptosis, extracellular matrix (ECM) degradation, and cell pyroptosis, and overexpression of nucleotide-binding domain and leucine-rich-repeat-containing (NLR) family, pyrin domain-containing 3 (NLRP3) revealed that quercetin reduced chondrocyte apoptosis and ECM degradation by inhibiting NLRP3-mediated pyroptosis.	Quercetin	20-29	NLR family pyrin domain containing 3	Homo sapiens	263-268
34830316-2	2021	We have previously shown that DC contains both microbial components and calcium phosphate crystals that induce an osteoclastogenic cytokine IL-1beta via the NLRP3 inflammasome in macrophages.	calcium phosphate	72-89	NLR family pyrin domain containing 3	Homo sapiens	157-162
34791735-6	2022	Results showed that quercetin could reduce LPS-induced C28/I2 cell apoptosis, extracellular matrix (ECM) degradation, and cell pyroptosis, and overexpression of nucleotide-binding domain and leucine-rich-repeat-containing (NLR) family, pyrin domain-containing 3 (NLRP3) revealed that quercetin reduced chondrocyte apoptosis and ECM degradation by inhibiting NLRP3-mediated pyroptosis.	Quercetin	20-29	NLR family pyrin domain containing 3	Homo sapiens	358-363
34791735-6	2022	Results showed that quercetin could reduce LPS-induced C28/I2 cell apoptosis, extracellular matrix (ECM) degradation, and cell pyroptosis, and overexpression of nucleotide-binding domain and leucine-rich-repeat-containing (NLR) family, pyrin domain-containing 3 (NLRP3) revealed that quercetin reduced chondrocyte apoptosis and ECM degradation by inhibiting NLRP3-mediated pyroptosis.	Quercetin	284-293	NLR family pyrin domain containing 3	Homo sapiens	263-268
34791735-6	2022	Results showed that quercetin could reduce LPS-induced C28/I2 cell apoptosis, extracellular matrix (ECM) degradation, and cell pyroptosis, and overexpression of nucleotide-binding domain and leucine-rich-repeat-containing (NLR) family, pyrin domain-containing 3 (NLRP3) revealed that quercetin reduced chondrocyte apoptosis and ECM degradation by inhibiting NLRP3-mediated pyroptosis.	Quercetin	284-293	NLR family pyrin domain containing 3	Homo sapiens	358-363
34791735-7	2022	Furthermore, quercetin could reduce chondrocyte apoptosis and ECM degradation, and inhibit NLRP3-mediated pyroptosis through blocking oxidative stress.	Quercetin	13-22	NLR family pyrin domain containing 3	Homo sapiens	91-96
34620721-14	2021	Here we show that increases of cAMP concentration within AII amacrine cells produce enhanced exocytosis from these glycinergic interneurons.	Cyclic AMP	31-35	NLR family pyrin domain containing 3	Homo sapiens	57-60
34767572-6	2021	RESULTS: PKD activation/auto-phosphorylation always preceded cleavage of caspase-1 and gasdermin D, and treatment with the PKD inhibitor CRT0066101 could block NLRP3 inflammasome assembly and interleukin-1beta production.	CRT 0066101	137-147	NLR family pyrin domain containing 3	Homo sapiens	160-165
34620721-15	2021	Therefore, we propose that light-sensitive neuromodulators may change the output of glycine release from AII amacrine cells.	Glycine	84-91	NLR family pyrin domain containing 3	Homo sapiens	105-108
34867921-1	2021	Nucleotide-binding domain and leucine-rich repeat-containing protein 3 (NLRP3) inflammasome-mediated interleukin-1 beta (IL-1beta) production is one of the crucial responses in innate immunity upon infection with viruses including influenza A virus (IAV) and is modulated by both viral and host cellular proteins.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	72-77
34858199-11	2021	miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro.	mir-204-5p	0-10	NLR family pyrin domain containing 3	Homo sapiens	20-25
34858199-11	2021	miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro.	mir-204-5p	0-10	NLR family pyrin domain containing 3	Homo sapiens	30-35
34858199-11	2021	miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro.	mir-204-5p	84-94	NLR family pyrin domain containing 3	Homo sapiens	20-25
34858199-11	2021	miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro.	mir-204-5p	84-94	NLR family pyrin domain containing 3	Homo sapiens	30-35
34858401-8	2021	Notably, TBK1 inhibition prevented LPS-induced NLRP3 inflammasome activation by targeting the mammalian target of rapamycin complex 1 (mTORC1).	Sirolimus	114-123	NLR family pyrin domain containing 3	Homo sapiens	47-52
34510229-0	2021	Cadmium induces renal inflammation by activating the NLRP3 inflammasome through ROS/MAPK/NF-kappaB pathway in vitro and in vivo.	Cadmium	0-7	NLR family pyrin domain containing 3	Homo sapiens	53-58
34524457-5	2021	NLRP3 is highly expressed during the mid-proliferative and mid-secretory phases of the human endometrium and transcriptionally up-regulated by estradiol (E2) through estrogen receptor beta (ERbeta).	Estradiol	143-152	NLR family pyrin domain containing 3	Homo sapiens	0-5
34524457-5	2021	NLRP3 is highly expressed during the mid-proliferative and mid-secretory phases of the human endometrium and transcriptionally up-regulated by estradiol (E2) through estrogen receptor beta (ERbeta).	Estradiol	154-156	NLR family pyrin domain containing 3	Homo sapiens	0-5
34524457-7	2021	Our findings suggest that NLRP3, which is transcriptionally regulated by E2, induces epithelial-mesenchymal transition of endometrial epithelial cells and promotes embryo adhesion.	Estradiol	73-75	NLR family pyrin domain containing 3	Homo sapiens	26-31
34819853-0	2021	Ethyl 2-Succinate-Anthraquinone Attenuates Inflammatory Response and Oxidative Stress via Regulating NLRP3 Signaling Pathway.	ethyl 2-succinate-anthraquinone	0-31	NLR family pyrin domain containing 3	Homo sapiens	101-106
34510229-5	2021	Results revealed that CdCl2 (2-8 muM) increased ROS production and activated NLRP3, thereby enhancing secretion of IL-1beta and IL-18 (P < 0.05).	Cadmium Chloride	22-27	NLR family pyrin domain containing 3	Homo sapiens	77-82
34510229-6	2021	Knock-down of NLRP3 rescued the RPTEC/TERT1 cells from Cd-induced inflammatory damage.	Cadmium	55-57	NLR family pyrin domain containing 3	Homo sapiens	14-19
34769294-0	2021	The Fibrotic Effects of TMAO on Human Renal Fibroblasts Is Mediated by NLRP3, Caspase-1 and the PERK/Akt/mTOR Pathway.	trimethyloxamine	24-28	NLR family pyrin domain containing 3	Homo sapiens	71-76
34562843-6	2021	Besides, EGCG significantly decreased overproduction of ROS and activation of MAPK signaling pathway induced by Hla, thereby markedly attenuating the expression of NLRP3 inflammasome-related proteins in THP-1 cells.	epigallocatechin gallate	9-13	NLR family pyrin domain containing 3	Homo sapiens	164-169
34555641-10	2021	In conclusion, ISL improves the ability of anti-oxidative stress, alleviates inflammatory reaction, apoptosis, and inhibits NLRP3 inflammasome to protect lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced ALF through activating the PGC-1alpha/Nrf2 pathway, which provides the possibility for the treatment of ALF.	Galactosamine	194-200	NLR family pyrin domain containing 3	Homo sapiens	124-129
34769294-5	2021	We found that TMAO promoted renal fibroblast activation and fibroblast proliferation via the PERK/Akt/mTOR pathway, NLRP3, and caspase-1 signaling.	trimethyloxamine	14-18	NLR family pyrin domain containing 3	Homo sapiens	116-121
34769294-8	2021	We have unraveled that the PERK/Akt/mTOR pathway, NLRP3, and caspase-1 mediates TMAO"s fibrotic effect on human renal fibroblasts.	trimethyloxamine	80-84	NLR family pyrin domain containing 3	Homo sapiens	50-55
34423507-0	2021	Ginsenoside Rg3 attenuates cisplatin-induced kidney injury through inhibition of apoptosis and autophagy-inhibited NLRP3.	ginsenoside Rg3	0-15	NLR family pyrin domain containing 3	Homo sapiens	115-120
34423507-0	2021	Ginsenoside Rg3 attenuates cisplatin-induced kidney injury through inhibition of apoptosis and autophagy-inhibited NLRP3.	Cisplatin	27-36	NLR family pyrin domain containing 3	Homo sapiens	115-120
34423507-1	2021	The NOD-like receptor family pyrin domain-containing (NLRP3) inflammasomes is centrally implicated in cisplatin (CP)-induced kidney injury.	Cisplatin	102-111	NLR family pyrin domain containing 3	Homo sapiens	54-59
34423507-7	2021	However, blockade of autophagy by 3-methyladenine reversed the suppression of SY on NLRP3 inflammasome activation and the protection of SY on HK-2 cells.	3-methyladenine	34-49	NLR family pyrin domain containing 3	Homo sapiens	84-89
34628106-0	2021	beta-hydroxybutyrate suppresses NLRP3 inflammasome-mediated placental inflammation and lipopolysaccharide-induced fetal absorption.	3-Hydroxybutyric Acid	0-20	NLR family pyrin domain containing 3	Homo sapiens	32-37
34664412-0	2021	Dexmedetomidine alleviates hepatic ischaemia-reperfusion injury via the PI3K/AKT/Nrf2-NLRP3 pathway.	Dexmedetomidine	0-15	NLR family pyrin domain containing 3	Homo sapiens	86-91
34664412-12	2021	Dex repressed NLRP3 inflammasome by activating the PI3K/AKT/Nrf2 pathway.	Dexmedetomidine	0-3	NLR family pyrin domain containing 3	Homo sapiens	14-19
34664412-14	2021	Overall, Dex repressed NLRP3 inflammasome and alleviated hepatic I/R injury via the miR-494/JUND/PI3K/AKT/Nrf2 axis.	Dexmedetomidine	9-12	NLR family pyrin domain containing 3	Homo sapiens	23-28
34173812-8	2021	Fisetin could also ameliorate and reduce oxLDL-induced upregulation of SREBP-1 and thereby expression of its downstream liposynthesis genes HMGCR and FAS via inhibiting ROS-induced NLRP3 activation.	fisetin	0-7	NLR family pyrin domain containing 3	Homo sapiens	181-186
34173812-8	2021	Fisetin could also ameliorate and reduce oxLDL-induced upregulation of SREBP-1 and thereby expression of its downstream liposynthesis genes HMGCR and FAS via inhibiting ROS-induced NLRP3 activation.	ros	169-172	NLR family pyrin domain containing 3	Homo sapiens	181-186
34173812-9	2021	In conclusion, fisetin could inhibit foam cell formation by blocking oxLDL induced ROS formation and subsequent NLRP3 activation, thereby inhibiting SREBP-1 and its downstream genes including FAS and HMGCR.	fisetin	15-22	NLR family pyrin domain containing 3	Homo sapiens	112-117
34554188-0	2021	BTK operates a phospho-tyrosine switch to regulate NLRP3 inflammasome activity.	Phosphotyrosine	15-31	NLR family pyrin domain containing 3	Homo sapiens	51-56
34554188-6	2021	As NLRP3 tyrosine modification by BTK also positively regulates IL-1beta release, we propose BTK as a multifunctional positive regulator of NLRP3 regulation and BTK phosphorylation of NLRP3 as a novel and therapeutically tractable step in the control of inflammation.	Tyrosine	9-17	NLR family pyrin domain containing 3	Homo sapiens	3-8
34628106-2	2021	Recently, the nucleotide-binding oligomerization domain, leucine-rich repeat-, and pyrin domain-containing 3 (NLRP3) inflammasome mechanisms ((a protein complex of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1)) have been reported to play roles in controlling placental inflammation involved in pregnancy pathologies.	Leucine	57-64	NLR family pyrin domain containing 3	Homo sapiens	164-169
34628106-3	2021	The ketone body beta-hydroxybutyrate (BHB) can suppress NLRP3 inflammasome activation and improve various inflammatory diseases.	3-Hydroxybutyric Acid	16-36	NLR family pyrin domain containing 3	Homo sapiens	56-61
34628106-3	2021	The ketone body beta-hydroxybutyrate (BHB) can suppress NLRP3 inflammasome activation and improve various inflammatory diseases.	3-Hydroxybutyric Acid	38-41	NLR family pyrin domain containing 3	Homo sapiens	56-61
34628106-4	2021	Therefore, we hypothesized that BHB could suppress activation of the NLRP3 inflammasome in the placenta, resulting in the improvement of pregnancy complications.	3-Hydroxybutyric Acid	32-35	NLR family pyrin domain containing 3	Homo sapiens	69-74
34238121-4	2021	Additionally, acrolein induces EAhy926 cells inflammatory response and pyroptosis by activating NOD-like receptor protein 3 (NLRP3) inflammasome.	Acrolein	14-22	NLR family pyrin domain containing 3	Homo sapiens	96-123
34536551-4	2021	Nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome, whose activation and assembly significantly affect the release of IL-1beta, is a crucial effector activated by a variety of metabolites.	Leucine	46-53	NLR family pyrin domain containing 3	Homo sapiens	82-87
34600334-5	2021	Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD.	celastrol	139-148	NLR family pyrin domain containing 3	Homo sapiens	58-63
34238121-4	2021	Additionally, acrolein induces EAhy926 cells inflammatory response and pyroptosis by activating NOD-like receptor protein 3 (NLRP3) inflammasome.	Acrolein	14-22	NLR family pyrin domain containing 3	Homo sapiens	125-130
34238121-7	2021	Notably, the present study also indicates that autophagy inhibited by inhibitor 3-methyladenine (3MA) and siAtg7 exacerbate acrolein-induced NLRP3 inflammasome activation and pyroptosis.	3-methyladenine	80-95	NLR family pyrin domain containing 3	Homo sapiens	141-146
34238121-7	2021	Notably, the present study also indicates that autophagy inhibited by inhibitor 3-methyladenine (3MA) and siAtg7 exacerbate acrolein-induced NLRP3 inflammasome activation and pyroptosis.	3-methyladenine	97-100	NLR family pyrin domain containing 3	Homo sapiens	141-146
34238121-7	2021	Notably, the present study also indicates that autophagy inhibited by inhibitor 3-methyladenine (3MA) and siAtg7 exacerbate acrolein-induced NLRP3 inflammasome activation and pyroptosis.	Acrolein	124-132	NLR family pyrin domain containing 3	Homo sapiens	141-146
34238121-8	2021	In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation.	Acrolein	12-20	NLR family pyrin domain containing 3	Homo sapiens	58-63
34238121-8	2021	In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation.	Reactive Oxygen Species	45-48	NLR family pyrin domain containing 3	Homo sapiens	58-63
34238121-8	2021	In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation.	Reactive Oxygen Species	93-96	NLR family pyrin domain containing 3	Homo sapiens	147-152
34238121-8	2021	In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation.	Reactive Oxygen Species	225-228	NLR family pyrin domain containing 3	Homo sapiens	147-152
34238121-8	2021	In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation.	Acrolein	232-240	NLR family pyrin domain containing 3	Homo sapiens	147-152
34760889-0	2021	Iguratimod Alleviates Myocardial Ischemia/Reperfusion Injury Through Inhibiting Inflammatory Response Induced by Cardiac Fibroblast Pyroptosis via COX2/NLRP3 Signaling Pathway.	iguratimod	0-10	NLR family pyrin domain containing 3	Homo sapiens	152-157
34951208-6	2021	In autoimmune diseases, NETs as important sources of autoantigens, can act as danger-associated molecular patterns( DAMPs) and activate the nucleotide-binding oligomerization domain leucine-rich repeats containing pyrin domain 3(NLRP3) inflammasome and complement system, thereby breaking self-tolerance and accelerating autoimmune inflammation.	Leucine	182-189	NLR family pyrin domain containing 3	Homo sapiens	229-234
34699250-0	2021	Tyrosine phosphorylation of NLRP3 by the Src family kinase Lyn suppresses the activity of the NLRP3 inflammasome.	Tyrosine	0-8	NLR family pyrin domain containing 3	Homo sapiens	28-33
34699250-0	2021	Tyrosine phosphorylation of NLRP3 by the Src family kinase Lyn suppresses the activity of the NLRP3 inflammasome.	Tyrosine	0-8	NLR family pyrin domain containing 3	Homo sapiens	94-99
34831052-3	2021	One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis.	Glucose	131-138	NLR family pyrin domain containing 3	Homo sapiens	38-43
34831052-3	2021	One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis.	Cholesterol	107-118	NLR family pyrin domain containing 3	Homo sapiens	38-43
34831052-3	2021	One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis.	Uric Acid	120-125	NLR family pyrin domain containing 3	Homo sapiens	38-43
34734090-8	2021	Western blot results showed that Man upregulated p-AMPKalpha levels and exhibited a significant AMPK activation effect, which was blocked by compound C. At the same time, Man downregulated the expression of NLRP3 inflammasome-related proteins and inhibited the activation of NLRP3 inflammasome, alleviating cell pyroptosis and inflammation effects.	mangiferin	33-36	NLR family pyrin domain containing 3	Homo sapiens	207-212
34734090-8	2021	Western blot results showed that Man upregulated p-AMPKalpha levels and exhibited a significant AMPK activation effect, which was blocked by compound C. At the same time, Man downregulated the expression of NLRP3 inflammasome-related proteins and inhibited the activation of NLRP3 inflammasome, alleviating cell pyroptosis and inflammation effects.	mangiferin	33-36	NLR family pyrin domain containing 3	Homo sapiens	275-280
34734090-8	2021	Western blot results showed that Man upregulated p-AMPKalpha levels and exhibited a significant AMPK activation effect, which was blocked by compound C. At the same time, Man downregulated the expression of NLRP3 inflammasome-related proteins and inhibited the activation of NLRP3 inflammasome, alleviating cell pyroptosis and inflammation effects.	mangiferin	171-174	NLR family pyrin domain containing 3	Homo sapiens	207-212
34734090-8	2021	Western blot results showed that Man upregulated p-AMPKalpha levels and exhibited a significant AMPK activation effect, which was blocked by compound C. At the same time, Man downregulated the expression of NLRP3 inflammasome-related proteins and inhibited the activation of NLRP3 inflammasome, alleviating cell pyroptosis and inflammation effects.	mangiferin	171-174	NLR family pyrin domain containing 3	Homo sapiens	275-280
34687223-3	2022	Herein, we for the first time revealed that micromolar range of PFOS exposure initiates the activation of NLR pyrin domain containing 3 (NLRP3) inflammasome to drive hepatocyte pyroptosis.	perfluorooctane sulfonic acid	64-68	NLR family pyrin domain containing 3	Homo sapiens	137-142
34671876-3	2022	Here, we present a patient with a rare leucine-rich repeat (LRR) domain mutation, p.Arg920Gln (p.R920Q), associated with an atypical NLRP3-AID with recurrent episodes of sore throat and extensive oropharyngeal ulceration.	Leucine	39-46	NLR family pyrin domain containing 3	Homo sapiens	133-138
34831052-4	2021	Furthermore, reactive oxygen species (ROS), act as an intermediate to activate NLRP3, contributing to subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	13-36	NLR family pyrin domain containing 3	Homo sapiens	79-84
34831052-4	2021	Furthermore, reactive oxygen species (ROS), act as an intermediate to activate NLRP3, contributing to subsequent inflammatory cascades and cell damage.	Reactive Oxygen Species	38-41	NLR family pyrin domain containing 3	Homo sapiens	79-84
34674097-6	2022	Moreover, activation of the NLRP3 inflammasome and pyroptosis were triggered by DCA.	Deoxycholic Acid	80-83	NLR family pyrin domain containing 3	Homo sapiens	28-33
34364127-0	2021	NLRP3 inflammasome blocked the glycolytic pathway via targeting to PKLR in arsenic-induced hepatic insulin resistance.	Arsenic	75-82	NLR family pyrin domain containing 3	Homo sapiens	0-5
34674097-8	2022	Collectively, our data showed that DCA-induced pyroptosis involves the inhibition of PINK1-mediated mitophagy and the activation of the NLRP3 inflammasome.	Deoxycholic Acid	35-38	NLR family pyrin domain containing 3	Homo sapiens	136-141
34745110-0	2021	Erianin: A Direct NLRP3 Inhibitor With Remarkable Anti-Inflammatory Activity.	Erianin	0-7	NLR family pyrin domain containing 3	Homo sapiens	18-23
34745125-3	2021	Furthermore, the NLRP3 agonists H2O2 and MSU elicited IL-1beta maturation without inducing specks.	Hydrogen Peroxide	32-36	NLR family pyrin domain containing 3	Homo sapiens	17-22
34668208-5	2022	Stimulation with the semiselective P2X7R agonist benzoyl ATP together with lipopolysaccharide treatment triggered P2X7R transfer to the cytoplasm and P2X7R/NLRP3 colocalization.	benzoyl atp	49-60	NLR family pyrin domain containing 3	Homo sapiens	156-161
34678326-10	2022	Inhibition of NLRP3 inflammasome responses reduces steroid-insensitive airway hyper-responsiveness but has no effect on IL-5 or IL-13 responses in experimental asthma.	Steroids	51-58	NLR family pyrin domain containing 3	Homo sapiens	14-19
34364127-4	2021	We found that NaAsO2 caused hepatic IR, activated NLRP3 inflammasome, and inhibited glycolysis pathway in vivo.	sodium arsenite	14-20	NLR family pyrin domain containing 3	Homo sapiens	50-55
34364127-10	2021	In summary, after treatment with NaAsO2, NLRP3 inflammasome blocked the glycolytic pathway via binding to PKLR, which in turn caused hepatic IR.	sodium arsenite	33-39	NLR family pyrin domain containing 3	Homo sapiens	41-46
34450555-0	2021	Corrigendum to "Magnesium isoglycyrrhizinate blocks fructose-induced hepatic NF-kappaB/NLRP3 inflammasome activation and lipid metabolism disorder" (Eur.	18alpha,20beta-hydroxy-11-oxo-norolean-12-en-3beta-yl-2-O-beta-D-glucopyranurosyl-alpha-D-glucopyranosiduronate magnesium tetrahydrate	16-44	NLR family pyrin domain containing 3	Homo sapiens	87-92
34450555-0	2021	Corrigendum to "Magnesium isoglycyrrhizinate blocks fructose-induced hepatic NF-kappaB/NLRP3 inflammasome activation and lipid metabolism disorder" (Eur.	Fructose	52-60	NLR family pyrin domain containing 3	Homo sapiens	87-92
34722576-0	2021	Elevated NLRP3 Inflammasome Levels Correlate With Vitamin D in the Vitreous of Proliferative Diabetic Retinopathy.	Vitamin D	50-59	NLR family pyrin domain containing 3	Homo sapiens	9-14
34681768-0	2021	NLRP3 Inflammasome Inhibitor BAY-117082 Reduces Oral Squamous Cell Carcinoma Progression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	29-39	NLR family pyrin domain containing 3	Homo sapiens	0-5
34681768-5	2021	This study aimed to investigate the effect of BAY-117082, an NLRP3 inflammasome inhibitor, in an in vitro and in vivo xenograft model of oral cancer.	3-(4-methylphenylsulfonyl)-2-propenenitrile	46-56	NLR family pyrin domain containing 3	Homo sapiens	61-66
34681768-7	2021	BAY-117082 at higher concentrations significantly reduced NLRP3, ASC, caspase-1, IL-1beta, and IL-18 expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	0-10	NLR family pyrin domain containing 3	Homo sapiens	58-63
34681768-9	2021	Furthermore, the in vivo study demonstrated that BAY-117082 at doses of 2.5 and 5 mg/kg significantly decreased subcutaneous tumor mass, and also reduced NLRP3 inflammasome pathway activation.	3-(4-methylphenylsulfonyl)-2-propenenitrile	49-59	NLR family pyrin domain containing 3	Homo sapiens	154-159
34681768-10	2021	Therefore, based on these results, the use of BAY-117082 could be considered a promising strategy to counteract oral cancer progression, thanks its ability to modulate the NLRP3 inflammasome and apoptosis pathways.	3-(4-methylphenylsulfonyl)-2-propenenitrile	46-56	NLR family pyrin domain containing 3	Homo sapiens	172-177
34722576-9	2021	Meanwhile, vitreous and serum vitamin D concentrations were significantly negatively correlated with vitreous NLRP3 expression in PDR patients.	Vitamin D	30-39	NLR family pyrin domain containing 3	Homo sapiens	110-115
34722576-13	2021	Conclusions: Our results demonstrate a strong correlation between increased NLRP3 inflammasome pathway and decreased vitamin D concentrations in the vitreous of PDR patients, which may be linked to PDR pathogenesis.	Vitamin D	117-126	NLR family pyrin domain containing 3	Homo sapiens	76-81
34722576-14	2021	In addition, vitamin D supplementation may play a key role in preventing, treating, and improving PDR prognosis due to its inhibitory impact on NLRP3 inflammasome pathway and VEGF.	Vitamin D	13-22	NLR family pyrin domain containing 3	Homo sapiens	144-149
34620711-0	2021	Identification of fluoxetine as a direct NLRP3 inhibitor to treat atrophic macular degeneration.	Fluoxetine	18-28	NLR family pyrin domain containing 3	Homo sapiens	41-46
34403689-6	2021	Also, EC dramatically inhibits the activation of NLRP3 inflammasome and reduces the CSE-induced pyroptosis, as indicated by decreasing lactate dehydrogenase release and the number of caspase-1-positive cells.	Catechin	6-8	NLR family pyrin domain containing 3	Homo sapiens	49-54
34684819-0	2021	Inhibitory Role of Berberine, an Isoquinoline Alkaloid, on NLRP3 Inflammasome Activation for the Treatment of Inflammatory Diseases.	Berberine	19-28	NLR family pyrin domain containing 3	Homo sapiens	59-64
34684819-3	2021	Various in vitro and in vivo studies have reported the anti-inflammatory role of berberine (BRB), an organic heteropentacyclic phytochemical and natural isoquinoline, in inhibiting NLRP3 inflammasome-dependent inflammation against many disorders.	Berberine	81-90	NLR family pyrin domain containing 3	Homo sapiens	181-186
34684819-3	2021	Various in vitro and in vivo studies have reported the anti-inflammatory role of berberine (BRB), an organic heteropentacyclic phytochemical and natural isoquinoline, in inhibiting NLRP3 inflammasome-dependent inflammation against many disorders.	isoquinoline	153-165	NLR family pyrin domain containing 3	Homo sapiens	181-186
34620711-6	2021	We report that fluoxetine, an FDA-approved drug for treating clinical depression, binds NLRP3 in silico, in vitro, and in vivo and inhibits activation of the NLRP3-ASC inflammasome and inflammatory cytokine release in RPE cells and macrophages, two critical cell types in dry AMD.	Fluoxetine	15-25	NLR family pyrin domain containing 3	Homo sapiens	88-93
34620711-6	2021	We report that fluoxetine, an FDA-approved drug for treating clinical depression, binds NLRP3 in silico, in vitro, and in vivo and inhibits activation of the NLRP3-ASC inflammasome and inflammatory cytokine release in RPE cells and macrophages, two critical cell types in dry AMD.	Fluoxetine	15-25	NLR family pyrin domain containing 3	Homo sapiens	158-163
34625906-0	2022	Mechanism of Baicalein in Brain Injury After Intracerebral Hemorrhage by Inhibiting the ROS/NLRP3 Inflammasome Pathway.	baicalein	13-22	NLR family pyrin domain containing 3	Homo sapiens	92-97
34384953-11	2021	CONCLUSIONS: AZD8055 ameliorated EAE through anti-inflammatory and anti-pyroptosis effects via the mammalian target of mTOR/ROS/NLRP3 pathway.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	13-20	NLR family pyrin domain containing 3	Homo sapiens	128-133
34384953-11	2021	CONCLUSIONS: AZD8055 ameliorated EAE through anti-inflammatory and anti-pyroptosis effects via the mammalian target of mTOR/ROS/NLRP3 pathway.	ros	124-127	NLR family pyrin domain containing 3	Homo sapiens	128-133
34625906-6	2022	The expression of NLRP3 inflammasome was detected after treatment with ROS scavenger.	Reactive Oxygen Species	71-74	NLR family pyrin domain containing 3	Homo sapiens	18-23
34650351-3	2021	COLCOT (in patients with recent MI) and LoDoCo2 (in patients with chronic coronary syndromes) tested oral colchicine (an NLRP3 inflammasome inhibitor) 0.5 mg daily vs. placebo, demonstrating prevention of MACE with a slightly increased risk of pneumonia in COLCOT (0.9 vs. 0.4%) but not in LoDoCo2.	Colchicine	106-116	NLR family pyrin domain containing 3	Homo sapiens	121-126
34625906-10	2022	Baicalein inhibited the high expression of NLRP3 inflammasome in ICH.	baicalein	0-9	NLR family pyrin domain containing 3	Homo sapiens	43-48
34625906-11	2022	ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	28-33
34692754-0	2021	Attenuating Effect of Chlorella Extract on NLRP3 Inflammasome Activation by Mitochondrial Reactive Oxygen Species.	chlorella extract	22-39	NLR family pyrin domain containing 3	Homo sapiens	43-48
34692754-0	2021	Attenuating Effect of Chlorella Extract on NLRP3 Inflammasome Activation by Mitochondrial Reactive Oxygen Species.	Reactive Oxygen Species	90-113	NLR family pyrin domain containing 3	Homo sapiens	43-48
34625906-11	2022	ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels.	Reactive Oxygen Species	70-73	NLR family pyrin domain containing 3	Homo sapiens	28-33
34692754-4	2021	In this study, we obtained a fat-soluble extract from Chlorella (CE) and demonstrated that it reduced NLRP3 inflammasome activation by inhibiting mitochondrial reactive oxygen species and caspase-1 activation.	Oxygen	169-175	NLR family pyrin domain containing 3	Homo sapiens	102-107
34625906-13	2022	Overall, baicalein alleviated the brain injury after ICH by inhibiting ROS and NLRP3 inflammasome.	baicalein	9-18	NLR family pyrin domain containing 3	Homo sapiens	79-84
34619679-0	2022	Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo.	beta-tricalcium phosphate	46-71	NLR family pyrin domain containing 3	Homo sapiens	14-19
34619679-6	2022	In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation.	beta-tricalcium phosphate	95-103	NLR family pyrin domain containing 3	Homo sapiens	62-67
34619679-4	2022	The present study aimed to determine the effects of beta-TCP particles on NLR family pyrin domain containing 3 (NLRP3) inflammasome complexes.	beta-tricalcium phosphate	52-60	NLR family pyrin domain containing 3	Homo sapiens	74-110
34619679-6	2022	In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation.	Potassium	130-139	NLR family pyrin domain containing 3	Homo sapiens	62-67
34619679-6	2022	In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation.	Reactive Oxygen Species	152-175	NLR family pyrin domain containing 3	Homo sapiens	62-67
34619679-6	2022	In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation.	Reactive Oxygen Species	177-180	NLR family pyrin domain containing 3	Homo sapiens	62-67
34619679-4	2022	The present study aimed to determine the effects of beta-TCP particles on NLR family pyrin domain containing 3 (NLRP3) inflammasome complexes.	beta-tricalcium phosphate	52-60	NLR family pyrin domain containing 3	Homo sapiens	112-117
34619679-6	2022	In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation.	beta-tricalcium phosphate	16-24	NLR family pyrin domain containing 3	Homo sapiens	62-67
34614009-8	2021	Additionally, treatment with C3G resulted in a significant reduction in the protein expression of inflammatory markers IL-1beta and NLRP3 (p<0.01) as well as an increase in LC3 autophagic marker (p<0.05) in human islets treated with amylin, Abeta1-42, rapamycin, or H2O2.	Hydrogen Peroxide	266-270	NLR family pyrin domain containing 3	Homo sapiens	132-137
34675809-7	2021	Notably, the increased expression levels of TLR4, NLRP3, interleukin 1beta, and interleukin 18 proteins and the elevated activities of caspase-1 and lactic dehydrogenase in in vivo and in vitro disease models were markedly reversed by the treatment with BHGZD.	bhgzd	254-259	NLR family pyrin domain containing 3	Homo sapiens	50-55
34403206-1	2021	The rapid formation and activation of the NLRP3 inflammasome is induced by co-stimulation with LPS and nigericin.	Nigericin	103-112	NLR family pyrin domain containing 3	Homo sapiens	42-47
34403206-3	2021	IKKbeta is not required for the nigericin-induced dispersion of the trans-Golgi network (TGN), but to bring NLRP3 in proximity with TGN38.	Nigericin	32-41	NLR family pyrin domain containing 3	Homo sapiens	108-113
34403206-5	2021	Prolonged stimulation with LPS to increase the expression of NLRP3, followed by stimulation with nigericin, produced larger TGN38-positive puncta, and the ensuing activation of the NLRP3 inflammasome was also suppressed by IKKbeta inhibitors added prior to stimulation with nigericin.	Nigericin	97-106	NLR family pyrin domain containing 3	Homo sapiens	181-186
34403206-5	2021	Prolonged stimulation with LPS to increase the expression of NLRP3, followed by stimulation with nigericin, produced larger TGN38-positive puncta, and the ensuing activation of the NLRP3 inflammasome was also suppressed by IKKbeta inhibitors added prior to stimulation with nigericin.	Nigericin	274-283	NLR family pyrin domain containing 3	Homo sapiens	61-66
34403206-5	2021	Prolonged stimulation with LPS to increase the expression of NLRP3, followed by stimulation with nigericin, produced larger TGN38-positive puncta, and the ensuing activation of the NLRP3 inflammasome was also suppressed by IKKbeta inhibitors added prior to stimulation with nigericin.	Nigericin	274-283	NLR family pyrin domain containing 3	Homo sapiens	181-186
34675809-8	2021	In conclusion, the above findings proved the immunomodulatory and anti-inflammatory activities of BHGZD, especially in pyroptosis, which may be attributed to the activation of TLR4-mediated NLRP3 inflammasome signaling.	bhgzd	98-103	NLR family pyrin domain containing 3	Homo sapiens	190-195
34599741-6	2021	BAF-312 also reduced the activation of astrocytes, by controlling NF-kB and NLRP3 induction and preventing the increase of proinflammatory cytokine and chemokines.	siponimod	0-7	NLR family pyrin domain containing 3	Homo sapiens	76-81
34089810-0	2021	Protective effect of pogostone on murine norovirus infected-RAW264.7 macrophages through inhibition of NF-kappaB/NLRP3-dependent pyroptosis.	Pogostone	21-30	NLR family pyrin domain containing 3	Homo sapiens	113-118
34790764-0	2021	Anti-inflammatory effects of artesunate on atherosclerosis via miR-16-5p and TXNIP regulation of the NLRP3 inflammasome.	Artesunate	29-39	NLR family pyrin domain containing 3	Homo sapiens	101-106
34790764-0	2021	Anti-inflammatory effects of artesunate on atherosclerosis via miR-16-5p and TXNIP regulation of the NLRP3 inflammasome.	mir-16-5p	63-72	NLR family pyrin domain containing 3	Homo sapiens	101-106
34790764-11	2021	Artesunate abrogated the activation of NLRP3 inflammasome in the presence of inflammasome activators in cultured macrophages.	Artesunate	0-10	NLR family pyrin domain containing 3	Homo sapiens	39-44
34790764-12	2021	Artesunate reduced TXNIP expression and impaired the interaction between TXNIP and NLRP3, thereby inhibiting release of inflammatory cytokines and ASC production in cultured macrophages.	Artesunate	0-10	NLR family pyrin domain containing 3	Homo sapiens	83-88
34469206-0	2021	Adipocyte factor CTRP6 inhibits homocysteine-induced proliferation, migration, and dedifferentiation of vascular smooth muscle cells through PPARgamma/NLRP3.	Homocysteine	32-44	NLR family pyrin domain containing 3	Homo sapiens	151-156
34492522-0	2021	Colchicine reduces extracellular vesicle NLRP3 inflammasome protein levels in chronic coronary disease: A LoDoCo2 biomarker substudy.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	41-46
34469206-10	2021	The addition of GW9662 and rosiglitazone further demonstrated that overexpression of CTRP6 inhibited HCY-induced VSMC proliferation, migration, and dedifferentiation through PPARgamma/NLRP3 signaling.	Homocysteine	101-104	NLR family pyrin domain containing 3	Homo sapiens	184-189
34492522-2	2021	Colchicine has broad anti-inflammatory effects and part of the atheroprotective effects have been suggested to be the result of NLRP3 inflammasome inhibition.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	128-133
34492522-10	2021	EV NLRP3 protein levels were lower in patients treated with colchicine (median 1.38 ng/mL), compared to placebo (median 1.58 ng/mL) (p = 0.025).	Colchicine	60-70	NLR family pyrin domain containing 3	Homo sapiens	3-8
34469206-11	2021	In conclusion, CTRP6 inhibited HCY-induced proliferation, migration, and dedifferentiation of VSMCs through PPARgamma/NLRP3.	Homocysteine	31-34	NLR family pyrin domain containing 3	Homo sapiens	118-123
34492522-14	2021	CONCLUSIONS: Colchicine leads to a reduction of EV NLRP3 protein levels.	Colchicine	13-23	NLR family pyrin domain containing 3	Homo sapiens	51-56
34492522-15	2021	This indicates that inhibitory effects on the NLRP3 inflammasome might contribute to the atheroprotective effects of colchicine in coronary disease.	Colchicine	117-127	NLR family pyrin domain containing 3	Homo sapiens	46-51
34332276-6	2021	RESULTS: The SP-induced hyperlipidemic cell model demonstrated increased expression of NLRP3 and caspase-1 proteins (P < 0.05) and elevated ROS levels (P < 0.01), and decreased phosphorylated-Akt and phosphorylated-eNOS expression (P < 0.05).	Palmitic Acid	13-15	NLR family pyrin domain containing 3	Homo sapiens	87-92
34599154-7	2021	Consistently, miR-138-5p inhibition reversed the effects of lncRNA NLRP3 silencing on the expression of NLRP3-related molecules and inhibition of the NLRP3/caspase-1/IL-1beta signalling pathway.	mir-138-5p	14-24	NLR family pyrin domain containing 3	Homo sapiens	67-72
34599154-7	2021	Consistently, miR-138-5p inhibition reversed the effects of lncRNA NLRP3 silencing on the expression of NLRP3-related molecules and inhibition of the NLRP3/caspase-1/IL-1beta signalling pathway.	mir-138-5p	14-24	NLR family pyrin domain containing 3	Homo sapiens	104-109
34599154-7	2021	Consistently, miR-138-5p inhibition reversed the effects of lncRNA NLRP3 silencing on the expression of NLRP3-related molecules and inhibition of the NLRP3/caspase-1/IL-1beta signalling pathway.	mir-138-5p	14-24	NLR family pyrin domain containing 3	Homo sapiens	150-155
34599390-3	2021	RECENT FINDINGS: Recently, it has been shown that the activation of the NLRP3 (NACHT, leucine-rich repeat, and pyrin domain-containing protein 3) inflammasome is central in the pathophysiology of pericarditis.	Leucine	86-93	NLR family pyrin domain containing 3	Homo sapiens	72-77
34599390-7	2021	Colchicine, an inhibitor of NLRP3 inflammasome formation, and IL-1-targeted therapies, such as anakinra and rilonacept, were found to effectively blunt the acute inflammation and reduce the risk for recurrences.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	28-33
34098069-0	2021	Acute cadmium exposure induces GSDME-mediated pyroptosis in triple-negative breast cancer cells through ROS generation and NLRP3 inflammasome pathway activation.	Cadmium	6-13	NLR family pyrin domain containing 3	Homo sapiens	123-128
34098069-0	2021	Acute cadmium exposure induces GSDME-mediated pyroptosis in triple-negative breast cancer cells through ROS generation and NLRP3 inflammasome pathway activation.	gsdme	31-36	NLR family pyrin domain containing 3	Homo sapiens	123-128
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	NLR family pyrin domain containing 3	Homo sapiens	17-22
34229177-0	2021	Licochalcone E improves insulin sensitivity in palmitic acid-treated HepG2 cells through inhibition of the NLRP3 signaling pathway.	licochalcone E	0-14	NLR family pyrin domain containing 3	Homo sapiens	107-112
34447480-14	2021	However, the NLRP3 activator Nigericin reversed the inhibitory effects of IL-22 on the induction of oxidative stress and fibrosis of HSCs induced by TGF-beta.	Nigericin	29-38	NLR family pyrin domain containing 3	Homo sapiens	13-18
34387860-4	2021	Upon NLRP3 activation, AKT activity is inhibited by second stimulus-induced ROS.	ros	76-79	NLR family pyrin domain containing 3	Homo sapiens	5-10
34447480-9	2021	Following addition of Nigericin, a NLRP3 activator, the levels of oxidative stress and fibrosis were measured.	Nigericin	22-31	NLR family pyrin domain containing 3	Homo sapiens	35-40
34229177-0	2021	Licochalcone E improves insulin sensitivity in palmitic acid-treated HepG2 cells through inhibition of the NLRP3 signaling pathway.	Palmitic Acid	47-60	NLR family pyrin domain containing 3	Homo sapiens	107-112
34229177-9	2021	Confocal microscopy results showed that licochalcone E dramatically reduced the generation of ROS and the expressions of NLRP3 and its downstream caspase-1 in PA-treated HepG2 model.	licochalcone E	40-54	NLR family pyrin domain containing 3	Homo sapiens	121-126
34229177-4	2021	Finally, molecular simulations were exploited to validate the interaction between licochalcone E and the NLRP3 inflammasome.	licochalcone E	82-96	NLR family pyrin domain containing 3	Homo sapiens	105-110
34229177-9	2021	Confocal microscopy results showed that licochalcone E dramatically reduced the generation of ROS and the expressions of NLRP3 and its downstream caspase-1 in PA-treated HepG2 model.	Palmitic Acid	159-161	NLR family pyrin domain containing 3	Homo sapiens	121-126
34229177-10	2021	Western blot results further indicated that licochalcone E significantly reduced the expression of NLRP3, caspase-1 and IL-1beta in the model.	licochalcone E	44-58	NLR family pyrin domain containing 3	Homo sapiens	99-104
34368883-0	2021	Oxymatrine attenuates oxidized low-density lipoprotein-induced HUVEC injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via the activation of the SIRT1/Nrf2 signaling pathway.	oxymatrine	0-10	NLR family pyrin domain containing 3	Homo sapiens	90-95
34368883-10	2021	Concurrently, oxymatrine inhibited ox-LDL-induced NLRP3 inflammasome-mediated pyroptosis in HUVECs, as evidenced by the significant decreases in the expression of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), cleaved caspase-1, interleukin (IL)-1beta and IL-18 in HUVECs.	oxymatrine	14-24	NLR family pyrin domain containing 3	Homo sapiens	50-55
34368883-3	2021	The present study was undertaken to investigate whether oxymatrine attenuates oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cell (HUVEC) injury, an in vitro cell model of atherosclerosis, by inhibiting NLRP3 inflammasome-mediated pyroptosis, and elucidate the role of the sirtuin (SIRT)1/nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway in this process.	oxymatrine	56-66	NLR family pyrin domain containing 3	Homo sapiens	239-244
34368883-10	2021	Concurrently, oxymatrine inhibited ox-LDL-induced NLRP3 inflammasome-mediated pyroptosis in HUVECs, as evidenced by the significant decreases in the expression of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), cleaved caspase-1, interleukin (IL)-1beta and IL-18 in HUVECs.	oxymatrine	14-24	NLR family pyrin domain containing 3	Homo sapiens	163-168
34664178-3	2021	Here, the promising yet unexplored antidepressant potential of dapagliflozin (Dapa), a sodium-glucose co-transporter-2 inhibitor, was investigated by assessing its role in the modulation of the NLRP3 inflammasome pathway and ETBR signal transduction, and their impact on neuroplasticity and BBB integrity in an animal model of depression.	dapagliflozin	63-76	NLR family pyrin domain containing 3	Homo sapiens	194-199
34368883-14	2021	Moreover, SIRT1 siRNA transfection blocked the inhibitory effect of oxymatrine on NLRP3 inflammasome-mediated pyroptosis in ox-LDL-treated HUVECs.	oxymatrine	68-78	NLR family pyrin domain containing 3	Homo sapiens	82-87
34368883-15	2021	Collectively, these results indicated that oxymatrine may attenuate ox-LDL-induced HUVEC injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via activating the SIRT1/Nrf2 signaling pathway.	oxymatrine	43-53	NLR family pyrin domain containing 3	Homo sapiens	110-115
34390315-1	2021	INTRODUCTION: The NLR family pyrin domain containing 3 (NLRP3) signaling pathway has an important role in inflammation mediated by monosodium urate crystals in gout, and the characterization of single nucleotide polymorphisms (SNPs) have helped to recognize disease susceptibility.	Uric Acid	131-147	NLR family pyrin domain containing 3	Homo sapiens	18-54
34390315-1	2021	INTRODUCTION: The NLR family pyrin domain containing 3 (NLRP3) signaling pathway has an important role in inflammation mediated by monosodium urate crystals in gout, and the characterization of single nucleotide polymorphisms (SNPs) have helped to recognize disease susceptibility.	Uric Acid	131-147	NLR family pyrin domain containing 3	Homo sapiens	56-61
34350498-4	2021	Some natural occurring compounds (NCs) have been reported to interact with the DOX-induced cardiotoxicity through targeting one or more of several pathways, including the Nrf2/NF-kB, TLR-4/NF-kB, MAPK/NF-kB, and NLRP3 inflammasome pathways.	Doxorubicin	79-82	NLR family pyrin domain containing 3	Homo sapiens	212-217
34664178-3	2021	Here, the promising yet unexplored antidepressant potential of dapagliflozin (Dapa), a sodium-glucose co-transporter-2 inhibitor, was investigated by assessing its role in the modulation of the NLRP3 inflammasome pathway and ETBR signal transduction, and their impact on neuroplasticity and BBB integrity in an animal model of depression.	dapagliflozin	78-82	NLR family pyrin domain containing 3	Homo sapiens	194-199
34664178-12	2021	Thus, Dapa may exert its antidepressant action by reinforcing BBB integrity and promoting neuroplasticity through manipulation of the NLRP3/ET-1/ETBR/BDNF/ZO-1 axis, with a significant role for ETBR signaling.	dapagliflozin	6-10	NLR family pyrin domain containing 3	Homo sapiens	134-139
34664178-14	2021	Dapa suppressed NLRP3 inflammasome activation and assembly with subsequent inhibition of pro-inflammatory ILs.	dapagliflozin	0-4	NLR family pyrin domain containing 3	Homo sapiens	16-21
34375537-0	2022	Black carbon induces complement activation via NLRP3 inflammasome in human corneal epithelial cells.	Carbon	6-12	NLR family pyrin domain containing 3	Homo sapiens	47-52
34375537-8	2022	NLRP3-siRNA transfection reduced C5b-9 protein levels in FBC treated and OBC treated HCECs compared to control (lowered by 27% in the FBC treated group and by 23% in the OBC treated group, all P < .05).	4-(3,5-difluorophenyl)benzoic acid	134-137	NLR family pyrin domain containing 3	Homo sapiens	0-5
34375537-10	2022	siRNA targeting NLRP3 to inhibit NLRP3 generation reduced C5b-9 protein level in HCECs treated with FBC or OBC particles, indicating that BC induces complement activation potentially through the NLRP3 inflammasome in HCECs.	4-(3,5-difluorophenyl)benzoic acid	100-103	NLR family pyrin domain containing 3	Homo sapiens	33-38
34616481-9	2021	Results: Our results showed that XXMD attenuated LPS-induced oxidative stress, barrier dysfunction, and the activation of NLRP3 inflammasome in vitro, as evidenced by enhanced ROS production, TEER levels, expression of NLRP3 and caspase 1 (p20) and release of IL-1beta and IL-18, and weakened cell permeability.	Reactive Oxygen Species	176-179	NLR family pyrin domain containing 3	Homo sapiens	122-127
34616481-12	2021	Conclusion: The findings showed that XXMD could alleviate LPS-induced ALI injury and inhibit inflammation and suppress ROS/NLRP3 signaling pathway, which were involved in these protective effects.	Reactive Oxygen Species	119-122	NLR family pyrin domain containing 3	Homo sapiens	123-128
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	98-100	NLR family pyrin domain containing 3	Homo sapiens	173-178
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	81-96	NLR family pyrin domain containing 3	Homo sapiens	173-178
34551296-8	2021	Together, our results suggest pTau activates IL-1beta via MyD88- and NLRP3-ASC-dependent pathways in myeloid cells, including microglia.	ptau	30-34	NLR family pyrin domain containing 3	Homo sapiens	69-74
34546972-13	2021	This effect of metformin is partially dependent on FOXO3 which can activate the transcription of NLRP3.	Metformin	15-24	NLR family pyrin domain containing 3	Homo sapiens	97-102
34587665-1	2021	We investigated two functional polymorphisms in NLRP3 inflammasome genes (NLRP3 rs35829419 and CARD8 rs2043211) and their association with alcohol dependence and related anxiety, depression, obsession-compulsion, or aggression in 88 hospitalised alcohol-dependent patients, 99 abstinent alcohol-dependent participants, and 94 controls, all male Caucasian.	Alcohols	246-253	NLR family pyrin domain containing 3	Homo sapiens	48-53
34146985-0	2021	2,2",4,4"-Tetrabromodiphenyl ether (BDE-47) activates Aryl hydrocarbon receptor (AhR) mediated ROS and NLRP3 inflammasome/p38 MAPK pathway inducing necrosis in cochlear hair cells.	2,2',4,4'-tetrabromodiphenyl ether	0-34	NLR family pyrin domain containing 3	Homo sapiens	103-108
34551296-4	2021	Treating microglia with pTau-containing neuronal media, exosomes, or PHFs causes IL-1beta activation, which is NLRP3, ASC, and caspase-1 dependent.	ptau	24-28	NLR family pyrin domain containing 3	Homo sapiens	111-116
34518217-10	2021	Mutagenesis of NLRP3 confirms serine 3 as an important phospho-switch site but, surprisingly, reveals that this is not the sole site regulated by either TBK1/IKKepsilon or PP2A, because all retain the control over the NLRP3 pathway even when serine 3 is mutated.	Serine	30-36	NLR family pyrin domain containing 3	Homo sapiens	15-20
34537816-0	2021	Trimetazidine attenuates dexamethasone-induced muscle atrophy via inhibiting NLRP3/GSDMD pathway-mediated pyroptosis.	Trimetazidine	0-13	NLR family pyrin domain containing 3	Homo sapiens	77-82
34537816-0	2021	Trimetazidine attenuates dexamethasone-induced muscle atrophy via inhibiting NLRP3/GSDMD pathway-mediated pyroptosis.	Dexamethasone	25-38	NLR family pyrin domain containing 3	Homo sapiens	77-82
34537816-5	2021	Dexamethasone also induced pyroptosis, indicated by upregulated pyroptosis-related protein NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and gasdermin-D (GSDMD).	Dexamethasone	0-13	NLR family pyrin domain containing 3	Homo sapiens	129-134
34537816-6	2021	Knockdown of NLRP3 or GSDMD attenuated dexamethasone-induced myotube pyroptosis and atrophy.	Dexamethasone	39-52	NLR family pyrin domain containing 3	Homo sapiens	13-18
34537816-8	2021	Activation of NLRP3 using LPS and ATP not only increased the cleavage and activation of Caspase-1 and GSDMD, but also increased the expression levels of atrophy markers MuRF1 and Atrogin-1 in trimetazidine-treated C2C12 myotubes.	Adenosine Triphosphate	34-37	NLR family pyrin domain containing 3	Homo sapiens	14-19
34537816-8	2021	Activation of NLRP3 using LPS and ATP not only increased the cleavage and activation of Caspase-1 and GSDMD, but also increased the expression levels of atrophy markers MuRF1 and Atrogin-1 in trimetazidine-treated C2C12 myotubes.	Trimetazidine	192-205	NLR family pyrin domain containing 3	Homo sapiens	14-19
34537816-10	2021	Conversely, co-treatment with a PI3K/AKT inhibitor, picropodophyllin, remarkably increased the expression of NLRP3 and reversed the protective effects of trimetazidine against dexamethasone-induced C2C12 myotube pyroptosis and atrophy.	picropodophyllin	52-68	NLR family pyrin domain containing 3	Homo sapiens	109-114
34537816-11	2021	Taken together, our study suggests that NLRP3/GSDMD-mediated pyroptosis might be a novel mechanism for dexamethasone-induced skeletal muscle atrophy.	Dexamethasone	103-116	NLR family pyrin domain containing 3	Homo sapiens	40-45
34524838-0	2021	Sensing low intracellular potassium by NLRP3 results in a stable open structure that promotes inflammasome activation.	Potassium	26-35	NLR family pyrin domain containing 3	Homo sapiens	39-44
34146985-0	2021	2,2",4,4"-Tetrabromodiphenyl ether (BDE-47) activates Aryl hydrocarbon receptor (AhR) mediated ROS and NLRP3 inflammasome/p38 MAPK pathway inducing necrosis in cochlear hair cells.	2,2',4,4'-tetrabromodiphenyl ether	36-42	NLR family pyrin domain containing 3	Homo sapiens	103-108
34431717-5	2021	NLRP3 is modified by lysine-63 ubiquitin chains in hepatocytes and is deubiquitinated during HCV infection.	Lysine	21-27	NLR family pyrin domain containing 3	Homo sapiens	0-5
34576117-0	2021	Acute Glucose Shift Induces the Activation of the NLRP3 Inflammasome in THP-1 Cells.	Glucose	6-13	NLR family pyrin domain containing 3	Homo sapiens	50-55
34576117-1	2021	We aimed to investigate the effect of acute glucose shift on the activation of the NLRP3 inflammasome, IL-1beta secretion, and underlying signaling pathways in THP-1 cells.	Glucose	44-51	NLR family pyrin domain containing 3	Homo sapiens	83-88
34576117-4	2021	Both directions of the acute glucose shift increased the activation of the NLRP3 inflammasome, generation of reactive oxygen species (ROS), and expression of phosphorylated p38 MAPK, JNK, and NF-kappaB compared with either constant NG or HG.	Glucose	29-36	NLR family pyrin domain containing 3	Homo sapiens	75-80
34576117-5	2021	Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-kappaB.	Acetylcysteine	15-31	NLR family pyrin domain containing 3	Homo sapiens	139-144
34576117-5	2021	Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-kappaB.	Glucose	84-91	NLR family pyrin domain containing 3	Homo sapiens	139-144
34576117-6	2021	Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells.	Glucose	87-94	NLR family pyrin domain containing 3	Homo sapiens	190-195
34576117-6	2021	Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells.	Reactive Oxygen Species	171-174	NLR family pyrin domain containing 3	Homo sapiens	190-195
34564408-0	2021	Ultramicronized Palmitoylethanolamide Inhibits NLRP3 Inflammasome Expression and Pro-Inflammatory Response Activated by SARS-CoV-2 Spike Protein in Cultured Murine Alveolar Macrophages.	palmidrol	16-37	NLR family pyrin domain containing 3	Homo sapiens	47-52
34285037-5	2021	CRC cell-originated 5-HT enhanced NLRP3 inflammasome activation in THP-1 cells and immortalized bone marrow-derived macrophages (iBMDM) via its ion channel receptor, HTR3A.	Serotonin	20-24	NLR family pyrin domain containing 3	Homo sapiens	34-39
34157359-0	2021	H2S alleviates aortic aneurysm and dissection: Crosstalk between transforming growth factor 1 signaling and NLRP3 inflammasome.	Deuterium	0-3	NLR family pyrin domain containing 3	Homo sapiens	108-113
34147915-0	2021	Celastrol inhibits rheumatoid arthritis through the ROS-NF-kappaB-NLRP3 inflammasome axis.	celastrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	66-71
34147915-9	2021	We speculated that Cel relieves RA symptoms and inhibits inflammation by inhibiting the ROS-NF-kappaB-NLRP3 axis.	Reactive Oxygen Species	88-91	NLR family pyrin domain containing 3	Homo sapiens	102-107
34116285-5	2021	RESULT: Lower expression levels of the P2X7R and NLRP3 proteins were observed in the EAM + BBG group than in the EAM1 group (P < 0.05).	bbg	91-94	NLR family pyrin domain containing 3	Homo sapiens	49-54
34157359-11	2021	In addition, H2S inhibited the expression of proteins involved in NLRP3 inflammasome.	Deuterium	13-16	NLR family pyrin domain containing 3	Homo sapiens	66-71
34116285-6	2021	The expression of NLRP3 in the EAM + glyburide group was lower than in the EAM2 group (P < 0.05).	Glyburide	37-46	NLR family pyrin domain containing 3	Homo sapiens	18-23
34116285-8	2021	NLRP3 was expressed at lower levels in the EAM + glyburide group than in the EAM2 group (P < 0.05).	Glyburide	49-58	NLR family pyrin domain containing 3	Homo sapiens	0-5
34157359-12	2021	Furthermore, H2S down-regulated TGF-beta1 signaling and then ameliorated vascular fibrosis by preventing NLRP3 inflammasome activation.	Deuterium	13-16	NLR family pyrin domain containing 3	Homo sapiens	105-110
34157359-13	2021	Finally, H2S inhibited NLRP3 inflammasome activation and decreased the level of IL-1beta by disrupting TGF-beta1 signaling.	Deuterium	9-12	NLR family pyrin domain containing 3	Homo sapiens	23-28
34116285-8	2021	NLRP3 was expressed at lower levels in the EAM + glyburide group than in the EAM2 group (P < 0.05).	eam2	77-81	NLR family pyrin domain containing 3	Homo sapiens	0-5
34312998-4	2021	In atherosclerosis, colchicine can inhibit the assembly and activation of NLRP3 inflammasome via various mechanisms to effectively reduce the expression of inflammatory factors, thereby reducing the inflammation.	Colchicine	20-30	NLR family pyrin domain containing 3	Homo sapiens	74-79
34467562-5	2022	Recently, increasing evidence highlights the NLRP3 (NOD-like, leucine-rich repeat domains, and pyrin domain-containing protein) inflammasome complex along with IL-1beta and effete neutrophils producing neutrophil extracellular traps (NETs) through NETosis.	Leucine	62-69	NLR family pyrin domain containing 3	Homo sapiens	45-50
34106394-10	2021	NaB ameliorated Glucocorticoid receptor and NLRP3 inflammasome expressions.	nab	0-3	NLR family pyrin domain containing 3	Homo sapiens	44-49
34296312-7	2021	The present study demonstrated that DI administration inhibited NLRP3 assembly, LDH release and GSDMD cleavage.	dimethyl itaconate	36-38	NLR family pyrin domain containing 3	Homo sapiens	64-69
34296312-10	2021	Moreover, DI induced cellular autophagy, whereas inhibition of autophagy with 3-methyladenine markedly reversed its inhibitory effect on NLRP3-dependent pyroptosis.	3-methyladenine	78-93	NLR family pyrin domain containing 3	Homo sapiens	137-142
34338401-0	2021	Proanthocyanidins attenuate the high glucose-induced damage of retinal pigment epithelial cells by attenuating oxidative stress and inhibiting activation of the NLRP3 inflammasome.	Proanthocyanidins	0-17	NLR family pyrin domain containing 3	Homo sapiens	161-166
34577552-1	2021	NLR family pyrin domain containing 3 (NLRP3) inflammasome formation is triggered by the damaged mitochondria releasing reactive oxygen species.	Reactive Oxygen Species	119-142	NLR family pyrin domain containing 3	Homo sapiens	38-43
34338401-10	2021	Additionally, exposure to nigericin sodium salt, an agonist of the NLRP3 inflammasome, upregulated expression of the NLRP3 inflammasome accompanied by the release of IL-1beta and IL-18.	Nigericin sodium	26-47	NLR family pyrin domain containing 3	Homo sapiens	67-72
34338401-10	2021	Additionally, exposure to nigericin sodium salt, an agonist of the NLRP3 inflammasome, upregulated expression of the NLRP3 inflammasome accompanied by the release of IL-1beta and IL-18.	Nigericin sodium	26-47	NLR family pyrin domain containing 3	Homo sapiens	117-122
34119876-4	2021	In the present study, we found that inhibition of SAHH by using its inhibitor adenosine dialdehyde (ADA) accumulates intracellular or plasma SAH levels and increases high glucose-induced podocyte injury and aggravates STZ-induced diabetic nephropathy, which is associated with Nod-like receptor protein 3 (NLRP3) inflammasome activation.	Adenosine	78-87	NLR family pyrin domain containing 3	Homo sapiens	306-311
34119876-4	2021	In the present study, we found that inhibition of SAHH by using its inhibitor adenosine dialdehyde (ADA) accumulates intracellular or plasma SAH levels and increases high glucose-induced podocyte injury and aggravates STZ-induced diabetic nephropathy, which is associated with Nod-like receptor protein 3 (NLRP3) inflammasome activation.	periodate-oxidized adenosine	100-103	NLR family pyrin domain containing 3	Homo sapiens	306-311
34462843-0	2021	Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway.	Selenium	0-8	NLR family pyrin domain containing 3	Homo sapiens	68-73
34436643-5	2022	Meanwhile, recent studies have revealed that vitamin B6 treatment increases cardiac levels of imidazole dipeptides (e.g., carnosine, anserine, and homocarnosine), histamine, and gamma-aminobutyric acid (GABA) and suppresses P2X7 receptor-mediated NLRP3 inflammasome.	Vitamin B 6	45-55	NLR family pyrin domain containing 3	Homo sapiens	247-252
34159683-4	2021	Thus, we have comprehensively searched and summarized the different targets of quercetin in different stages of liver diseases and concluded that quercetin inhibited inflammation of the liver mainly through NF-kappaB/TLR/NLRP3, reduced PI3K/Nrf2-mediated oxidative stress, mTOR activation in autophagy, and inhibited the expression of apoptotic factors associated with the development of liver diseases.	Quercetin	79-88	NLR family pyrin domain containing 3	Homo sapiens	221-226
34159683-4	2021	Thus, we have comprehensively searched and summarized the different targets of quercetin in different stages of liver diseases and concluded that quercetin inhibited inflammation of the liver mainly through NF-kappaB/TLR/NLRP3, reduced PI3K/Nrf2-mediated oxidative stress, mTOR activation in autophagy, and inhibited the expression of apoptotic factors associated with the development of liver diseases.	Quercetin	146-155	NLR family pyrin domain containing 3	Homo sapiens	221-226
34577552-0	2021	Doxycycline Attenuates Cancer Cell Growth by Suppressing NLRP3-Mediated Inflammation.	Doxycycline	0-11	NLR family pyrin domain containing 3	Homo sapiens	57-62
34577552-1	2021	NLR family pyrin domain containing 3 (NLRP3) inflammasome formation is triggered by the damaged mitochondria releasing reactive oxygen species.	Reactive Oxygen Species	119-142	NLR family pyrin domain containing 3	Homo sapiens	0-36
34577552-2	2021	Doxycycline was shown to regulate inflammation; however, its effect on NLRP3 in cancer remains largely unknown.	Doxycycline	0-11	NLR family pyrin domain containing 3	Homo sapiens	71-76
34577552-3	2021	Therefore, we sought to determine the effect of doxycycline on NLRP3 regulation in cancer using an in vitro model.	Doxycycline	48-59	NLR family pyrin domain containing 3	Homo sapiens	63-68
34577552-4	2021	NLRP3 was activated in a prostate cancer cell line (PC3) and a lung cancer cell line (A549) before treatment with doxycycline.	Doxycycline	114-125	NLR family pyrin domain containing 3	Homo sapiens	0-5
34577552-10	2021	Doxycycline treatment decreased NLRP3 formation in PC3 and A549 cells compared to untreated and LPS only treated cells (p < 0.05).	Doxycycline	0-11	NLR family pyrin domain containing 3	Homo sapiens	32-37
34577552-12	2021	Our findings suggest that doxycycline inhibits LPS priming of NLRP3 and reduces tumor progression through early apoptosis in cancer.	Doxycycline	26-37	NLR family pyrin domain containing 3	Homo sapiens	62-67
34412584-0	2021	Human umbilical cord mesenchymal stem cells deliver exogenous miR-26a-5p via exosomes to inhibit nucleus pulposus cell pyroptosis through METTL14/NLRP3.	mir-26a-5p	62-72	NLR family pyrin domain containing 3	Homo sapiens	146-151
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	pelargonic acid vanillylamide	218-222	NLR family pyrin domain containing 3	Homo sapiens	25-30
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	pelargonic acid vanillylamide	218-222	NLR family pyrin domain containing 3	Homo sapiens	93-98
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	Rosuvastatin Calcium	227-230	NLR family pyrin domain containing 3	Homo sapiens	25-30
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	Rosuvastatin Calcium	227-230	NLR family pyrin domain containing 3	Homo sapiens	93-98
34217687-8	2021	The combination of PAVA and RSV reduced ox-LDL-induced recruitment of monocytes to the site of inflammation, inhibited activation of the NLRP3 inflammasome, and ameliorated the impairment of cell-cell junctions through the NF-kappaB pathway.	pelargonic acid vanillylamide	19-23	NLR family pyrin domain containing 3	Homo sapiens	137-142
34217687-8	2021	The combination of PAVA and RSV reduced ox-LDL-induced recruitment of monocytes to the site of inflammation, inhibited activation of the NLRP3 inflammasome, and ameliorated the impairment of cell-cell junctions through the NF-kappaB pathway.	Rosuvastatin Calcium	28-31	NLR family pyrin domain containing 3	Homo sapiens	137-142
34522180-3	2021	Observations: Cholesterol promotes the development of atherosclerosis by activating NLR family pyrin domain containing 3 (NLRP3), and the resulting inflammatory environment indirectly contributes to COVID-19 infection and subsequent deterioration.	Cholesterol	14-25	NLR family pyrin domain containing 3	Homo sapiens	84-120
34522180-3	2021	Observations: Cholesterol promotes the development of atherosclerosis by activating NLR family pyrin domain containing 3 (NLRP3), and the resulting inflammatory environment indirectly contributes to COVID-19 infection and subsequent deterioration.	Cholesterol	14-25	NLR family pyrin domain containing 3	Homo sapiens	122-127
34522180-8	2021	Conclusions and Relevance: Cholesterol can indirectly increase the susceptibility of patients to SARS-CoV-2 and increase the risk of death from COVID-19, which are mediated by NLRP3 and atherosclerotic plaques, respectively.	Cholesterol	27-38	NLR family pyrin domain containing 3	Homo sapiens	176-181
34217685-2	2021	In this study, the effect of luteolin on pyroptosis and the underlying mechanism were investigated using the canonical NLRP3 inflammasome in THP-1 macrophages induced by LPS/ATP.	Adenosine Triphosphate	174-177	NLR family pyrin domain containing 3	Homo sapiens	119-124
34217685-4	2021	Moreover, luteolin was found to significantly reduce the expression of NLRP3, pro-CASP-1 and CASP-1, which are the key components of NLRP3 inflammasome, as well as the expression of N-GSDMD and IL-1beta, and we proved that the inhibition of luteolin on NLRP3 inflammasome activation is ROS-dependent.	ros	286-289	NLR family pyrin domain containing 3	Homo sapiens	253-258
34217687-0	2021	Pelargonic acid vanillylamide and rosuvastatin protect against oxidized low-density lipoprotein-induced endothelial dysfunction by inhibiting the NF-kappaB/NLRP3 pathway and improving cell-cell junctions.	pelargonic acid	0-15	NLR family pyrin domain containing 3	Homo sapiens	156-161
34217687-0	2021	Pelargonic acid vanillylamide and rosuvastatin protect against oxidized low-density lipoprotein-induced endothelial dysfunction by inhibiting the NF-kappaB/NLRP3 pathway and improving cell-cell junctions.	4-Hydroxy-3-methoxybenzamide	16-29	NLR family pyrin domain containing 3	Homo sapiens	156-161
34217687-0	2021	Pelargonic acid vanillylamide and rosuvastatin protect against oxidized low-density lipoprotein-induced endothelial dysfunction by inhibiting the NF-kappaB/NLRP3 pathway and improving cell-cell junctions.	Rosuvastatin Calcium	34-46	NLR family pyrin domain containing 3	Homo sapiens	156-161
34564598-0	2021	Mycotoxin Zearalenone Attenuates Innate Immune Responses and Suppresses NLRP3 Inflammasome Activation in LPS-Activated Macrophages.	Zearalenone	10-21	NLR family pyrin domain containing 3	Homo sapiens	72-77
34426748-0	2021	CY-09 Inhibits NLRP3 Inflammasome Activation to Relieve Pain via TRPA1.	CY5.5 cyanine dye	0-5	NLR family pyrin domain containing 3	Homo sapiens	15-20
34457115-6	2021	In this research, we found that A740003 suppressed reactive oxygen species (ROS) generation and inhibited the activation of Nod-like receptor pyrin-domain protein 3 (NLRP3) inflammasome and nuclear factor-kappaB (NF-kappaB) pathway.	(N-(1-(((cyanoimino)(5-quinolinylamino) methyl) amino)-2,2-dimethylpropyl)-2-(3,4-dimethoxyphenyl)acetamide)	32-39	NLR family pyrin domain containing 3	Homo sapiens	124-164
34457115-6	2021	In this research, we found that A740003 suppressed reactive oxygen species (ROS) generation and inhibited the activation of Nod-like receptor pyrin-domain protein 3 (NLRP3) inflammasome and nuclear factor-kappaB (NF-kappaB) pathway.	(N-(1-(((cyanoimino)(5-quinolinylamino) methyl) amino)-2,2-dimethylpropyl)-2-(3,4-dimethoxyphenyl)acetamide)	32-39	NLR family pyrin domain containing 3	Homo sapiens	166-171
34457117-0	2021	Salidroside Suppresses the Proliferation and Migration of Human Lung Cancer Cells through AMPK-Dependent NLRP3 Inflammasome Regulation.	rhodioloside	0-11	NLR family pyrin domain containing 3	Homo sapiens	105-110
34457117-3	2021	It has been shown that SAL improves metabolic inflammation in diabetic rodents through AMP-activated protein kinase- (AMPK-) dependent inhibition of the NLRP3 inflammasome.	rhodioloside	23-26	NLR family pyrin domain containing 3	Homo sapiens	153-158
34457117-4	2021	However, whether the NLRP3 inflammasome is regulated by SAL in NSCLC cells and how its underlying mechanism(s) can be determined require clarification.	rhodioloside	56-59	NLR family pyrin domain containing 3	Homo sapiens	21-26
34457117-7	2021	Moreover, SAL protected A549 cells against LPS-induced AMPK inhibition, ROS production, and NLRP3 inflammasome activation.	rhodioloside	10-13	NLR family pyrin domain containing 3	Homo sapiens	92-97
34457117-9	2021	In summary, these results indicate that SAL suppresses the proliferation and migration of human lung cancer cells through AMPK-dependent NLRP3 inflammasome regulation.	rhodioloside	40-43	NLR family pyrin domain containing 3	Homo sapiens	137-142
34119493-0	2021	Necrosulfonamide reverses pyroptosis-induced inhibition of proliferation and differentiation of osteoblasts through the NLRP3/caspase-1/GSDMD pathway.	N-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamide	0-16	NLR family pyrin domain containing 3	Homo sapiens	120-125
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	Chloroquine	23-25	NLR family pyrin domain containing 3	Homo sapiens	45-50
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	Chloroquine	23-25	NLR family pyrin domain containing 3	Homo sapiens	117-122
34165285-10	2021	Further, the DXM-MMF conjugate significantly inhibited expression of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome-associated genes.	Dexamethasone	13-16	NLR family pyrin domain containing 3	Homo sapiens	69-118
34165285-10	2021	Further, the DXM-MMF conjugate significantly inhibited expression of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome-associated genes.	Dexamethasone	13-16	NLR family pyrin domain containing 3	Homo sapiens	120-125
34400791-9	2021	Immunomodulatory effects of melatonin were demonstrated with marked effects in the children with Down syndrome with a reduction of MyD88, IL-1ss and NLRP3 expression in whole-blood samples.	Melatonin	28-37	NLR family pyrin domain containing 3	Homo sapiens	149-154
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	3-methyladenine	14-18	NLR family pyrin domain containing 3	Homo sapiens	45-50
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	3-methyladenine	14-18	NLR family pyrin domain containing 3	Homo sapiens	117-122
34426748-8	2021	Our findings indicate that CY-09 relieves inflammation and pain via inhibiting TRPA1-mediated activation of NLRP3 inflammasomes.	CY5.5 cyanine dye	27-32	NLR family pyrin domain containing 3	Homo sapiens	108-113
34422213-9	2021	MGO induced cell death by apoptosis, whereas 3-DGal and 3,4-DGE induced nuclear translocation of the proinflammatory NF-kappaB transcription pathway, and the activation of the pyroptosis-related NLRP3 inflammasome cascade.	3-deoxygalactosone	45-51	NLR family pyrin domain containing 3	Homo sapiens	195-200
34439523-0	2021	Isoorientin Attenuated the Pyroptotic Hepatocyte Damage Induced by Benzo(a)pyrene via ROS/NF-kappaB/NLRP3/Caspase-1 Signaling Pathway.	homoorientin	0-11	NLR family pyrin domain containing 3	Homo sapiens	100-105
34439523-0	2021	Isoorientin Attenuated the Pyroptotic Hepatocyte Damage Induced by Benzo(a)pyrene via ROS/NF-kappaB/NLRP3/Caspase-1 Signaling Pathway.	Benzo(a)pyrene	67-81	NLR family pyrin domain containing 3	Homo sapiens	100-105
34408814-2	2021	H2S has previously been shown to induce the secretion of the pro-inflammatory cytokines IL-1beta and IL-18 via the NLRP3 inflammasome in monocytes.	Deuterium	0-3	NLR family pyrin domain containing 3	Homo sapiens	115-120
34408814-3	2021	Objective: To investigate the non-NLRP3 inflammasome-dependent immunological response of human peripheral blood mononuclear cells (PBMCs) of periodontitis patients and healthy controls exposed to H2S in vitro.	Deuterium	196-199	NLR family pyrin domain containing 3	Homo sapiens	34-39
34422213-9	2021	MGO induced cell death by apoptosis, whereas 3-DGal and 3,4-DGE induced nuclear translocation of the proinflammatory NF-kappaB transcription pathway, and the activation of the pyroptosis-related NLRP3 inflammasome cascade.	3,4-dideoxyglucosone-3-ene	56-63	NLR family pyrin domain containing 3	Homo sapiens	195-200
34118452-4	2021	Accumulation of damaged ROS-generating mitochondria, accompanied by the release of mitochondrial DAMPs, can activate PRRs such as the NLRP3 inflammasome, TLR9, cGAS/STING, and ZBP1.	ros	24-27	NLR family pyrin domain containing 3	Homo sapiens	134-139
34515145-0	2022	Hydrogen Peroxide Is Crucial for NLRP3 Inflammasome-Mediated IL-1beta Production and Cell Death in Pneumococcal Infections of Bronchial Epithelial Cells.	Hydrogen Peroxide	0-17	NLR family pyrin domain containing 3	Homo sapiens	33-38
34515145-6	2022	We demonstrate that H2O2 primes as well as activates the NLRP3 inflammasome and thereby mediates IL-1beta production and release.	Hydrogen Peroxide	20-24	NLR family pyrin domain containing 3	Homo sapiens	57-62
34393801-7	2021	Western blot was performed to evaluate the expression of NLRP3 and the related proteins in osteosarcoma cell lines after the blockade of NLRP3 using CY-09 and lentivirus intervention.	CY5.5 cyanine dye	149-154	NLR family pyrin domain containing 3	Homo sapiens	57-62
34145545-4	2021	increased plasma glucose, fatty acids, and beta-amyloid are augmented during obesity and activate NLRP3 inflammasome expression.	Glucose	17-24	NLR family pyrin domain containing 3	Homo sapiens	98-103
34145545-4	2021	increased plasma glucose, fatty acids, and beta-amyloid are augmented during obesity and activate NLRP3 inflammasome expression.	Fatty Acids	26-37	NLR family pyrin domain containing 3	Homo sapiens	98-103
34171753-0	2021	Chitin-derived polymer deacetylation regulates mitochondrial reactive oxygen species dependent cGAS-STING and NLRP3 inflammasome activation.	oxygen species	70-84	NLR family pyrin domain containing 3	Homo sapiens	110-115
34171753-5	2021	Additionally, the capacity of the polymers to activate the NLRP3 inflammasome was strictly dependent on the degree and pattern of deacetylation and mtROS generation.	Polymers	34-42	NLR family pyrin domain containing 3	Homo sapiens	59-64
34171753-7	2021	Furthermore, this polyglucosamine polymer enhanced antigen-specific Th1 responses in a NLRP3 and STING-type I IFN-dependent manner.	polyglucosamine polymer	18-41	NLR family pyrin domain containing 3	Homo sapiens	87-92
34216617-5	2021	AIM2 and NLRP3 appeared to be the responsible inflammasome receptors upon antimycin A-induced mitochondrial damage.	Antimycin A	74-85	NLR family pyrin domain containing 3	Homo sapiens	9-14
34257710-0	2021	BMP-2 alleviates heart failure with type 2 diabetes mellitus and doxorubicin-induced AC16 cell injury by inhibiting NLRP3 inflammasome-mediated pyroptosis.	Doxorubicin	65-76	NLR family pyrin domain containing 3	Homo sapiens	116-121
34098486-0	2021	Tanshinones inhibit NLRP3 inflammasome activation by alleviating mitochondrial damage to protect against septic and gouty inflammation.	tanshinone	0-11	NLR family pyrin domain containing 3	Homo sapiens	20-25
34216224-5	2021	The anti-inflammatory role of resolvin D1 (RvD1), a pro-resolving mediator derived from omega-3 fatty acids, has demonstrated that the NF-kappaB/NLRP3 inflammasome pathway in different tissues is attenuated after treatment with RvD1.	Fatty Acids, Omega-3	88-107	NLR family pyrin domain containing 3	Homo sapiens	145-150
34350135-4	2021	Much research has focused on toll-like receptors and more recently the nucleotide-binding domain and leucine-rich repeat pyrin containing protein-3 (NLRP3) inflammasome, which is required for the processing and release of IL-1beta.	Leucine	101-108	NLR family pyrin domain containing 3	Homo sapiens	149-154
34393801-7	2021	Western blot was performed to evaluate the expression of NLRP3 and the related proteins in osteosarcoma cell lines after the blockade of NLRP3 using CY-09 and lentivirus intervention.	CY5.5 cyanine dye	149-154	NLR family pyrin domain containing 3	Homo sapiens	137-142
34393801-10	2021	Moreover, NLRP3 suppression by the inhibitor of CY-09 or lentivirus-induced gene knockdown inhibited the cell proliferation, migration, invasion and promoted the cell apoptosis and G1 cell cycle arrest in osteosarcoma via targeting the inflammasome pathway.	CY5.5 cyanine dye	48-53	NLR family pyrin domain containing 3	Homo sapiens	10-15
34366853-0	2021	Magnoflorine Alleviates "M1" Polarized Macrophage-Induced Intervertebral Disc Degeneration Through Repressing the HMGB1/Myd88/NF-kappaB Pathway and NLRP3 Inflammasome.	magnoflorine	0-12	NLR family pyrin domain containing 3	Homo sapiens	148-153
34313166-1	2022	We investigated the effects of the NACHT leucine-rich repeat- and PYD-containing proteins (NLRP3) inflammasome, interleukin -18 (IL-18) and interleukin-1 beta (IL-1beta) cytokines on the expression of filaggrin-2 (FLG-2) protein in psoriasis patients.	Leucine	41-48	NLR family pyrin domain containing 3	Homo sapiens	91-96
34362072-8	2021	A significant positive correlation of NLRP3 levels with age (r = 0.20, p = 0.04), BMI (r = 0.32, p < 0.01) and waist (r = 0.24, p = 0.02) and a significant negative correlation between NLRP3 and HDL-cholesterol (r= -0.21, p = 0.03) were also observed in females.	Cholesterol	199-210	NLR family pyrin domain containing 3	Homo sapiens	38-43
34381452-1	2021	The nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor protein 3 (NLRP3) is an important pattern recognition receptor in human innate immunity.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	98-103
34381452-3	2021	Theories explaining activation of the NLRP3 inflammasome include the reactive oxygen species theory, the lysosomal damage theory and the mitochondrial DNA theory.	oxygen species	78-92	NLR family pyrin domain containing 3	Homo sapiens	38-43
34366853-9	2021	As a result, LPS evidently promoted the expression of pro-inflammatory cytokines and HMGB1, the MyD88-NF-kappaB activation, and the NLRP3 inflammasome profile in THP-1 cells, while MAG obviously inhibited the "M1"" polarization of THP-1 cells.	magnoflorine	181-184	NLR family pyrin domain containing 3	Homo sapiens	132-137
34366853-12	2021	Furthermore, MAG dampened the HMGB1 expression and inactivated the MyD88/NF-kappaB pathway and NLRP3 inflammasome in NP cells.	magnoflorine	13-16	NLR family pyrin domain containing 3	Homo sapiens	95-100
34335248-0	2021	Atractylenolide I Inhibits NLRP3 Inflammasome Activation in Colitis-Associated Colorectal Cancer via Suppressing Drp1-Mediated Mitochondrial Fission.	atractylenolide I	0-17	NLR family pyrin domain containing 3	Homo sapiens	27-32
34366853-13	2021	In conclusion, this study confirmed that MAG alleviates "M1" polarized macrophage-mediated NP cell damage by inactivating the HMGB1-MyD88-NF-kappaB pathway and NLRP3 inflammasome, which provides a new reference for IDD treatment.	magnoflorine	41-44	NLR family pyrin domain containing 3	Homo sapiens	160-165
34266494-7	2021	Further results showed that Rabeprazole inhibited cell pyroptosis in gastric epithelial cells by alleviating GSDMD-executed pyroptosis, leading to decrease IL-1beta and IL-18 mature and secretion, which is attributed to NLRP3 inflammasome activation inhibition.	Rabeprazole	28-39	NLR family pyrin domain containing 3	Homo sapiens	220-225
34266494-8	2021	Further analysis showed that ASC, NLRP3 and Caspase-1, was significantly repressed in response to Rabeprazole stimulation, resulting in decreasing cleaved-caspase-1 expression.	Rabeprazole	98-109	NLR family pyrin domain containing 3	Homo sapiens	34-39
34301174-2	2021	This study intends to discuss miR-135"s function in inflammatory response in PE by modulating proprotein convertase subtilisin/kexin-6 (PCSK6) and NLR pyrin domain containing 3 (NLRP3).	mir-135	30-37	NLR family pyrin domain containing 3	Homo sapiens	178-183
34301174-9	2021	CONCLUSIONS: Altogether, we demonstrate that up-regulated miR-135 or reduced PCSK6 attenuates inflammatory response in PE by restricting NLRP3 inflammasome, which provides novel therapy for PE treatment.	mir-135	58-65	NLR family pyrin domain containing 3	Homo sapiens	137-142
34336106-0	2021	The Ameliorative Effects of Arctiin and Arctigenin on the Oxidative Injury of Lung Induced by Silica via TLR-4/NLRP3/TGF-beta Signaling Pathway.	Silicon Dioxide	94-100	NLR family pyrin domain containing 3	Homo sapiens	111-116
34336106-3	2021	Further, our study revealed that arctiin and arctigenin suppressed the activation of NLRP3 inflammasome through the TLR-4/Myd88/NF-kappaB pathway and the silica-induced secretion of TNF-alpha, IL-1beta, TGF-beta, and alpha-SMA.	Silicon Dioxide	154-160	NLR family pyrin domain containing 3	Homo sapiens	85-90
34357072-3	2021	However, excessive extracellular ATP levels, such as observed in ventilator-induced lung injury, act as a danger-associated signal that activates NLRP3 inflammasome contributing to lung damage.	Adenosine Triphosphate	33-36	NLR family pyrin domain containing 3	Homo sapiens	146-151
34115964-0	2021	Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation.	Metformin	0-9	NLR family pyrin domain containing 3	Homo sapiens	70-75
34130054-12	2021	CONCLUSION: Cyn protects against blue light-induced retinal degeneration by modulating autophagy and decreasing the NLRP3 inflammasome.	luteolin-7-glucoside	12-15	NLR family pyrin domain containing 3	Homo sapiens	116-121
34371919-0	2021	Caffeine Has Different Immunomodulatory Effect on the Cytokine Expression and NLRP3 Inflammasome Function in Various Human Macrophage Subpopulations.	Caffeine	0-8	NLR family pyrin domain containing 3	Homo sapiens	78-83
34371919-8	2021	We hypothesized that these alterations play an important modulatory role in the upregulation of NLRP3 inflammasome-mediated IL-1beta secretion in LPS-activated M-MPhis following caffeine treatment.	Caffeine	178-186	NLR family pyrin domain containing 3	Homo sapiens	96-101
34115964-0	2021	Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation.	Adenosine Triphosphate	38-41	NLR family pyrin domain containing 3	Homo sapiens	70-75
34115964-3	2021	We show that metformin inhibited NLRP3 inflammasome activation and interleukin (IL)-1beta production in cultured and alveolar macrophages along with inflammasome-independent IL-6 secretion, thus attenuating lipopolysaccharide (LPS)- and SARS-CoV-2-induced ARDS.	Metformin	13-22	NLR family pyrin domain containing 3	Homo sapiens	33-38
34115964-4	2021	By targeting electron transport chain complex 1 and independently of AMP-activated protein kinase (AMPK) or NF-kappaB, metformin blocked LPS-induced and ATP-dependent mitochondrial (mt) DNA synthesis and generation of oxidized mtDNA, an NLRP3 ligand.	Metformin	119-128	NLR family pyrin domain containing 3	Homo sapiens	237-242
34281264-5	2021	In doing so, H2 suppresses oxidative stress, which is implicated in several mechanisms at the root of chronic inflammation, including the activation of NLRP3 inflammasomes.	Deuterium	13-15	NLR family pyrin domain containing 3	Homo sapiens	152-157
34356813-0	2021	The Marine-Derived Natural Product Epiloliolide Isolated from Sargassum horneri Regulates NLRP3 via PKA/CREB, Promoting Proliferation and Anti-Inflammatory Effects of Human Periodontal Ligament Cells.	7-epi-Loliolide	35-47	NLR family pyrin domain containing 3	Homo sapiens	90-95
34356813-6	2021	Epiloliolide effectively increased the proliferation and migration of human periodontal ligament cells without cytotoxicity and suppressed the protein expression of proinflammatory mediators and cytokines, such as iNOS, COX-2, TNF-alpha, IL-6, and IL-1beta, by downregulating NLRP3 activated by PG-LPS.	7-epi-Loliolide	0-12	NLR family pyrin domain containing 3	Homo sapiens	276-281
34356813-6	2021	Epiloliolide effectively increased the proliferation and migration of human periodontal ligament cells without cytotoxicity and suppressed the protein expression of proinflammatory mediators and cytokines, such as iNOS, COX-2, TNF-alpha, IL-6, and IL-1beta, by downregulating NLRP3 activated by PG-LPS.	pg-lps	295-301	NLR family pyrin domain containing 3	Homo sapiens	276-281
34307357-8	2021	In addition, mitochondrial dysfunction may amplify the activation of NLRP3 through the production of mitochondrial ROS, which together aggravate accumulating mitochondrial damage.	ros	115-118	NLR family pyrin domain containing 3	Homo sapiens	69-74
34262321-0	2021	Calcitriol Alleviates Hyperosmotic Stress-Induced Corneal Epithelial Cell Damage via Inhibiting the NLRP3-ASC-Caspase-1-GSDMD Pyroptosis Pathway in Dry Eye Disease.	Calcitriol	0-10	NLR family pyrin domain containing 3	Homo sapiens	100-105
34262321-11	2021	More importantly, we demonstrated that, in line with the effect of disulfiram, calcitriol could also alleviate HS-induced pyroptosis, through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Disulfiram	67-77	NLR family pyrin domain containing 3	Homo sapiens	157-162
34262321-11	2021	More importantly, we demonstrated that, in line with the effect of disulfiram, calcitriol could also alleviate HS-induced pyroptosis, through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Calcitriol	79-89	NLR family pyrin domain containing 3	Homo sapiens	157-162
34305534-0	2021	NLRP3 Inflammasome: A Potential Target in Isoflurane Pretreatment Alleviates Stroke-Induced Retinal Injury in Diabetes.	Isoflurane	42-52	NLR family pyrin domain containing 3	Homo sapiens	0-5
34305534-7	2021	Isoflurane has been demonstrated to inhibit the activation of the NLRP3 inflammasome and show neuroprotective effects.	Isoflurane	0-10	NLR family pyrin domain containing 3	Homo sapiens	66-71
34305534-11	2021	Of note, isoflurane pretreatment inhibited the NLRP3 inflammasome activation in the retina, indicating that isoflurane pretreatment may provide substantial retinal protection in stroke-induced retinal injury in diabetes.	Isoflurane	9-19	NLR family pyrin domain containing 3	Homo sapiens	47-52
34305534-11	2021	Of note, isoflurane pretreatment inhibited the NLRP3 inflammasome activation in the retina, indicating that isoflurane pretreatment may provide substantial retinal protection in stroke-induced retinal injury in diabetes.	Isoflurane	108-118	NLR family pyrin domain containing 3	Homo sapiens	47-52
34262321-13	2021	We demonstrated that calcitriol was able to effectively alleviate HS-induced corneal epithelial cell damage through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Calcitriol	21-31	NLR family pyrin domain containing 3	Homo sapiens	131-136
34209843-0	2021	Chemical Modulation of the 1-(Piperidin-4-yl)-1,3-dihydro-2H-benzo(d)imidazole-2-one Scaffold as a Novel NLRP3 Inhibitor.	1-(piperidin-4-yl)-1,3-dihydro-2h-benzo(d)imidazole-2-one	27-84	NLR family pyrin domain containing 3	Homo sapiens	105-110
34323410-0	2021	Screening-based identification of xanthone as a novel NLRP3 inflammasome inhibitor via metabolic reprogramming.	xanthone	34-42	NLR family pyrin domain containing 3	Homo sapiens	54-59
34196654-8	2021	Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway.	Deuterium	40-42	NLR family pyrin domain containing 3	Homo sapiens	146-151
34196654-8	2021	Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway.	Methylnitrosourea	57-60	NLR family pyrin domain containing 3	Homo sapiens	146-151
33318439-0	2021	Role of N4-acetylcytidine for continuously activating NLRP3 inflammosome by HMGB1 pathway in microglia.	N-acetylcytidine	8-25	NLR family pyrin domain containing 3	Homo sapiens	54-59
34108686-5	2021	Conditional deletion of TIM-3 in DCs led to increased accumulation of reactive oxygen species resulting in NLRP3 inflammasome activation.	Oxygen	79-85	NLR family pyrin domain containing 3	Homo sapiens	107-112
34193972-0	2021	Auranofin prevents liver fibrosis by system Xc-mediated inhibition of NLRP3 inflammasome.	Auranofin	0-9	NLR family pyrin domain containing 3	Homo sapiens	70-75
34193972-5	2021	Previous studies showed that the anti-rheumatic agent auranofin inhibits the NLRP3 inflammasome; thus, this study evaluates the antifibrotic effect of auranofin in vivo and explores the underlying molecular mechanism.	Auranofin	54-63	NLR family pyrin domain containing 3	Homo sapiens	77-82
34193972-5	2021	Previous studies showed that the anti-rheumatic agent auranofin inhibits the NLRP3 inflammasome; thus, this study evaluates the antifibrotic effect of auranofin in vivo and explores the underlying molecular mechanism.	Auranofin	151-160	NLR family pyrin domain containing 3	Homo sapiens	77-82
34193972-8	2021	Auranofin potently inhibits activation of the NLRP3 inflammasome in BMDM and kupffer cell.	Auranofin	0-9	NLR family pyrin domain containing 3	Homo sapiens	46-51
34193972-11	2021	Auranofin inhibits system Xc activity and instantly induced oxidative burst, which mediated inhibition of the NLRP3 inflammasome in macrophages and HSCs.	Auranofin	0-9	NLR family pyrin domain containing 3	Homo sapiens	110-115
34209843-1	2021	In the search for new chemical scaffolds able to afford NLRP3 inflammasome inhibitors, we used a pharmacophore-hybridization strategy by combining the structure of the acrylic acid derivative INF39 with the 1-(piperidin-4-yl)1,3-dihydro-2H-benzo(d)imidazole-2-one substructure present in HS203873, a recently identified NLRP3 binder.	acrylic acid	168-180	NLR family pyrin domain containing 3	Homo sapiens	56-61
34209843-1	2021	In the search for new chemical scaffolds able to afford NLRP3 inflammasome inhibitors, we used a pharmacophore-hybridization strategy by combining the structure of the acrylic acid derivative INF39 with the 1-(piperidin-4-yl)1,3-dihydro-2H-benzo(d)imidazole-2-one substructure present in HS203873, a recently identified NLRP3 binder.	1-(piperidin-4-yl)1,3-dihydro-2h-benzo(d)imidazole-2-one	207-263	NLR family pyrin domain containing 3	Homo sapiens	56-61
34209843-1	2021	In the search for new chemical scaffolds able to afford NLRP3 inflammasome inhibitors, we used a pharmacophore-hybridization strategy by combining the structure of the acrylic acid derivative INF39 with the 1-(piperidin-4-yl)1,3-dihydro-2H-benzo(d)imidazole-2-one substructure present in HS203873, a recently identified NLRP3 binder.	1-(piperidin-4-yl)1,3-dihydro-2h-benzo(d)imidazole-2-one	207-263	NLR family pyrin domain containing 3	Homo sapiens	320-325
34209843-3	2021	The obtained compounds were screened in vitro to test their ability to inhibit NLRP3-dependent pyroptosis and IL-1beta release in PMA-differentiated THP-1 cells stimulated with LPS/ATP.	Adenosine Triphosphate	181-184	NLR family pyrin domain containing 3	Homo sapiens	79-84
34262463-10	2021	Collectively, our results indicate that the ROS-NLRP3 inflammasome-interleukin-1beta axis may contribute to platelet hyperactivity in active CD.	Reactive Oxygen Species	44-47	NLR family pyrin domain containing 3	Homo sapiens	48-53
34209843-5	2021	From this screening, compounds 9, 13 and 18, able to concentration-dependently inhibit IL-1beta release in LPS/ATP-stimulated human macrophages, emerged as the most promising NLRP3 inhibitors of the series.	Adenosine Triphosphate	111-114	NLR family pyrin domain containing 3	Homo sapiens	175-180
34234503-0	2021	Hydrogen Sulfide Contributes to Uterine Quiescence Through Inhibition of NLRP3 Inflammasome Activation by Suppressing the TLR4/NF-kappaB Signalling Pathway.	Hydrogen Sulfide	0-16	NLR family pyrin domain containing 3	Homo sapiens	73-78
34234503-12	2021	In addition, treatment with the H2S donor NaHS inhibited NLRP3 inflammasome activation, reduced the expression of uterine contraction-associated proteins and inflammatory cytokines and reduced the activation of TLR4 and NF-kappaB compared with stimulation with IL-1beta in human uterine smooth muscle cells.	Deuterium	32-35	NLR family pyrin domain containing 3	Homo sapiens	57-62
34172780-1	2021	Nucleotide-binding domain and leucine-rich repeat (LRR)-containing family protein 3 (NLRP3) regulated the maturation of inflammation-related cytokines by forming NLRP3 inflammasome, which plays pivotal roles in sepsis pathogenesis.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	85-90
34172780-1	2021	Nucleotide-binding domain and leucine-rich repeat (LRR)-containing family protein 3 (NLRP3) regulated the maturation of inflammation-related cytokines by forming NLRP3 inflammasome, which plays pivotal roles in sepsis pathogenesis.	Leucine	30-37	NLR family pyrin domain containing 3	Homo sapiens	162-167
34234503-12	2021	In addition, treatment with the H2S donor NaHS inhibited NLRP3 inflammasome activation, reduced the expression of uterine contraction-associated proteins and inflammatory cytokines and reduced the activation of TLR4 and NF-kappaB compared with stimulation with IL-1beta in human uterine smooth muscle cells.	sodium bisulfide	42-46	NLR family pyrin domain containing 3	Homo sapiens	57-62
34234503-13	2021	Furthermore, treatment of uterine smooth muscle cells with BAY 11-7082 and TAK-242 found that NLRP3 activation was regulated by the TLR4 and NF-kappaB pathways.	3-(4-methylphenylsulfonyl)-2-propenenitrile	59-70	NLR family pyrin domain containing 3	Homo sapiens	94-99
34175493-5	2022	ATP activates purinergic receptors in the cell membranes of infected cells and promotes parasite control by inducing leukotriene B4 release and NLRP3 inflammasome activation.	Adenosine Triphosphate	0-3	NLR family pyrin domain containing 3	Homo sapiens	144-149
34234503-13	2021	Furthermore, treatment of uterine smooth muscle cells with BAY 11-7082 and TAK-242 found that NLRP3 activation was regulated by the TLR4 and NF-kappaB pathways.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	75-82	NLR family pyrin domain containing 3	Homo sapiens	94-99
34234503-14	2021	Conclusion: H2S suppresses CAP expression and the inflammatory response and contributes to uterine quiescence by inhibiting the TLR4/NF-kappaB signalling pathway and downstream NLRP3 inflammasome activation.	Deuterium	12-15	NLR family pyrin domain containing 3	Homo sapiens	177-182
34202842-0	2021	The Role of Melatonin on NLRP3 Inflammasome Activation in Diseases.	Melatonin	12-21	NLR family pyrin domain containing 3	Homo sapiens	25-30
34234503-15	2021	Thus, H2S contributes to uterine quiescence through inhibition of NLRP3 inflammasome activation by suppressing the TLR4/NF-kappaB signalling pathway.	Deuterium	6-9	NLR family pyrin domain containing 3	Homo sapiens	66-71
34202842-1	2021	NLRP3 inflammasome is a part of the innate immune system and responsible for the rapid identification and eradication of pathogenic microbes, metabolic stress products, reactive oxygen species, and other exogenous agents.	Reactive Oxygen Species	169-192	NLR family pyrin domain containing 3	Homo sapiens	0-5
34202842-6	2021	Many in vitro and in vivo studies have proved that melatonin alleviates NLRP3 inflammasome activity via various intracellular signaling pathways.	Melatonin	51-60	NLR family pyrin domain containing 3	Homo sapiens	72-77
34326697-6	2021	Furthermore, knockdown of MEG3 not only partly abolished the activation effect of DDP on NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis, but also reversed the suppression of DDP on tumor growth and metastasis ability in vitro and in vivo, further confirming that MEG3 may partially mediate the pyroptotic signaling upon DDP treatment.	Cisplatin	323-326	NLR family pyrin domain containing 3	Homo sapiens	89-94
34202842-7	2021	In this review, the effect of melatonin on the NLRP3 inflammasome in the context of diseases will be discussed.	Melatonin	30-39	NLR family pyrin domain containing 3	Homo sapiens	47-52
34326697-0	2021	Cisplatin Induces Pyroptosis via Activation of MEG3/NLRP3/caspase-1/GSDMD Pathway in Triple-Negative Breast Cancer.	Cisplatin	0-9	NLR family pyrin domain containing 3	Homo sapiens	52-57
34249981-9	2021	Pedigree analysis revealed another four relatives with similar symptoms, and a heterozygous NLRP3 gene mutation c.1316C>T, p.Ala439Val was identified by whole-exome sequencing and Sanger sequencing.	ala439val	125-134	NLR family pyrin domain containing 3	Homo sapiens	92-97
34326697-4	2021	In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo, providing evidence that DDP might induce pyroptosis in TNBC.	Cisplatin	83-86	NLR family pyrin domain containing 3	Homo sapiens	22-27
34145842-10	2021	Furthermore, treatment with S-MWCNT, L-MWCNT and L-MWCNT-COOH increased NLRP3 expression in a time-dependent manner at 6.25 mug/cm2.	Carbonic Acid	57-61	NLR family pyrin domain containing 3	Homo sapiens	72-77
34326697-4	2021	In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo, providing evidence that DDP might induce pyroptosis in TNBC.	Cisplatin	167-170	NLR family pyrin domain containing 3	Homo sapiens	22-27
34198548-3	2021	Macrophage-specific deletion of Glucose Transporter 1 (GLUT1) significantly reduced tumor burden, which was accompanied by increased Natural Killer and CD8+ T cell activity and suppression of the NLRP3-IL1beta inflammasome axis.	Glucose	32-39	NLR family pyrin domain containing 3	Homo sapiens	196-201
34212035-3	2021	When treated with Carvacrol or tert-butylhydroquinone (TBHQ) that activates Nrf2, the expression of Keap1/Nrf2/HO-1, epithelial-mesenchymal transition- (EMT-) related proteins, and NALP3 was examined in OSCC cells.	carvacrol	18-27	NLR family pyrin domain containing 3	Homo sapiens	181-186
34178667-0	2021	Polydatin Reduces Cardiotoxicity and Enhances the Anticancer Effects of Sunitinib by Decreasing Pro-Oxidative Stress, Pro-Inflammatory Cytokines, and NLRP3 Inflammasome Expression.	polydatin	0-9	NLR family pyrin domain containing 3	Homo sapiens	150-155
34178667-0	2021	Polydatin Reduces Cardiotoxicity and Enhances the Anticancer Effects of Sunitinib by Decreasing Pro-Oxidative Stress, Pro-Inflammatory Cytokines, and NLRP3 Inflammasome Expression.	Sunitinib	72-81	NLR family pyrin domain containing 3	Homo sapiens	150-155
34212035-9	2021	Carvacrol or silencing Nrf2 markedly inhibited the expression of Keap1/Nrf2/HO-1, EMT-related proteins, and NALP3 inflammasome in OSCC cells.	carvacrol	0-9	NLR family pyrin domain containing 3	Homo sapiens	108-113
34204067-11	2021	NAC concurrently reduced the NLRP3 levels but had no effect on IL-18 release.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	29-34
34099830-1	2021	Recent studies suggested that ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor, developed for the treatment of chronic lymphocytic leukemia, may prevent NLRP3 inflammasome activation in macrophages, IL-1beta secretion and subsequent development of inflammation and organ fibrosis.	ibrutinib	30-39	NLR family pyrin domain containing 3	Homo sapiens	156-161
34204067-0	2021	Hydroquinone Induces NLRP3-Independent IL-18 Release from ARPE-19 Cells.	hydroquinone	0-12	NLR family pyrin domain containing 3	Homo sapiens	21-26
34204067-9	2021	Cytoplasmic NLRP3 levels increased after the hydroquinone treatment of IL-1alpha-primed RPE cells, but IL-18 was equally released from primed and nonprimed cells.	hydroquinone	45-57	NLR family pyrin domain containing 3	Homo sapiens	12-17
34204067-13	2021	Collectively, hydroquinone caused DNA damage seen as reduced intracellular PARP levels and induced NLRP3-independent IL-18 secretion in human RPE cells.	hydroquinone	14-26	NLR family pyrin domain containing 3	Homo sapiens	99-104
34350239-10	2021	A NLRP3 activator Nigericin was used to verify the effect of NLRP3 in the neuroprotective mechanism of UTI.	Nigericin	18-27	NLR family pyrin domain containing 3	Homo sapiens	2-7
34349888-2	2021	ROS induces NLRP3, a protein involved in the synthesis of interleukin (IL)-1 and IL-18; vaspin is a serine protease inhibitor that has an important role in suppressing the activation of NLRP3 inflammasome.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	12-17
34350239-12	2021	We also found decreased DA secretion and TH expression, as well as increased NLRP3, caspase-1, ASC, IL-1alpha, and IL-18 expression in the MPP+ induced PD model.	mangion-purified polysaccharide (Candida albicans)	139-143	NLR family pyrin domain containing 3	Homo sapiens	77-82
34350239-14	2021	NLRP3 activator Nigericin markedly increased LDH release, accelerated apoptosis, increased inflammation levels and decreased DA secretion and TH expression, suggesting that Nigericin eliminated the neuroprotective effect of UTI on MPP+ treated cells.	Nigericin	16-25	NLR family pyrin domain containing 3	Homo sapiens	0-5
34350239-14	2021	NLRP3 activator Nigericin markedly increased LDH release, accelerated apoptosis, increased inflammation levels and decreased DA secretion and TH expression, suggesting that Nigericin eliminated the neuroprotective effect of UTI on MPP+ treated cells.	amsonic acid	125-127	NLR family pyrin domain containing 3	Homo sapiens	0-5
34350239-14	2021	NLRP3 activator Nigericin markedly increased LDH release, accelerated apoptosis, increased inflammation levels and decreased DA secretion and TH expression, suggesting that Nigericin eliminated the neuroprotective effect of UTI on MPP+ treated cells.	Nigericin	173-182	NLR family pyrin domain containing 3	Homo sapiens	0-5
34350239-15	2021	Conclusions: Our data demonstrated that UTI pre-treatment performed a neuroprotective role in the MPP+ induced PD cell models by inhibiting the NLRP3 pathway.	mangion-purified polysaccharide (Candida albicans)	98-102	NLR family pyrin domain containing 3	Homo sapiens	144-149
34115948-3	2021	The opioid, morphine, initiates a Toll-like receptor 4 (TLR4) signaling cascade that drives the activation of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome proteins, resulting in cytokine production and effectively creating a positive feedback loop for continuous TLR4 activation.	Morphine	12-20	NLR family pyrin domain containing 3	Homo sapiens	110-159
34069836-0	2021	Antioxidant Ascorbic Acid Modulates NLRP3 Inflammasome in LPS-G Treated Oral Stem Cells through NFkappaB/Caspase-1/IL-1beta Pathway.	Ascorbic Acid	12-25	NLR family pyrin domain containing 3	Homo sapiens	36-41
34115948-3	2021	The opioid, morphine, initiates a Toll-like receptor 4 (TLR4) signaling cascade that drives the activation of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome proteins, resulting in cytokine production and effectively creating a positive feedback loop for continuous TLR4 activation.	Morphine	12-20	NLR family pyrin domain containing 3	Homo sapiens	161-166
34093539-0	2021	Remdesivir Alleviates Acute Kidney Injury by Inhibiting the Activation of NLRP3 Inflammasome.	remdesivir	0-10	NLR family pyrin domain containing 3	Homo sapiens	74-79
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	31-41	NLR family pyrin domain containing 3	Homo sapiens	147-196
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	31-41	NLR family pyrin domain containing 3	Homo sapiens	198-203
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	43-46	NLR family pyrin domain containing 3	Homo sapiens	147-196
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	43-46	NLR family pyrin domain containing 3	Homo sapiens	198-203
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	48-55	NLR family pyrin domain containing 3	Homo sapiens	147-196
34093539-3	2021	Here, we firstly reported that remdesivir (RDV, GS-5734), a broad-spectrum antiviral nucleotide prodrug, alleviated AKI by specifically inhibiting NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in macrophages.	remdesivir	48-55	NLR family pyrin domain containing 3	Homo sapiens	198-203
34093539-4	2021	Mechanically, RDV effectively suppressed the activities of nuclear transcription factor (NF)-kappaB, mitogen-activated protein kinase (MAPK), which further led to the reduction of the inflammasome genes of NLRP3 transcription, limiting the activation of NLRP3 inflammasome in vivo and in vitro.	remdesivir	14-17	NLR family pyrin domain containing 3	Homo sapiens	206-211
34093539-4	2021	Mechanically, RDV effectively suppressed the activities of nuclear transcription factor (NF)-kappaB, mitogen-activated protein kinase (MAPK), which further led to the reduction of the inflammasome genes of NLRP3 transcription, limiting the activation of NLRP3 inflammasome in vivo and in vitro.	remdesivir	14-17	NLR family pyrin domain containing 3	Homo sapiens	254-259
34093588-6	2021	TLR4-mediated internalization of the HAdV-lactoferrin complex induced an NLRP3-associated response that consisted of cytokine release and transient disruption of plasma membrane integrity, without causing cell death.	hadv-lactoferrin complex	37-61	NLR family pyrin domain containing 3	Homo sapiens	73-78
34093086-4	2021	The coculture system of spleen CD4+ T and bone marrow CD11c+ DC cells was set to explore the orchestration of NLRP3 and Th17 in the pathological development of VMC in vitro.	2-methoxy-4-(1-{2-[(2S)-1-methylpyrrolidin-2-yl]ethyl}-4-phenyl-1H-imidazol-5-yl)phenol	160-163	NLR family pyrin domain containing 3	Homo sapiens	110-115
34084773-10	2021	Additionally, high glucose markedly activated NLRP3 inflammasome in RPMCs that was blunted by mPGES-1 inhibition.	Glucose	19-26	NLR family pyrin domain containing 3	Homo sapiens	46-51
34084773-13	2021	Conclusion: These data demonstrate that mPGES-1-derived PGE2 plays a critical role in PD-associated peritoneal fibrosis through activation of the NLRP3 inflammasome.	Dinoprostone	56-60	NLR family pyrin domain containing 3	Homo sapiens	146-151
34064821-0	2021	Leukotriene B4 Receptors Are Necessary for the Stimulation of NLRP3 Inflammasome and IL-1beta Synthesis in Neutrophil-Dominant Asthmatic Airway Inflammation.	Leukotrienes	0-11	NLR family pyrin domain containing 3	Homo sapiens	62-67
34064821-6	2021	The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands (LTB4, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)), were also critically associated with the stimulation of NLRP3 and IL-1beta synthesis.	Leukotriene B4	96-100	NLR family pyrin domain containing 3	Homo sapiens	255-260
34062977-0	2021	TAS-116, a Well-Tolerated Hsp90 Inhibitor, Prevents the Activation of the NLRP3 Inflammasome in Human Retinal Pigment Epithelial Cells.	TAS-116	0-7	NLR family pyrin domain containing 3	Homo sapiens	74-79
34064821-6	2021	The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands (LTB4, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)), were also critically associated with the stimulation of NLRP3 and IL-1beta synthesis.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	102-136	NLR family pyrin domain containing 3	Homo sapiens	255-260
34064821-6	2021	The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands (LTB4, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)), were also critically associated with the stimulation of NLRP3 and IL-1beta synthesis.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	138-148	NLR family pyrin domain containing 3	Homo sapiens	255-260
34064821-6	2021	The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands (LTB4, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)), were also critically associated with the stimulation of NLRP3 and IL-1beta synthesis.	12-hydroxyheptadecatreinoic acid	155-187	NLR family pyrin domain containing 3	Homo sapiens	255-260
34064821-6	2021	The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands (LTB4, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)), were also critically associated with the stimulation of NLRP3 and IL-1beta synthesis.	12-hydroxy-5,8,10-heptadecatrienoic acid	189-195	NLR family pyrin domain containing 3	Homo sapiens	255-260
34066647-0	2021	Ethyl Pyruvate Attenuates Microglial NLRP3 Inflammasome Activation via Inhibition of HMGB1/NF-kappaB/miR-223 Signaling.	ethyl pyruvate	0-14	NLR family pyrin domain containing 3	Homo sapiens	37-42
34066647-4	2021	Our study aimed to investigate the mechanism of the impact of Ethyl pyruvate on NLRP3 inflammasome activation in the N9 microglial cell line.	ethyl pyruvate	62-76	NLR family pyrin domain containing 3	Homo sapiens	80-85
34066647-5	2021	Our results indicated that ethyl pyruvate significantly suppressed LPS and ATP-induced NLRP3 inflammasome activation, decreased active caspase-1 level, secretion of IL-1beta and IL-18 cytokines, and reduced the level of pyroptotic cell death resulting from inflammasome activation.	ethyl pyruvate	27-41	NLR family pyrin domain containing 3	Homo sapiens	87-92
34066647-5	2021	Our results indicated that ethyl pyruvate significantly suppressed LPS and ATP-induced NLRP3 inflammasome activation, decreased active caspase-1 level, secretion of IL-1beta and IL-18 cytokines, and reduced the level of pyroptotic cell death resulting from inflammasome activation.	Adenosine Triphosphate	75-78	NLR family pyrin domain containing 3	Homo sapiens	87-92
34066647-7	2021	Our study suggests that ethyl pyruvate effectively suppresses the NLRP3 inflammasome activation in microglial cells regulation by miR-223 and NF-kappaB/HMGB1 axis.	ethyl pyruvate	24-38	NLR family pyrin domain containing 3	Homo sapiens	66-71
34062977-5	2021	Here, we have tested the effects of a novel Hsp90 inhibitor, TAS-116, on NLRP3 activation using geldanamycin as a reference compound.	TAS-116	61-68	NLR family pyrin domain containing 3	Homo sapiens	73-78
34870152-0	2021	Can NLRP3 inhibitors improve on dexamethasone for the treatment of COVID-19?	Dexamethasone	32-45	NLR family pyrin domain containing 3	Homo sapiens	4-9
34268377-4	2021	The roles of Andro in BLM-induced NLRP3 inflammasome activation, EMT and AKT/mTOR signaling were investigated using human alveolar epithelial A549 cells.	andrographolide	13-18	NLR family pyrin domain containing 3	Homo sapiens	34-39
34530705-5	2021	Experimental models of AD have suggested that Abeta accumulation induces, through microglia, activation of the NLRP3 inflammasome.	UNII-042A8N37WH	46-51	NLR family pyrin domain containing 3	Homo sapiens	111-116
34870152-4	2021	The NLRP3 inflammasome is an intracellular signalling complex which is responsible for the cleavage and release of the cytokines IL-1beta and IL-18 and has also been shown to be inhibited by dexamethasone.	Dexamethasone	191-204	NLR family pyrin domain containing 3	Homo sapiens	4-9
34879371-8	2021	miRNA-141-3p induced NLRP3, IL-1beta, and IL-18 production, decreased CXCR4, MMP, and MMP2 production, and suppressed cell growth and invasion.	mirna-141-3p	0-12	NLR family pyrin domain containing 3	Homo sapiens	21-26
34870152-5	2021	NLRP3 inflammasome activation is strongly correlated with COVID-19 severity and part of dexamethasone"s clinical effect in COVID-19 may be via NLRP3 inhibition.	Dexamethasone	88-101	NLR family pyrin domain containing 3	Homo sapiens	0-5
34870152-5	2021	NLRP3 inflammasome activation is strongly correlated with COVID-19 severity and part of dexamethasone"s clinical effect in COVID-19 may be via NLRP3 inhibition.	Dexamethasone	88-101	NLR family pyrin domain containing 3	Homo sapiens	143-148
34879371-9	2021	Furthermore, we observed that NLRP3 plays an important mediatory role in the effects of miR-141-3p described above.	mir-141-3p	88-98	NLR family pyrin domain containing 3	Homo sapiens	30-35
34396831-4	2021	Binding between insulin amyloid fibrils and NLRP3 was evaluated by immunoprecipitation followed by native polyacrylamide gel electrophoresis.	polyacrylamide	106-120	NLR family pyrin domain containing 3	Homo sapiens	44-49
35297523-9	2022	In BPDE combined with 4-PBA intervention group, the rate of PI-positive cells was reduced, the expression levels of GRP78, GSDMD-N, and cleaved-caspase 1 were decreased, and the expression levels of IL-1beta, IL-18, and NLRP3 were decreased.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	3-7	NLR family pyrin domain containing 3	Homo sapiens	220-225
34747666-10	2021	Furthermore, tube formation by human umbilical vein endothelial cells, TNF-alpha and VEGF secretion, and the levels of MRP1, ABCG1, ABCA1, and NLRP3 expression in cisplatin-resistant Eca-109 and TE1 cells were all reduced by miR-495 mimics.	Cisplatin	163-172	NLR family pyrin domain containing 3	Homo sapiens	143-148
35551917-0	2022	RESOLVIN E1 ATTENUATES DOXORUBICIN-INDUCED ENDOTHELIAL SENESCENCE BY MODULATING NLRP3 INFLAMMASOME ACTIVATION.	Doxorubicin	23-34	NLR family pyrin domain containing 3	Homo sapiens	80-85
35551917-7	2022	Moreover, we identified Doxo-induced senescence to be mediated by the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome, a key player of the immune innate system capable of releasing interleukin (IL)-1beta.	Doxorubicin	24-28	NLR family pyrin domain containing 3	Homo sapiens	70-119
35551917-7	2022	Moreover, we identified Doxo-induced senescence to be mediated by the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome, a key player of the immune innate system capable of releasing interleukin (IL)-1beta.	Doxorubicin	24-28	NLR family pyrin domain containing 3	Homo sapiens	121-126
35551917-8	2022	In fact, IL-1beta itself mimicked the stimulatory action of Doxo on both NLRP3 activation and cellular senescence, while the pharmacological blockade of IL-1 receptors markedly attenuated the pro-senescence effects of Doxo.	Doxorubicin	60-64	NLR family pyrin domain containing 3	Homo sapiens	73-78
35403328-8	2022	Finally, the intracellular reactive oxygen species (ROS) was measured and the ROS inhibitor N-acetyl-L-cysteine (NAC) was used to investigate whether ROS was required for PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions.	Reactive Oxygen Species	150-153	NLR family pyrin domain containing 3	Homo sapiens	185-190
35403328-10	2022	Furthermore, PM2.5 exposure aggravated NLRP3 inflammasome activation and pyroptosis after OGD/R, as indicated by an increased expression of NLRP3, ASC, pro-caspase-1, Caspase-1, GSDMD, and GSDMD-N; increased production of IL-1beta and IL-18; and enhanced Caspase-1 activity and SYTOX green uptake.	gsdmd-n	189-196	NLR family pyrin domain containing 3	Homo sapiens	39-44
35403328-10	2022	Furthermore, PM2.5 exposure aggravated NLRP3 inflammasome activation and pyroptosis after OGD/R, as indicated by an increased expression of NLRP3, ASC, pro-caspase-1, Caspase-1, GSDMD, and GSDMD-N; increased production of IL-1beta and IL-18; and enhanced Caspase-1 activity and SYTOX green uptake.	SYTOX Green	278-289	NLR family pyrin domain containing 3	Homo sapiens	39-44
35403328-12	2022	Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions.	Reactive Oxygen Species	84-87	NLR family pyrin domain containing 3	Homo sapiens	181-186
35403328-12	2022	Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions.	Reactive Oxygen Species	122-125	NLR family pyrin domain containing 3	Homo sapiens	181-186
35403328-12	2022	Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions.	Acetylcysteine	142-145	NLR family pyrin domain containing 3	Homo sapiens	181-186
35403328-13	2022	CONCLUSION: These results suggested that PM2.5 exposure triggered the activation of NLRP3 inflammasome and pyroptosis under ischemic conditions, which may be mediated by increased ROS production after ischemic stroke.	Reactive Oxygen Species	180-183	NLR family pyrin domain containing 3	Homo sapiens	84-89
34997266-10	2022	Furthermore, PQQ abolished mitochondrial dysfunction and the activation of NF-kappaB/IkappaB, and decreased NLRP3 inflammation-mediated pyroptosis in AC16 cells under high-glucose conditions.	PQQ Cofactor	13-16	NLR family pyrin domain containing 3	Homo sapiens	108-113
35477273-8	2022	sDPP4 activates the metabotropic receptor PAR2 (protease-activated receptor 2), COX-2 (cyclooxygenase 2) activity, and the production of TXA2 (thromboxane A2) acting over TP (thromboxane receptor) receptors (PAR2-COX-2-TP axis), leading to NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3) inflammasome activation.	sdpp4	0-5	NLR family pyrin domain containing 3	Homo sapiens	240-245
35354089-0	2022	Cucurbitacin E glucoside alleviates concanavalin A-induced hepatitis through enhancing SIRT1/Nrf2/HO-1 and inhibiting NF-kB/NLRP3 signaling pathways.	cucurbitacin E	0-14	NLR family pyrin domain containing 3	Homo sapiens	124-129
35354089-0	2022	Cucurbitacin E glucoside alleviates concanavalin A-induced hepatitis through enhancing SIRT1/Nrf2/HO-1 and inhibiting NF-kB/NLRP3 signaling pathways.	Glucosides	15-24	NLR family pyrin domain containing 3	Homo sapiens	124-129
35439536-3	2022	The results showed that BPA increased the mRNA levels of IL-18, ASC, GSDMD and protein levels of NLRP3, caspase-1 and GSDMD in both cell lines in a nonlinear manner.	bisphenol A	24-27	NLR family pyrin domain containing 3	Homo sapiens	97-102
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	bisphenol A	12-15	NLR family pyrin domain containing 3	Homo sapiens	69-74
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	bisphenol A	173-176	NLR family pyrin domain containing 3	Homo sapiens	69-74
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	epigallocatechin gallate	220-224	NLR family pyrin domain containing 3	Homo sapiens	69-74
35346830-0	2022	MiR-1656 targets GPX4 to trigger pyroptosis in broilers kidney tissues by activating NLRP3 inflammasome under Se deficiency.	mir-1656	0-8	NLR family pyrin domain containing 3	Homo sapiens	85-90
35346830-8	2022	The overexpression of miR-1656 can induce increased expression of pyroptosis-related genes including NLRP3, Caspase-1, IL-18, and IL-1beta by inhibiting the release of GPX4.	mir-1656	22-30	NLR family pyrin domain containing 3	Homo sapiens	101-106
35346830-9	2022	This study showed that miR-1656 could increase the release of ROS by targeting GPX4, activated the NLRP3 inflammasome, and release the inflammatory factors IL-1beta and IL-18 to trigger pyroptosis in the kidney tissue of Se-deficient broilers.	ros	62-65	NLR family pyrin domain containing 3	Homo sapiens	99-104
35633614-0	2022	3,4,5-O-tricaffeoylquinic acid with anti-radiation activity suppresses LPS-induced NLRP3 inflammasome activation via autophagy in THP-1 macrophages.	3,4,5-o-tricaffeoylquinic acid	0-30	NLR family pyrin domain containing 3	Homo sapiens	83-88
35633614-8	2022	Furthermore, we found that the autophagy inhibitor chloroquine, not the proteasome inhibitor MG132, could counteract the promoting effect of tCQA on NLRP3 degradation and the inhibitory effect on cell death.	Chloroquine	51-62	NLR family pyrin domain containing 3	Homo sapiens	149-154
35633614-8	2022	Furthermore, we found that the autophagy inhibitor chloroquine, not the proteasome inhibitor MG132, could counteract the promoting effect of tCQA on NLRP3 degradation and the inhibitory effect on cell death.	tcqa	141-145	NLR family pyrin domain containing 3	Homo sapiens	149-154
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	62-66	NLR family pyrin domain containing 3	Homo sapiens	204-209
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	62-66	NLR family pyrin domain containing 3	Homo sapiens	276-281
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	196-200	NLR family pyrin domain containing 3	Homo sapiens	204-209
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	196-200	NLR family pyrin domain containing 3	Homo sapiens	276-281
35439536-0	2022	Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis in BPA-Induced Apoptosis of Human Neuroblastoma Cells.	bisphenol A	61-64	NLR family pyrin domain containing 3	Homo sapiens	15-20
34997266-10	2022	Furthermore, PQQ abolished mitochondrial dysfunction and the activation of NF-kappaB/IkappaB, and decreased NLRP3 inflammation-mediated pyroptosis in AC16 cells under high-glucose conditions.	Glucose	172-179	NLR family pyrin domain containing 3	Homo sapiens	108-113
35313270-0	2022	Chlorogenic acid attenuates inflammation in LPS-induced Human gingival fibroblasts via CysLT1R/Nrf2/NLRP3 signaling.	Chlorogenic Acid	0-16	NLR family pyrin domain containing 3	Homo sapiens	100-105
35608902-0	2022	Citric acid of ovarian cancer metabolite induces pyroptosis via the caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer.	Citric Acid	0-11	NLR family pyrin domain containing 3	Homo sapiens	84-89
35481558-4	2022	In the study, we found for the first time that apigenin could alleviate palmitic acid (PA)-induced NLRP3 inflammasome activation and pyroptosis in HepG2 cells and primary mouse hepatic cells.	Apigenin	47-55	NLR family pyrin domain containing 3	Homo sapiens	99-104
35271969-1	2022	BACKGROUND: Chronic low-grade systemic inflammation (SI), including activation of the NLRP3 inflammasome, is a feature of obesity, associated with increased circulating saturated fatty acids, such as palmitic acid (PA), and bacterial endotoxin lipopolysaccharide (LPS).	Fatty Acids	169-190	NLR family pyrin domain containing 3	Homo sapiens	86-91
35271969-1	2022	BACKGROUND: Chronic low-grade systemic inflammation (SI), including activation of the NLRP3 inflammasome, is a feature of obesity, associated with increased circulating saturated fatty acids, such as palmitic acid (PA), and bacterial endotoxin lipopolysaccharide (LPS).	Palmitic Acid	200-213	NLR family pyrin domain containing 3	Homo sapiens	86-91
35271969-1	2022	BACKGROUND: Chronic low-grade systemic inflammation (SI), including activation of the NLRP3 inflammasome, is a feature of obesity, associated with increased circulating saturated fatty acids, such as palmitic acid (PA), and bacterial endotoxin lipopolysaccharide (LPS).	Palmitic Acid	215-217	NLR family pyrin domain containing 3	Homo sapiens	86-91
35271969-2	2022	PA and LPS may contribute to SI observed in obesity, while the dietary antioxidant sulforaphane has been shown to reduce activation of the NLRP3 inflammasome.	sulforaphane	83-95	NLR family pyrin domain containing 3	Homo sapiens	139-144
35271969-3	2022	This study investigated immune cell responses from obese subjects to PA, and the effects of sulforaphane on NLRP3 activation/inflammation.	sulforaphane	92-104	NLR family pyrin domain containing 3	Homo sapiens	108-113
35271969-6	2022	RESULTS: IL-1beta and NLRP3 expression were higher in both unstimulated and PA treated monocytes from obese compared to non-obese subjects.	Palmitic Acid	76-78	NLR family pyrin domain containing 3	Homo sapiens	22-27
35271969-10	2022	CONCLUSION: NLRP3 inflammasome activation by PA is higher in obesity, which maybe driven by baseline activation of the NLRP3 inflammasome.	Palmitic Acid	45-47	NLR family pyrin domain containing 3	Homo sapiens	12-17
35271969-10	2022	CONCLUSION: NLRP3 inflammasome activation by PA is higher in obesity, which maybe driven by baseline activation of the NLRP3 inflammasome.	Palmitic Acid	45-47	NLR family pyrin domain containing 3	Homo sapiens	119-124
35385822-8	2022	Moreover, the expression of Caspase-1, NLRP3, GSDMA, IL-18, and IL-1beta and caused membrane perforation, suggesting the development of pyroptosis by chTERT in LMH cells.	chtert	150-156	NLR family pyrin domain containing 3	Homo sapiens	39-44
35331853-7	2022	Puerarin ameliorated LPS-induced cytotoxicity and apoptosis, while repressing LPS-stimulated NLRP3 inflammasome-mediated pyroptosis in GES-1 cells, as evidenced by significantly decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1beta and IL-18.	puerarin	0-8	NLR family pyrin domain containing 3	Homo sapiens	93-98
35331853-7	2022	Puerarin ameliorated LPS-induced cytotoxicity and apoptosis, while repressing LPS-stimulated NLRP3 inflammasome-mediated pyroptosis in GES-1 cells, as evidenced by significantly decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1beta and IL-18.	puerarin	0-8	NLR family pyrin domain containing 3	Homo sapiens	202-207
35612721-3	2022	RECENT FINDINGS: The latest research on this topic has focused on the critical role of the NLRP3 (NACHT, leucine-rich repeat, and pyrin domain-containing protein) inflammasome.	Leucine	105-112	NLR family pyrin domain containing 3	Homo sapiens	91-96
35481558-4	2022	In the study, we found for the first time that apigenin could alleviate palmitic acid (PA)-induced NLRP3 inflammasome activation and pyroptosis in HepG2 cells and primary mouse hepatic cells.	Palmitic Acid	72-85	NLR family pyrin domain containing 3	Homo sapiens	99-104
35481558-4	2022	In the study, we found for the first time that apigenin could alleviate palmitic acid (PA)-induced NLRP3 inflammasome activation and pyroptosis in HepG2 cells and primary mouse hepatic cells.	Palmitic Acid	87-89	NLR family pyrin domain containing 3	Homo sapiens	99-104
35584771-0	2022	Agonism of GPR120 Prevented High Glucose-Induced Apoptosis of Retinal Endothelial Cells through Inhibiting NLRP3 Inflammasome.	Glucose	33-40	NLR family pyrin domain containing 3	Homo sapiens	107-112
35629435-10	2022	From bedside to bench, ROS scavenger attenuates PCS-activated expressions of cPLA2/COX2, pro-caspase-1 and NLRP3 in the HASMC model.	ros	23-26	NLR family pyrin domain containing 3	Homo sapiens	107-112
35584771-10	2022	GW9508 can attenuate inflammation by reducing the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 under HG.	GW9508	0-6	NLR family pyrin domain containing 3	Homo sapiens	64-69
35629435-0	2022	Translational Medicine in Uremic Vascular Calcification: Scavenging ROS Attenuates p-Cresyl Sulfate-Activated Caspase-1, NLRP3 Inflammasome and Eicosanoid Inflammation in Human Arterial Smooth Muscle Cells.	ros	68-71	NLR family pyrin domain containing 3	Homo sapiens	121-126
35635948-0	2022	Development of sulfonamide-based NLRP3 inhibitors: Further modifications and optimization through structure-activity relationship studies.	Sulfonamides	15-26	NLR family pyrin domain containing 3	Homo sapiens	33-38
35635948-3	2022	In our continuing efforts to develop NLRP3 inhibitors, a recently identified lead inhibitor, YQ128, was further modified and optimized.	YQ128	93-98	NLR family pyrin domain containing 3	Homo sapiens	37-42
35628574-11	2022	Gene Set Enrichment Analysis revealed that gold nanorod-induced NLRP3 inflammasome activation was accompanied by downregulated sterol/cholesterol biosynthesis, oxidative phosphorylation, and purinergic receptor signalling.	Sterols	127-133	NLR family pyrin domain containing 3	Homo sapiens	64-69
35628574-11	2022	Gene Set Enrichment Analysis revealed that gold nanorod-induced NLRP3 inflammasome activation was accompanied by downregulated sterol/cholesterol biosynthesis, oxidative phosphorylation, and purinergic receptor signalling.	Cholesterol	134-145	NLR family pyrin domain containing 3	Homo sapiens	64-69
35584771-12	2022	Additionally, knockdown of GPR120 by siRNA weakened the effects of GW9508 on NLRP3 inflammasome expression.	GW9508	67-73	NLR family pyrin domain containing 3	Homo sapiens	77-82
35634294-6	2022	Consistently, SHED could inhibit the elevated expression of NLRP3, GSDMD and Caspase-1 induced by CCl4 treatment in vitro co-culture system, which was mediated by decreasing reactive oxygen species (ROS) generation.	Reactive Oxygen Species	199-202	NLR family pyrin domain containing 3	Homo sapiens	60-65
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Olanzapine	32-42	NLR family pyrin domain containing 3	Homo sapiens	148-153
35619689-8	2022	Additionally, the overexpression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) or 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase (HMGCR), the known target of statins, reversed the effects of simvastatin.	Simvastatin	234-245	NLR family pyrin domain containing 3	Homo sapiens	36-101
35619689-8	2022	Additionally, the overexpression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) or 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase (HMGCR), the known target of statins, reversed the effects of simvastatin.	Simvastatin	234-245	NLR family pyrin domain containing 3	Homo sapiens	103-108
35619689-10	2022	Furthermore, the immunoprecipitation results confirmed the interaction between NLRP3 and HMGCR, and this interaction was inhibited by simvastatin.	Simvastatin	134-145	NLR family pyrin domain containing 3	Homo sapiens	79-84
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Quetiapine Fumarate	44-54	NLR family pyrin domain containing 3	Homo sapiens	148-153
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Risperidone	56-67	NLR family pyrin domain containing 3	Homo sapiens	148-153
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Haloperidol	72-83	NLR family pyrin domain containing 3	Homo sapiens	148-153
35615587-6	2022	Co-treatment with a histamine H1 receptor agonist, 2-(3-trifluoromethylphenyl) histamine (FMPH), dose-dependently reduced the increased expression of NLRP3, caspase-1 and GSDMD induced by olanzapine, quetiapine, risperidone, or haloperidol.	2-(3-trifluoromethylphenyl)histamine	51-88	NLR family pyrin domain containing 3	Homo sapiens	150-155
35615587-6	2022	Co-treatment with a histamine H1 receptor agonist, 2-(3-trifluoromethylphenyl) histamine (FMPH), dose-dependently reduced the increased expression of NLRP3, caspase-1 and GSDMD induced by olanzapine, quetiapine, risperidone, or haloperidol.	fmph	90-94	NLR family pyrin domain containing 3	Homo sapiens	150-155
35631400-3	2022	Here, we demonstrate the role of the host nucleotide-binding domain, leucine-rich containing family, pyrin domain-containing 3 (NLRP3) inflammasome in metastatic breast cancer.	Leucine	69-76	NLR family pyrin domain containing 3	Homo sapiens	128-133
35506157-0	2022	Ganoderic Acid A alleviates the degeneration of intervertebral disc via suppressing the activation of TLR4/NLRP3 signaling pathway.	ganoderic acid A	0-16	NLR family pyrin domain containing 3	Homo sapiens	107-112
35513901-1	2022	The nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome has emerged as a key mediator of pathological inflammation in many diseases and is an exciting drug target.	Leucine	47-54	NLR family pyrin domain containing 3	Homo sapiens	106-111
35092164-6	2022	Mechanistically, we revealed that the enhanced autophagic turnover by RAPA inhibited NLRP3 inflammasome activity through NLRP3 degradation.	Sirolimus	70-74	NLR family pyrin domain containing 3	Homo sapiens	85-90
35092164-6	2022	Mechanistically, we revealed that the enhanced autophagic turnover by RAPA inhibited NLRP3 inflammasome activity through NLRP3 degradation.	Sirolimus	70-74	NLR family pyrin domain containing 3	Homo sapiens	121-126
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	NLR family pyrin domain containing 3	Homo sapiens	97-102
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	NLR family pyrin domain containing 3	Homo sapiens	202-207
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	Sirolimus	136-140	NLR family pyrin domain containing 3	Homo sapiens	97-102
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	Sirolimus	136-140	NLR family pyrin domain containing 3	Homo sapiens	202-207
35563447-0	2022	A2A Adenosine Receptor: A Possible Therapeutic Target for Alzheimer"s Disease by Regulating NLRP3 Inflammasome Activity?	Adenosine	4-13	NLR family pyrin domain containing 3	Homo sapiens	92-97
35563447-8	2022	NLRP3 inhibition provides neuroprotection, and in recent years adenosine, through the A2A receptor, has been reported to modulate NLRP3 functions to reduce organ damage.	Adenosine	63-72	NLR family pyrin domain containing 3	Homo sapiens	0-5
35563447-8	2022	NLRP3 inhibition provides neuroprotection, and in recent years adenosine, through the A2A receptor, has been reported to modulate NLRP3 functions to reduce organ damage.	Adenosine	63-72	NLR family pyrin domain containing 3	Homo sapiens	130-135
35474599-5	2022	Deactivated AMPK induces metabolic dysregulation, mitochondrial fragmentation, and reactive oxygen species formation, leading to the activation of the NLRP3 inflammasome.	Oxygen	92-98	NLR family pyrin domain containing 3	Homo sapiens	151-156
35474599-6	2022	In addition, flufenamic acid (FA), a member of non-steroidal anti-inflammatory drugs, was found to effectively inhibit activation of the microglial NLRP3 inflammasome by regulating Syk and AMPK.	Flufenamic Acid	13-28	NLR family pyrin domain containing 3	Homo sapiens	148-153
35506157-7	2022	Furthermore, we also demonstrated that GAA suppressed the activation of TLR4/NLRP3 in H2O2-stimulated NP cells.	Hydrogen Peroxide	86-90	NLR family pyrin domain containing 3	Homo sapiens	77-82
35506157-8	2022	Thus, our results demonstrate that GAA inhibited the H2O2 induced apoptosis, oxidative stress, and inflammatory responses through the depression of TLR4/NLRP3 signaling axis.	Hydrogen Peroxide	53-57	NLR family pyrin domain containing 3	Homo sapiens	153-158
35060675-0	2022	The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS-mediated MAPK, NF-kappaB signaling pathways and NLRP3 inflammasome.	cooking oil	16-27	NLR family pyrin domain containing 3	Homo sapiens	130-135
35278669-0	2022	ATRA-mediated-crosstalk between stellate cells and Kupffer cells inhibits autophagy and promotes NLRP3 activation in acute liver injury.	Tretinoin	0-4	NLR family pyrin domain containing 3	Homo sapiens	97-102
35278669-7	2022	ATRA also blocked autophagic flow by activating the AKT/mTOR pathway, leading to an excessive accumulation of ROS, which further activated the NLRP3 inflammasome.	Tretinoin	0-4	NLR family pyrin domain containing 3	Homo sapiens	143-148
35278669-7	2022	ATRA also blocked autophagic flow by activating the AKT/mTOR pathway, leading to an excessive accumulation of ROS, which further activated the NLRP3 inflammasome.	ros	110-113	NLR family pyrin domain containing 3	Homo sapiens	143-148
35278669-9	2022	In conclusion, we have uncovered a novel crosstalk pattern between HSCs and KCs, and ATRA-mediated-crosstalk between HSCs and KCs inhibits autophagy and promotes NLRP3 activation to aggravate acute liver injury.	Tretinoin	85-89	NLR family pyrin domain containing 3	Homo sapiens	162-167
35182568-7	2022	When REC were treated with ATP to stimulate P2X7R, NLRP3 inflammasome proteins were all increased compared to high glucose only.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	51-56
35182568-10	2022	Epac1 and PKA can inhibit of P2X7, which will reduce NLRP3 inflammasome proteins in REC grown in high glucose.	Glucose	102-109	NLR family pyrin domain containing 3	Homo sapiens	53-58
35400286-3	2022	This study aimed to evaluate the vitamin D (VD) immunomodulatory effect on the NLRP1/NLRP3 inflammasomes in placental explants from preeclamptic (PE) and normotensive (NT) pregnant women.	Vitamin D	33-42	NLR family pyrin domain containing 3	Homo sapiens	85-90
35234268-2	2022	Studies have suggested that hydrogen sulfide (H2S) plays a protective role against COPD by inhibiting the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Hydrogen Sulfide	28-44	NLR family pyrin domain containing 3	Homo sapiens	124-160
35234268-2	2022	Studies have suggested that hydrogen sulfide (H2S) plays a protective role against COPD by inhibiting the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Hydrogen Sulfide	28-44	NLR family pyrin domain containing 3	Homo sapiens	162-167
35234268-7	2022	In addition, H2S significantly attenuated the effects of CS extract (CSE) on pyroptosis, cell viability and the expression levels of pyroptosis-related proteins, indicating that H2S inhibited pyroptosis by decreasing NLRP3 expression and promoting GSDMD activation.	Deuterium	178-181	NLR family pyrin domain containing 3	Homo sapiens	217-222
35234268-2	2022	Studies have suggested that hydrogen sulfide (H2S) plays a protective role against COPD by inhibiting the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Deuterium	46-49	NLR family pyrin domain containing 3	Homo sapiens	124-160
35234268-2	2022	Studies have suggested that hydrogen sulfide (H2S) plays a protective role against COPD by inhibiting the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Deuterium	46-49	NLR family pyrin domain containing 3	Homo sapiens	162-167
35234268-6	2022	The cellular experiments also revealed that CS induced the pyroptosis of the cells in a NLRP3/gasdermin D (GSDMD)-dependent manner.	Cesium	44-46	NLR family pyrin domain containing 3	Homo sapiens	88-93
35234268-7	2022	In addition, H2S significantly attenuated the effects of CS extract (CSE) on pyroptosis, cell viability and the expression levels of pyroptosis-related proteins, indicating that H2S inhibited pyroptosis by decreasing NLRP3 expression and promoting GSDMD activation.	Deuterium	13-16	NLR family pyrin domain containing 3	Homo sapiens	217-222
35234268-7	2022	In addition, H2S significantly attenuated the effects of CS extract (CSE) on pyroptosis, cell viability and the expression levels of pyroptosis-related proteins, indicating that H2S inhibited pyroptosis by decreasing NLRP3 expression and promoting GSDMD activation.	Cesium	57-59	NLR family pyrin domain containing 3	Homo sapiens	217-222
35147911-0	2022	All-Trans Retinoic Acid-Preconditioned Mesenchymal Stem Cells Improve Motor Function and Alleviate Tissue Damage After Spinal Cord Injury by Inhibition of HMGB1/NF-kappaB/NLRP3 Pathway Through Autophagy Activation.	Tretinoin	0-23	NLR family pyrin domain containing 3	Homo sapiens	171-176
35194373-6	2022	Korean Red Ginseng (KRG) inhibits several inflammatory responses, including the NLRP3 inflammasome signaling.	CHEMBL1828984	20-23	NLR family pyrin domain containing 3	Homo sapiens	80-85
35218026-5	2022	The inflammatory cell infiltration, expression level of keratinocyte proliferation marker Ki67, keratinocyte proliferation, inflammatory cytokines, and ROS/NLRP3 pathway-related proteins in vivo and in vitro were examined by hematoxylin and eosin, immunohistochemistry, ELISA, CCK-8, flow cytometry, and western blot.	Hematoxylin	225-236	NLR family pyrin domain containing 3	Homo sapiens	156-161
35138513-5	2022	Moreover, TGF-beta increased the expression of p-Smad2/3-NOX4 in LX-2 cells and consequently increased ROS content, which is a trigger for NLRP3 inflammasome activation.	ros	103-106	NLR family pyrin domain containing 3	Homo sapiens	139-144
35561274-2	2022	Pretreatment and delayed treatment of S. herbacea extract (SHE) in bone marrow-derived macrophages (BMDMs) reduced the activity of NLRP3 inflammasome induced by lipopolysaccharide (LPS) and adenosine triphosphate stimulation and downregulated interleukin (IL)-1beta production.	she	59-62	NLR family pyrin domain containing 3	Homo sapiens	131-136
35561274-2	2022	Pretreatment and delayed treatment of S. herbacea extract (SHE) in bone marrow-derived macrophages (BMDMs) reduced the activity of NLRP3 inflammasome induced by lipopolysaccharide (LPS) and adenosine triphosphate stimulation and downregulated interleukin (IL)-1beta production.	Adenosine	190-199	NLR family pyrin domain containing 3	Homo sapiens	131-136
35561274-6	2022	Finally, 3,5-dicaffeoylquinic acid (3,5-DCQA), one of the components of S. herbacea, inhibited IL-1beta produced by NLRP3 inflammasome activity.	3,5-dicaffeoylquinic acid	9-34	NLR family pyrin domain containing 3	Homo sapiens	116-121
35561274-6	2022	Finally, 3,5-dicaffeoylquinic acid (3,5-DCQA), one of the components of S. herbacea, inhibited IL-1beta produced by NLRP3 inflammasome activity.	3,5-dicaffeoylquinic acid	36-44	NLR family pyrin domain containing 3	Homo sapiens	116-121
35303531-4	2022	Sulforaphane mediates the inhibitory effect on NLRP3 inflammasome activation and we believe that this could be the main mechanism where sulforaphane is useful for patients with COVID-19.	sulforaphane	0-12	NLR family pyrin domain containing 3	Homo sapiens	47-52
35303531-4	2022	Sulforaphane mediates the inhibitory effect on NLRP3 inflammasome activation and we believe that this could be the main mechanism where sulforaphane is useful for patients with COVID-19.	sulforaphane	136-148	NLR family pyrin domain containing 3	Homo sapiens	47-52
35490837-1	2022	We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE).	Reactive Oxygen Species	39-62	NLR family pyrin domain containing 3	Homo sapiens	91-96
35484409-0	2022	Creating ATP via creatine kinase B for NLRP3 activation.	Adenosine Triphosphate	9-12	NLR family pyrin domain containing 3	Homo sapiens	39-44
35490837-1	2022	We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE).	Reactive Oxygen Species	64-67	NLR family pyrin domain containing 3	Homo sapiens	91-96
35571141-5	2022	Further exploration with the inflammatory model in THP-1 cells indicated that DHA reduced the protein expression of hypoxia-inducible factor (HIF)-1alpha and the phosphorylation in Janus kinase (JAK) 3 and signal transducer and activator of transcription (STAT) 3 protein, which resulted in a decrease in NOD-like receptor protein (NLRP) 3 expression and interleukin (IL)-1beta release.	dihydroarteannuin	78-81	NLR family pyrin domain containing 3	Homo sapiens	305-339
35473933-6	2022	We further identified that necrotic TECs-induced NLRP3 inflammasome activation was dependent on ATP secretion via Pannexin-1 (Panx1) channel in macrophages.	Adenosine Triphosphate	96-99	NLR family pyrin domain containing 3	Homo sapiens	49-54
35563208-0	2022	The Role of H2S Regulating NLRP3 Inflammasome in Diabetes.	Deuterium	12-15	NLR family pyrin domain containing 3	Homo sapiens	27-32
35563208-7	2022	In recent years, it has been reported that H2S regulation of the NLRP3 inflammasome contributes to a variety of diseases.	Deuterium	43-46	NLR family pyrin domain containing 3	Homo sapiens	65-70
35563208-9	2022	In this review, we summarized the recent role and mechanism of H2S in regulating the NLRP3 inflammasome in diabetes, in order to provide a theoretical basis for future research.	Deuterium	63-66	NLR family pyrin domain containing 3	Homo sapiens	85-90
35468877-6	2022	Ageing-associated hypothyroidism as well as acute thyroidectomy augmented transport of liver-derived ApoE4 reach exosomes into the brain, where ApoE4 activated nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome by increasing cholesterol level in neural cells.	Cholesterol	284-295	NLR family pyrin domain containing 3	Homo sapiens	160-248
35625713-10	2022	TNF-alpha and NLRP3 were upregulated in ziprasidone-treated myocytes, and the level of phosphorylated calcium/calmodulin-dependent protein kinase II protein was increased.	Calcium	102-109	NLR family pyrin domain containing 3	Homo sapiens	14-19
35509841-0	2022	Simvastatin Inhibits NLRP3 Inflammasome Activation and Ameliorates Lung Injury in Hyperoxia-Induced Bronchopulmonary Dysplasia via the KLF2-Mediated Mechanism.	Simvastatin	0-11	NLR family pyrin domain containing 3	Homo sapiens	21-26
35509841-8	2022	Simvastatin suppressed NLRP3 inflammasome activation and played anti-inflammatory and antioxidant roles by increasing KLF2 (Kruppel-like factor 2) expression.	Simvastatin	0-11	NLR family pyrin domain containing 3	Homo sapiens	23-28
35509841-10	2022	In summary, our findings indicate that simvastatin could downregulate NLRP3 inflammasome activation and attenuate lung injury in hyperoxia-induced bronchopulmonary dysplasia via KLF2-mediated mechanism.	Simvastatin	39-50	NLR family pyrin domain containing 3	Homo sapiens	70-75
35625713-10	2022	TNF-alpha and NLRP3 were upregulated in ziprasidone-treated myocytes, and the level of phosphorylated calcium/calmodulin-dependent protein kinase II protein was increased.	ziprasidone	40-51	NLR family pyrin domain containing 3	Homo sapiens	14-19
35625713-11	2022	CONCLUSIONS: Our results suggest that ziprasidone increases the occurrence of atrial triggered activity and causes intracellular Ca2+ and Na+ dysregulation, which may result from enhanced oxidative stress and activation of the TNF-alpha/NLRP3 inflammasome pathway in ziprasidone-treated myocytes.	ziprasidone	38-49	NLR family pyrin domain containing 3	Homo sapiens	237-242
35528000-0	2022	rs3806265 and rs4612666 of the NLRP3 Gene Are Associated With the Titer of Glutamic Acid Decarboxylase Antibody in Type 1 Diabetes.	Glutamic Acid	75-88	NLR family pyrin domain containing 3	Homo sapiens	31-36
35448938-6	2022	In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU.	Fluorouracil	141-145	NLR family pyrin domain containing 3	Homo sapiens	63-68
35528000-14	2022	Conclusion: rs3806265 and rs4612666 of the NLRP3 gene were significantly associated with GADA titers in Chinese Han T1D patients.	gada	89-93	NLR family pyrin domain containing 3	Homo sapiens	43-48
35394753-10	2022	The presence of mitochondrial reactive oxygen species (mitoROS) led to oxidative damage of mitochondrial DNA (mitoDNA), which further activates NLRP3/Caspase-1/gasdermin D (GSDMD)-dependent pyroptosis and could promote dendritic cell (DC) maturation by pyroptosis.	Reactive Oxygen Species	30-53	NLR family pyrin domain containing 3	Homo sapiens	144-149
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Cannabidiol	26-29	NLR family pyrin domain containing 3	Homo sapiens	83-88
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Dronabinol	55-58	NLR family pyrin domain containing 3	Homo sapiens	83-88
35529876-0	2022	Cochlear Marginal Cell Pyroptosis Is Induced by Cisplatin via NLRP3 Inflammasome Activation.	Cisplatin	48-57	NLR family pyrin domain containing 3	Homo sapiens	62-67
35563697-8	2022	Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs.	Adenosine Triphosphate	129-132	NLR family pyrin domain containing 3	Homo sapiens	83-88
35529876-3	2022	In this study, a stable model of cisplatin-induced MC damage was established in vitro, and the results of PCR and Western blotting showed increased expressions of NLRP3, Caspase-1, IL-1beta, and GSDMD in MCs.	Cisplatin	33-42	NLR family pyrin domain containing 3	Homo sapiens	163-168
35563697-12	2022	Overall, CBD and THC were found to be effective in alleviating the LPS-induced cytokine storm in human macrophages and primary HBECs, at least via modulation of NLRP3 inflammasome and STAT3 signaling pathways.	Cannabidiol	9-12	NLR family pyrin domain containing 3	Homo sapiens	161-166
35529876-5	2022	In addition, downregulation of NLRP3 by small interfering RNA can alleviate cisplatin-induced MC pyroptosis, and reducing the expression level of TXNIP possesses the inhibition effect on NLRP3 inflammasome activation and its mediated pyroptosis.	Cisplatin	76-85	NLR family pyrin domain containing 3	Homo sapiens	31-36
35529876-5	2022	In addition, downregulation of NLRP3 by small interfering RNA can alleviate cisplatin-induced MC pyroptosis, and reducing the expression level of TXNIP possesses the inhibition effect on NLRP3 inflammasome activation and its mediated pyroptosis.	Cisplatin	76-85	NLR family pyrin domain containing 3	Homo sapiens	187-192
35529876-6	2022	Taken together, our results suggest that NLRP3 inflammasome activation may mediate cisplatin-induced MC pyroptosis in cochlear stria vascularis, and TXNIP is a possible upstream regulator, which may be a promising therapeutic target for alleviating cisplatin-induced hearing loss.	Cisplatin	83-92	NLR family pyrin domain containing 3	Homo sapiens	41-46
35563697-0	2022	Cannabinoids Alleviate the LPS-Induced Cytokine Storm via Attenuating NLRP3 Inflammasome Signaling and TYK2-Mediated STAT3 Signaling Pathways In Vitro.	Cannabinoids	0-12	NLR family pyrin domain containing 3	Homo sapiens	70-75
35563697-12	2022	Overall, CBD and THC were found to be effective in alleviating the LPS-induced cytokine storm in human macrophages and primary HBECs, at least via modulation of NLRP3 inflammasome and STAT3 signaling pathways.	Dronabinol	17-20	NLR family pyrin domain containing 3	Homo sapiens	161-166
35429346-6	2022	Whilst the cleavage of IL-37 was found to be constitutive, the release of mature IL-37 (mIL-37) was blocked in NLRP3 deficient THP-1 cells and by NLRP3 inhibitor MCC950 in THP-1s and primary human monocytes.	mil-37	88-94	NLR family pyrin domain containing 3	Homo sapiens	111-116
35514993-0	2022	Oleamide-Mediated Polarization of M1 Macrophages and IL-1beta Production by Regulating NLRP3-Inflammasome Activation in Primary Human Monocyte-Derived Macrophages.	oleylamide	0-8	NLR family pyrin domain containing 3	Homo sapiens	87-92
35514993-10	2022	Whether oleamide functioned as a second signal that activated the NLRP3 inflammasome and mediated IL-1beta production was further investigated using LPS-primed MDMs followed by oleamide treatment that induced activation of inflammasome-related proteins including NLRP3, ASC, cleaved casp-1, and cleaved IL-1beta.	oleylamide	8-16	NLR family pyrin domain containing 3	Homo sapiens	66-71
35514993-10	2022	Whether oleamide functioned as a second signal that activated the NLRP3 inflammasome and mediated IL-1beta production was further investigated using LPS-primed MDMs followed by oleamide treatment that induced activation of inflammasome-related proteins including NLRP3, ASC, cleaved casp-1, and cleaved IL-1beta.	oleylamide	8-16	NLR family pyrin domain containing 3	Homo sapiens	263-268
35514993-11	2022	These findings suggested that oleamide promoted M1 macrophage polarization and increased IL-1beta production by activating the NLRP3 inflammasome in primary MDMs.	oleylamide	30-38	NLR family pyrin domain containing 3	Homo sapiens	127-132
35440074-4	2022	Here, we found that DHEA inhibited the NLRP3 inflammasome components expression by blocking inflammatory signals in lipopolysaccharide (LPS)-primed macrophages, and prevented the bacterial toxin nigericin (Nig)-induced NLRP3 inflammasome assembly.	Dehydroepiandrosterone	20-24	NLR family pyrin domain containing 3	Homo sapiens	39-44
35440074-4	2022	Here, we found that DHEA inhibited the NLRP3 inflammasome components expression by blocking inflammatory signals in lipopolysaccharide (LPS)-primed macrophages, and prevented the bacterial toxin nigericin (Nig)-induced NLRP3 inflammasome assembly.	Dehydroepiandrosterone	20-24	NLR family pyrin domain containing 3	Homo sapiens	219-224
35440074-4	2022	Here, we found that DHEA inhibited the NLRP3 inflammasome components expression by blocking inflammatory signals in lipopolysaccharide (LPS)-primed macrophages, and prevented the bacterial toxin nigericin (Nig)-induced NLRP3 inflammasome assembly.	Nigericin	195-204	NLR family pyrin domain containing 3	Homo sapiens	219-224
35440074-5	2022	However, DHEA exacerbated NLRP3-independent cell death in Nig-treated inflammatory macrophages.	Dehydroepiandrosterone	9-13	NLR family pyrin domain containing 3	Homo sapiens	26-31
35437791-0	2022	ROS-mediated activation of NLRP3 inflammasome associated with pyroptosis in Het-1A cells induced by the co-exposure of nitrosamines.	Reactive Oxygen Species	0-3	NLR family pyrin domain containing 3	Homo sapiens	27-32
35437791-0	2022	ROS-mediated activation of NLRP3 inflammasome associated with pyroptosis in Het-1A cells induced by the co-exposure of nitrosamines.	Nitrosamines	119-131	NLR family pyrin domain containing 3	Homo sapiens	27-32
35437791-4	2022	In this study, the human esophageal epithelial cells (Het-1A) were used to explore potential mechanisms of the activation of NLRP3 inflammasome under co-exposure to nine nitrosamines commonly found in drinking water at the doses of 0, 4, 20, 100, 500 and 2500 ng/mL.	Nitrosamines	170-182	NLR family pyrin domain containing 3	Homo sapiens	125-130
35437791-4	2022	In this study, the human esophageal epithelial cells (Het-1A) were used to explore potential mechanisms of the activation of NLRP3 inflammasome under co-exposure to nine nitrosamines commonly found in drinking water at the doses of 0, 4, 20, 100, 500 and 2500 ng/mL.	Water	210-215	NLR family pyrin domain containing 3	Homo sapiens	125-130
35437791-5	2022	The results showed that nitrosamines stimulated activation of the NLRP3 inflammasome and induced cellular oxidative damage in a dose-dependent manner.	Nitrosamines	24-36	NLR family pyrin domain containing 3	Homo sapiens	66-71
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	oxygen species	25-39	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	50-69	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	50-69	NLR family pyrin domain containing 3	Homo sapiens	272-277
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	71-74	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	71-74	NLR family pyrin domain containing 3	Homo sapiens	272-277
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	reactive oxygen	104-119	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	reactive oxygen	104-119	NLR family pyrin domain containing 3	Homo sapiens	272-277
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Nitrosamines	227-239	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Reactive Oxygen Species	309-332	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	Nitrosamines	27-39	NLR family pyrin domain containing 3	Homo sapiens	94-99
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	Nitrosamines	27-39	NLR family pyrin domain containing 3	Homo sapiens	210-215
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	182-192	NLR family pyrin domain containing 3	Homo sapiens	94-99
35437791-8	2022	This study revealed the underlying mechanism of the activation of NLRP3 inflammasome initiated by nitrosamines co-exposure and provided new perspectives on the toxic effects of nitrosamines.	Nitrosamines	98-110	NLR family pyrin domain containing 3	Homo sapiens	66-71
35437791-8	2022	This study revealed the underlying mechanism of the activation of NLRP3 inflammasome initiated by nitrosamines co-exposure and provided new perspectives on the toxic effects of nitrosamines.	Nitrosamines	177-189	NLR family pyrin domain containing 3	Homo sapiens	66-71
35429346-6	2022	Whilst the cleavage of IL-37 was found to be constitutive, the release of mature IL-37 (mIL-37) was blocked in NLRP3 deficient THP-1 cells and by NLRP3 inhibitor MCC950 in THP-1s and primary human monocytes.	mil-37	88-94	NLR family pyrin domain containing 3	Homo sapiens	146-151
35496300-20	2022	Conclusion: The results show that PTS exhibits protective effects against DOX-induced liver injuries via suppression of oxidative stress, fibrosis, NLRP3 inflammasome stimulation, and cell apoptosis which might lead to a new approach of preventing DOX-induced hepatotoxicity.	pterostilbene	34-37	NLR family pyrin domain containing 3	Homo sapiens	148-153
35436742-15	2022	Taken together, our results demonstrate that ATRA disrupts the osteogenesis and mineralizationof PDLSCs by promoting IL-1beta expression via activating NF-kappaB signaling and NLRP3 inflammasome, which may offer a new method for improving the ATRA-induced disruption of osteoblast differentiation.	Tretinoin	45-49	NLR family pyrin domain containing 3	Homo sapiens	176-181
35422229-7	2022	DA mediates neuroprotection via inhibition of the A1 astrocytic pathway through blockage of NF-kB and nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3); and promotion of A2 astrocytic pathways leading to the formation of neurotrophic factors like BDNF and GDNF.	Dopamine	0-2	NLR family pyrin domain containing 3	Homo sapiens	102-183
35422229-7	2022	DA mediates neuroprotection via inhibition of the A1 astrocytic pathway through blockage of NF-kB and nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3); and promotion of A2 astrocytic pathways leading to the formation of neurotrophic factors like BDNF and GDNF.	Dopamine	0-2	NLR family pyrin domain containing 3	Homo sapiens	185-190
35495623-0	2022	Corrigendum: Sevoflurane Alleviates Myocardial Ischemia Reperfusion Injury by Inhibiting P2X7-NLRP3 Mediated Pyroptosis.	Sevoflurane	13-24	NLR family pyrin domain containing 3	Homo sapiens	94-99
35462936-0	2022	(-)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-kappaB Signaling Pathway.	Catechin	0-15	NLR family pyrin domain containing 3	Homo sapiens	94-99
35496295-0	2022	Farrerol Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting Macrophages and NLRP3.	farrerol	0-8	NLR family pyrin domain containing 3	Homo sapiens	88-93
35410608-0	2022	The NLRP3 inflammasome in stress response: another target for the promiscuous cannabidiol?	Cannabidiol	78-89	NLR family pyrin domain containing 3	Homo sapiens	4-9
35464445-2	2022	Acute gout symptoms are triggered by the inflammatory response to monosodium urate crystals, which is mediated by the innate immune system and immune cells (e.g., macrophages and neutrophils), the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation, and pro-inflammatory cytokine (e.g., IL-1beta) release.	Uric Acid	66-82	NLR family pyrin domain containing 3	Homo sapiens	197-245
35421403-3	2022	In this study, we observed that AGEs, NLRP3 and IL-18 were increased in the dermis of sun-exposed skin and lesions of melasma and solar lentigo and that dermal deposition of AGEs was positively correlated with epidermal melanin levels.	Melanins	220-227	NLR family pyrin domain containing 3	Homo sapiens	38-43
35464445-2	2022	Acute gout symptoms are triggered by the inflammatory response to monosodium urate crystals, which is mediated by the innate immune system and immune cells (e.g., macrophages and neutrophils), the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation, and pro-inflammatory cytokine (e.g., IL-1beta) release.	Uric Acid	66-82	NLR family pyrin domain containing 3	Homo sapiens	247-252
35462936-0	2022	(-)-Epicatechin Ameliorates Monosodium Urate-Induced Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and the NF-kappaB Signaling Pathway.	Uric Acid	28-44	NLR family pyrin domain containing 3	Homo sapiens	94-99
35462936-7	2022	Furthermore, the secretion of inflammatory cytokines (IL-1beta, IL-18, IL-6, and TNF-alpha) activation of NLRP3 inflammasome and NF-kappaB signaling pathway were markedly suppressed by EC in vitro and in vivo.	Catechin	185-187	NLR family pyrin domain containing 3	Homo sapiens	106-111
35462936-8	2022	Conclusion: These results indicated that EC could effectively improve MSU-induced acute gouty arthritis via inhibiting NLRP3 inflammasome and the NF-kappaB signaling pathway in vitro and in vivo, which suggested that EC might be a promising active ingredient for the prevention and treatment of gouty arthritis.	Catechin	41-43	NLR family pyrin domain containing 3	Homo sapiens	119-124
35462936-8	2022	Conclusion: These results indicated that EC could effectively improve MSU-induced acute gouty arthritis via inhibiting NLRP3 inflammasome and the NF-kappaB signaling pathway in vitro and in vivo, which suggested that EC might be a promising active ingredient for the prevention and treatment of gouty arthritis.	Uric Acid	70-73	NLR family pyrin domain containing 3	Homo sapiens	119-124
35462936-8	2022	Conclusion: These results indicated that EC could effectively improve MSU-induced acute gouty arthritis via inhibiting NLRP3 inflammasome and the NF-kappaB signaling pathway in vitro and in vivo, which suggested that EC might be a promising active ingredient for the prevention and treatment of gouty arthritis.	Catechin	217-219	NLR family pyrin domain containing 3	Homo sapiens	119-124
34990072-6	2022	The mechanistic investigation revealed that CTRP9 overexpression restrained the activation of the nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome in IL-1beta-stimulated chondrocytes via the adiponectin receptor 1 (AdipoR1)/adenosine monophosphate-activated protein kinase (AMPK) axis.	Adenosine	254-263	NLR family pyrin domain containing 3	Homo sapiens	98-155
35433045-0	2022	Examining the Effect of Consuming C8 Medium-Chain Triglyceride Oil for 14 Days on Markers of NLRP3 Activation in Healthy Humans.	Triglycerides	50-62	NLR family pyrin domain containing 3	Homo sapiens	93-98
35433045-2	2022	The ketone body beta-hydroxybutyrate (betaHB) suppresses the NLRP3 inflammasome and alters intracellular signalling pathways in vitro and in animal models; however, this effect has not yet been shown in vivo in humans.	3-Hydroxybutyric Acid	16-36	NLR family pyrin domain containing 3	Homo sapiens	61-66
35433045-2	2022	The ketone body beta-hydroxybutyrate (betaHB) suppresses the NLRP3 inflammasome and alters intracellular signalling pathways in vitro and in animal models; however, this effect has not yet been shown in vivo in humans.	3-Hydroxybutyric Acid	38-44	NLR family pyrin domain containing 3	Homo sapiens	61-66
35433045-3	2022	The purpose of this single-arm pilot trial was to determine if consuming 15 mL of C8 medium-chain triglyceride (trioctanoin; MCT) oil, which induces mild elevation of betaHB, twice daily (30 mL total) for 14 days would suppress markers of NLRP3 inflammasome activation in young, healthy humans while following their habitual diet.	c8 medium-chain triglyceride	82-110	NLR family pyrin domain containing 3	Homo sapiens	239-244
35021019-2	2022	Adenosine-5"-Triphosphate (ATP) triggers interleukin (IL)-1beta secretion via the P2X7 receptor (P2X7R) and activation of the NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome.	Adenosine Triphosphate	27-30	NLR family pyrin domain containing 3	Homo sapiens	126-131
34538111-4	2022	Recent Advances: Reactive oxygen species (ROS), especially derived from the mitochondria, are one of the critical mediators of NLRP3 inflammasome activation.	Reactive Oxygen Species	17-40	NLR family pyrin domain containing 3	Homo sapiens	127-132
34538111-4	2022	Recent Advances: Reactive oxygen species (ROS), especially derived from the mitochondria, are one of the critical mediators of NLRP3 inflammasome activation.	Reactive Oxygen Species	42-45	NLR family pyrin domain containing 3	Homo sapiens	127-132
34538111-5	2022	Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome.	Reactive Oxygen Species	140-143	NLR family pyrin domain containing 3	Homo sapiens	13-18
34538111-5	2022	Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome.	Reactive Oxygen Species	140-143	NLR family pyrin domain containing 3	Homo sapiens	199-204
34538111-5	2022	Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome.	Reactive Oxygen Species	191-194	NLR family pyrin domain containing 3	Homo sapiens	13-18
34538111-5	2022	Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome.	Reactive Oxygen Species	191-194	NLR family pyrin domain containing 3	Homo sapiens	199-204
34538111-6	2022	CRITICAL ISSUES: The precise mechanism of how ROS affects NLRP3 inflammasome activation still need to be addressed.	Reactive Oxygen Species	46-49	NLR family pyrin domain containing 3	Homo sapiens	58-63
34538111-7	2022	This review will summarize the current knowledge on the molecular mechanisms underlying the activation of NLRP3 inflammasome with particular emphasis on the intricate balance of feedback loop between ROS and inflammasome activation.	Reactive Oxygen Species	200-203	NLR family pyrin domain containing 3	Homo sapiens	106-111
35286854-0	2022	An AIEgen-based oral-administration nanosystem for detection and therapy of ulcerative colitis via 3D-MSOT/NIR-II fluorescent imaging and inhibiting NLRP3 inflammasome.	aiegen	3-9	NLR family pyrin domain containing 3	Homo sapiens	149-154
35133600-0	2022	Correction to: PM2.5 exposure inducing ATP alteration links with NLRP3 inflammasome activation.	Adenosine Triphosphate	39-42	NLR family pyrin domain containing 3	Homo sapiens	65-70
35178861-0	2022	Colchicine prevents disease progression in viral myocarditis via modulating the NLRP3 inflammasome in the cardiosplenic axis.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	80-85
35178861-3	2022	The anti-inflammatory drug colchicine exerts its effects, in part, via reducing NLRP3 activity, and has been shown to improve several cardiac diseases, including acute coronary syndrome and pericarditis.	Colchicine	27-37	NLR family pyrin domain containing 3	Homo sapiens	80-85
35178861-11	2022	Evaluation of components of the NLRP3 inflammasome revealed an increased percentage of apoptosis-associated speck-like protein containing a CARD domain (ASC)-expressing, caspase-1-expressing, and interleukin-1beta-expressing cells in the myocardium and in the spleen of CVB3 + PBS vs. control mice, which was reduced in CVB3 + colchicine compared with CVB3 + PBS mice.	pbs	277-280	NLR family pyrin domain containing 3	Homo sapiens	32-37
35178861-11	2022	Evaluation of components of the NLRP3 inflammasome revealed an increased percentage of apoptosis-associated speck-like protein containing a CARD domain (ASC)-expressing, caspase-1-expressing, and interleukin-1beta-expressing cells in the myocardium and in the spleen of CVB3 + PBS vs. control mice, which was reduced in CVB3 + colchicine compared with CVB3 + PBS mice.	Colchicine	327-337	NLR family pyrin domain containing 3	Homo sapiens	32-37
35178861-11	2022	Evaluation of components of the NLRP3 inflammasome revealed an increased percentage of apoptosis-associated speck-like protein containing a CARD domain (ASC)-expressing, caspase-1-expressing, and interleukin-1beta-expressing cells in the myocardium and in the spleen of CVB3 + PBS vs. control mice, which was reduced in CVB3 + colchicine compared with CVB3 + PBS mice.	pbs	359-362	NLR family pyrin domain containing 3	Homo sapiens	32-37
35178861-15	2022	In both CVB3 FB and HL-1 cells, colchicine down-regulated the NLRP3 inflammasome-related components ASC, caspase-1, and IL-1beta.	Colchicine	32-42	NLR family pyrin domain containing 3	Homo sapiens	62-67
35178861-16	2022	CONCLUSIONS: Colchicine improves LV function in CVB3-induced myocarditis, involving a decrease in cardiac and splenic NLRP3 inflammasome activity, without exacerbation of CVB3 load.	Colchicine	13-23	NLR family pyrin domain containing 3	Homo sapiens	118-123
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	Dimethyl Fumarate	109-126	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	Dimethyl Fumarate	128-131	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	dimethyl itaconate	0-3	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	(1~{R},2~{R})-~{N}-(1~{H}-pyrazol-4-yl)-2-pyridin-3-yl-cyclopropane-1-carboxamide	5-8	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	Dimethyl Fumarate	10-13	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	citraconic acid	18-37	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	citraconic acid	39-42	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	Fumarates	53-61	NLR family pyrin domain containing 3	Homo sapiens	121-126
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	Dimethyl Fumarate	0-3	NLR family pyrin domain containing 3	Homo sapiens	90-95
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	Dimethyl Fumarate	0-3	NLR family pyrin domain containing 3	Homo sapiens	271-276
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	dimethyl itaconate	62-65	NLR family pyrin domain containing 3	Homo sapiens	90-95
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	Lysophosphatidylcholines	137-160	NLR family pyrin domain containing 3	Homo sapiens	90-95
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	Lysophosphatidylcholines	137-160	NLR family pyrin domain containing 3	Homo sapiens	271-276
35137954-6	2022	DMF, an approved treatment for multiple sclerosis, as well as DMI, 4OI and MMF, inhibited NLRP3 activation in macrophages in response to lysophosphatidylcholine, which is used to induce demyelination, suggesting a possible mechanism for DMF in multiple sclerosis through NLRP3 inhibition.	Dimethyl Fumarate	237-240	NLR family pyrin domain containing 3	Homo sapiens	90-95
35137954-9	2022	Furthermore, we highlight itaconate and fumarate derivatives as potential therapeutic options in NLRP3- and IL-1alpha-driven diseases, including in the brain.	Fumarates	40-48	NLR family pyrin domain containing 3	Homo sapiens	97-102
35384439-0	2022	Quercetin ameliorates renal tubulointerstitial transformation and renal fibrosis by regulating NLRP3 in obstructive nephropathy.	Quercetin	0-9	NLR family pyrin domain containing 3	Homo sapiens	95-100
35171697-5	2022	The NLRP3 inflammasome can be activated by multiple stimuli such as extracellular ATP, microbial toxins, ROS, mitochondria DNA or particulate matter.	Adenosine Triphosphate	82-85	NLR family pyrin domain containing 3	Homo sapiens	4-9
35171697-5	2022	The NLRP3 inflammasome can be activated by multiple stimuli such as extracellular ATP, microbial toxins, ROS, mitochondria DNA or particulate matter.	ros	105-108	NLR family pyrin domain containing 3	Homo sapiens	4-9
35171697-6	2022	Although the precise mechanisms of NLRP3 activation and regulation by these diverse agonists remain unclear, multiple reports indicate that all NLRP3 agonists ultimately lead to a drop in intracellular concentration of potassium (K+ efflux) and chloride (Cl- efflux).	Potassium	219-228	NLR family pyrin domain containing 3	Homo sapiens	35-40
35171697-6	2022	Although the precise mechanisms of NLRP3 activation and regulation by these diverse agonists remain unclear, multiple reports indicate that all NLRP3 agonists ultimately lead to a drop in intracellular concentration of potassium (K+ efflux) and chloride (Cl- efflux).	Potassium	219-228	NLR family pyrin domain containing 3	Homo sapiens	144-149
35171697-6	2022	Although the precise mechanisms of NLRP3 activation and regulation by these diverse agonists remain unclear, multiple reports indicate that all NLRP3 agonists ultimately lead to a drop in intracellular concentration of potassium (K+ efflux) and chloride (Cl- efflux).	Chlorides	245-253	NLR family pyrin domain containing 3	Homo sapiens	35-40
35171697-6	2022	Although the precise mechanisms of NLRP3 activation and regulation by these diverse agonists remain unclear, multiple reports indicate that all NLRP3 agonists ultimately lead to a drop in intracellular concentration of potassium (K+ efflux) and chloride (Cl- efflux).	Chlorides	245-253	NLR family pyrin domain containing 3	Homo sapiens	144-149
35571391-9	2022	The protein expression levels of Caspase-1, NLRP3, TLR4, MyD88, and NF-kappaB in the LPS + EB1089 group were evidently lower than those in the LPS group; however, the VDR protein expression evidently increased in the LPS + EB1089 group.	seocalcitol	91-97	NLR family pyrin domain containing 3	Homo sapiens	44-49
35441575-8	2022	Nucleotide-binding domain leucine-rich repeat family protein 3 (NLRP3) inflammasome activation is vital for cell pyroptosis, and FTO functions as a pivotal modulator in the N6-methyladenosine modifications of various genes.	Leucine	26-33	NLR family pyrin domain containing 3	Homo sapiens	64-69
35441575-8	2022	Nucleotide-binding domain leucine-rich repeat family protein 3 (NLRP3) inflammasome activation is vital for cell pyroptosis, and FTO functions as a pivotal modulator in the N6-methyladenosine modifications of various genes.	N-methyladenosine	173-191	NLR family pyrin domain containing 3	Homo sapiens	64-69
35350102-8	2022	In addition, spermine significantly reduced NLR family pyrin domain containing 3, cleaved caspase-1, N-gasdermin D and IL-1beta expression, as well as IL-1beta levels in the supernatant.	Spermine	13-21	NLR family pyrin domain containing 3	Homo sapiens	44-80
35137954-0	2022	Itaconate and fumarate derivatives inhibit priming and activation of the canonical NLRP3 inflammasome in macrophages.	itaconic acid	0-9	NLR family pyrin domain containing 3	Homo sapiens	83-88
35137954-0	2022	Itaconate and fumarate derivatives inhibit priming and activation of the canonical NLRP3 inflammasome in macrophages.	Fumarates	14-22	NLR family pyrin domain containing 3	Homo sapiens	83-88
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	itaconic acid	31-40	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	Fumarates	45-53	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	dimethyl itaconate	55-73	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	dimethyl itaconate	75-78	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	4-Octyl Itaconate	81-98	NLR family pyrin domain containing 3	Homo sapiens	190-195
35137954-2	2022	Derivatives of the metabolites itaconate and fumarate, dimethyl itaconate (DMI), 4-octyl itaconate (4OI) and dimethyl fumarate (DMF), limit both expression and release of IL-1beta following NLRP3 inflammasome activation.	(1~{R},2~{R})-~{N}-(1~{H}-pyrazol-4-yl)-2-pyridin-3-yl-cyclopropane-1-carboxamide	100-103	NLR family pyrin domain containing 3	Homo sapiens	190-195
34990072-6	2022	The mechanistic investigation revealed that CTRP9 overexpression restrained the activation of the nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome in IL-1beta-stimulated chondrocytes via the adiponectin receptor 1 (AdipoR1)/adenosine monophosphate-activated protein kinase (AMPK) axis.	Adenosine	254-263	NLR family pyrin domain containing 3	Homo sapiens	157-162
35114687-0	2022	Structure of the NLRP3 decamer bound to the cytokine release inhibitor CRID3.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	71-76	NLR family pyrin domain containing 3	Homo sapiens	17-22
35412034-3	2022	The NLRP3 (NACHT, leucine-rich repeat, and pyrin domain-containing protein 3) inflammasome is a protein complex that functions as a platform for rapid induction of the inflammatory response to infection or sterile injury through pro-inflammatory cytokines, now recognized as a new important therapeutic target for myopericardial diseases.	Leucine	18-25	NLR family pyrin domain containing 3	Homo sapiens	4-9
35022530-1	2022	In coronavirus disease (COVID-19), the nucleotide-binding domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome is activated in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.	Leucine	66-73	NLR family pyrin domain containing 3	Homo sapiens	125-130
35114687-4	2022	Inactive, ADP-bound NLRP3 is a decamer composed of homodimers of intertwined LRR domains that assemble back-to-back as pentamers.	Adenosine Diphosphate	10-13	NLR family pyrin domain containing 3	Homo sapiens	20-25
35114687-9	2022	Its central sulfonylurea group interacts with the Walker A motif of the NLRP3 nucleotide-binding domain and is sandwiched between two arginines, explaining the specificity of NLRP3 for this chemical entity.	Sulfonylurea Compounds	12-24	NLR family pyrin domain containing 3	Homo sapiens	72-77
35114687-9	2022	Its central sulfonylurea group interacts with the Walker A motif of the NLRP3 nucleotide-binding domain and is sandwiched between two arginines, explaining the specificity of NLRP3 for this chemical entity.	Sulfonylurea Compounds	12-24	NLR family pyrin domain containing 3	Homo sapiens	175-180
35114687-9	2022	Its central sulfonylurea group interacts with the Walker A motif of the NLRP3 nucleotide-binding domain and is sandwiched between two arginines, explaining the specificity of NLRP3 for this chemical entity.	Arginine	134-143	NLR family pyrin domain containing 3	Homo sapiens	72-77
35114687-9	2022	Its central sulfonylurea group interacts with the Walker A motif of the NLRP3 nucleotide-binding domain and is sandwiched between two arginines, explaining the specificity of NLRP3 for this chemical entity.	Arginine	134-143	NLR family pyrin domain containing 3	Homo sapiens	175-180
35131633-0	2022	VX-765 prevents intestinal ischemia-reperfusion injury by inhibiting NLRP3 inflammasome.	belnacasan	0-6	NLR family pyrin domain containing 3	Homo sapiens	69-74
35131633-12	2022	Moreover, VX-765 inhibited the nuclear translocation of P65, reduced oxidative stress and down-regulated the activation of NLRP3 inflammasome.	belnacasan	10-16	NLR family pyrin domain containing 3	Homo sapiens	123-128
35260874-0	2022	Lycopene ameliorates atrazine-induced pyroptosis in spleen by suppressing the Ox-mtDNA/Nlrp3 inflammasome pathway.	Lycopene	0-8	NLR family pyrin domain containing 3	Homo sapiens	87-92
35245615-6	2022	Treatment of human THP-1 macrophages with phthalates revealed increased NLRP3 and NLRP6 expression and induction of a pro-inflammatory macrophage population.	phthalic acid	42-52	NLR family pyrin domain containing 3	Homo sapiens	72-77
35418866-0	2022	Canagliflozin Ameliorates NLRP3 Inflammasome-Mediated Inflammation Through Inhibiting NF-kappaB Signaling and Upregulating Bif-1.	Canagliflozin	0-13	NLR family pyrin domain containing 3	Homo sapiens	26-31
35418866-3	2022	In this study, we found that canagliflozin (CAN) transcriptionally inhibited NLRP3 inflammasome-related proteins by inhibiting the transduction of the nuclear factor kappaB signal.	Canagliflozin	29-42	NLR family pyrin domain containing 3	Homo sapiens	77-82
35454970-6	2022	Specific checkpoints identified in managing SARS-CoV-2 induced cytokine storm include a decrease in the level of Nod-Like Receptor 3 (NLRP3) inflammasome where drugs such as quercetin and anakinra were effective.	Quercetin	174-183	NLR family pyrin domain containing 3	Homo sapiens	134-139
35360199-10	2022	In addition, IP-Se-06 displayed significant inhibition of p38 MAPK and p-p38, leading to inhibition of inflammasome complex proteins (NLRP3 and caspase-1) in glioblastoma cells.	ip-se-06	13-21	NLR family pyrin domain containing 3	Homo sapiens	134-139
34981119-0	2022	New insights into the regulatory roles of glutathione in NLRP3-inflammasome-mediated immune and inflammatory responses.	Glutathione	42-53	NLR family pyrin domain containing 3	Homo sapiens	57-62
34981119-4	2022	Recent findings revealed that altered GSH levels are closely associated with a wide range of pathologies including bacterial and viral infections, neurodegenerative diseases, and autoimmune disorders, all of which are also characterized by aberrant activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Glutathione	38-41	NLR family pyrin domain containing 3	Homo sapiens	267-303
34981119-4	2022	Recent findings revealed that altered GSH levels are closely associated with a wide range of pathologies including bacterial and viral infections, neurodegenerative diseases, and autoimmune disorders, all of which are also characterized by aberrant activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome.	Glutathione	38-41	NLR family pyrin domain containing 3	Homo sapiens	305-310
34981119-5	2022	As a result of these findings, GSH was assigned a central role in influencing the activation of the NLRP3 inflammasome.	Glutathione	31-34	NLR family pyrin domain containing 3	Homo sapiens	100-105
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Nigericin	137-146	NLR family pyrin domain containing 3	Homo sapiens	99-104
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	poly(dA)	151-158	NLR family pyrin domain containing 3	Homo sapiens	99-104
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Thymidine	159-161	NLR family pyrin domain containing 3	Homo sapiens	99-104
35312958-7	2022	Excessive Cu exposure can modulate a huge number of cytokines in both directions, increase and/or decrease through a variety of molecular and cellular signaling pathways including nuclear factor kappa-B (NF-kappaB) pathway, mitogen-activated protein kinase (MAPKs) pathway, JAK-STAT (Janus Kinase- signal transducer and activator of transcription) pathway, and NOD-like receptor protein 3 (NLRP3) inflammasome.	Copper	10-12	NLR family pyrin domain containing 3	Homo sapiens	361-388
35312958-7	2022	Excessive Cu exposure can modulate a huge number of cytokines in both directions, increase and/or decrease through a variety of molecular and cellular signaling pathways including nuclear factor kappa-B (NF-kappaB) pathway, mitogen-activated protein kinase (MAPKs) pathway, JAK-STAT (Janus Kinase- signal transducer and activator of transcription) pathway, and NOD-like receptor protein 3 (NLRP3) inflammasome.	Copper	10-12	NLR family pyrin domain containing 3	Homo sapiens	390-395
35260874-6	2022	Lastly, atrazine induced pyroptosis in spleen, mediating the activation of Nlrp3 inflammasome.	Atrazine	8-16	NLR family pyrin domain containing 3	Homo sapiens	75-80
35260874-9	2022	The results also provided evidence that lycopene had a potential role in the prevention of Nlrp3 inflammasome activation by depleting the ox-mtDNA.	Lycopene	40-48	NLR family pyrin domain containing 3	Homo sapiens	91-96
35253245-0	2022	Astragaloside IV alleviates oxidative stress-related damage via inhibiting NLRP3 inflammasome in a MAPK signaling dependent pathway in human lens epithelial cells.	astragaloside	0-13	NLR family pyrin domain containing 3	Homo sapiens	75-80
35370636-0	2022	Fucoidan Alleviates Renal Fibrosis in Diabetic Kidney Disease via Inhibition of NLRP3 Inflammasome-Mediated Podocyte Pyroptosis.	fucoidan	0-8	NLR family pyrin domain containing 3	Homo sapiens	80-85
35286219-3	2022	The present study aimed to examine the involvement of NLRP3 inflammasomes in the anti-breast cancer effects of raloxifene and its underlying mechanisms.	Raloxifene Hydrochloride	111-121	NLR family pyrin domain containing 3	Homo sapiens	54-59
35286219-4	2022	RESULTS: Raloxifene significantly inhibited activation of NLRP3 inflammasomes in various breast cancer cell lines.	Raloxifene Hydrochloride	9-19	NLR family pyrin domain containing 3	Homo sapiens	58-63
35286219-5	2022	Importantly, forced expression of a gain-of-function variant of NLRP3 rescued breast cancer cells from growth arrest by raloxifene, suggesting that suppression of NLRP3 inflammasomes activation mediates the raloxifene-induced inhibition of breast cancer growth.	Raloxifene Hydrochloride	120-130	NLR family pyrin domain containing 3	Homo sapiens	64-69
35286219-5	2022	Importantly, forced expression of a gain-of-function variant of NLRP3 rescued breast cancer cells from growth arrest by raloxifene, suggesting that suppression of NLRP3 inflammasomes activation mediates the raloxifene-induced inhibition of breast cancer growth.	Raloxifene Hydrochloride	120-130	NLR family pyrin domain containing 3	Homo sapiens	163-168
35286219-5	2022	Importantly, forced expression of a gain-of-function variant of NLRP3 rescued breast cancer cells from growth arrest by raloxifene, suggesting that suppression of NLRP3 inflammasomes activation mediates the raloxifene-induced inhibition of breast cancer growth.	Raloxifene Hydrochloride	207-217	NLR family pyrin domain containing 3	Homo sapiens	64-69
35286219-5	2022	Importantly, forced expression of a gain-of-function variant of NLRP3 rescued breast cancer cells from growth arrest by raloxifene, suggesting that suppression of NLRP3 inflammasomes activation mediates the raloxifene-induced inhibition of breast cancer growth.	Raloxifene Hydrochloride	207-217	NLR family pyrin domain containing 3	Homo sapiens	163-168
35286219-6	2022	Mechanistically, raloxifene suppressed NLRP3 inflammasomes activation by lowering the cellular levels of ROS through the modulation of redox signaling mediated via aryl hydrocarbon receptor (AhR)-Nrf2-HO-1 axis or the impaired generation of mitochondrial ROS in a mitophagy-dependent manner.	Raloxifene Hydrochloride	17-27	NLR family pyrin domain containing 3	Homo sapiens	39-44
35286219-6	2022	Mechanistically, raloxifene suppressed NLRP3 inflammasomes activation by lowering the cellular levels of ROS through the modulation of redox signaling mediated via aryl hydrocarbon receptor (AhR)-Nrf2-HO-1 axis or the impaired generation of mitochondrial ROS in a mitophagy-dependent manner.	ros	105-108	NLR family pyrin domain containing 3	Homo sapiens	39-44
35286219-9	2022	CONCLUSIONS: The results observed in this study suggest that modulation of NLRP3 inflammasomes activation is a critical event in inhibition of breast tumor growth by raloxifene.	Raloxifene Hydrochloride	166-176	NLR family pyrin domain containing 3	Homo sapiens	75-80
35330829-3	2022	Our previous study showed that C646, an inhibitor of histone acetyltransferase p300, has a protective role in dextran sulfate sodium (DSS)-induced colitis by targeting the NLRP3 inflammasome, making us further study the inhibitors of histone deacetylases (HDACs) in the treatment of colitis.	C646	31-35	NLR family pyrin domain containing 3	Homo sapiens	172-177
35330829-3	2022	Our previous study showed that C646, an inhibitor of histone acetyltransferase p300, has a protective role in dextran sulfate sodium (DSS)-induced colitis by targeting the NLRP3 inflammasome, making us further study the inhibitors of histone deacetylases (HDACs) in the treatment of colitis.	Dextran Sulfate	134-137	NLR family pyrin domain containing 3	Homo sapiens	172-177
35298317-0	2022	Effect of NLRP3 repression on NLRP3 inflammasome activation in human corneal epithelial cells with black carbon exposure.	Carbon	105-111	NLR family pyrin domain containing 3	Homo sapiens	10-15
35298317-1	2022	PURPOSE: To investigate the inhibitory effects of NLRP3 siRNA on NLRP3 inflammasome activation in human corneal epithelial cells (HCECs) with fresh black carbon (FBC) particles and ozone-oxidized BC (OBC) particles treatment.	4-(3,5-difluorophenyl)benzoic acid	162-165	NLR family pyrin domain containing 3	Homo sapiens	50-55
35298317-6	2022	Under FBC treatment, the reductions of NLRP3 and Caspase-1 mRNA levels were 53.5% (p < 0.001) and 34.2% (p < 0.	4-(3,5-difluorophenyl)benzoic acid	6-9	NLR family pyrin domain containing 3	Homo sapiens	39-44
35370689-7	2022	Therefore, this report can provide an overview of natural extractions targeted to prevent or treat NLRP3 inflammasome-mediated gout in the MSU-induced gout model.	msu	139-142	NLR family pyrin domain containing 3	Homo sapiens	99-104
35183871-7	2022	Further studies showed that J114 displayed remarkable inhibitory activity against NLRP3- and AIM2-but not NLRC4-dependent activation of caspase-1 and the release of IL-1beta in human THP-1 macrophages.	Cancell	28-32	NLR family pyrin domain containing 3	Homo sapiens	82-87
35309841-9	2022	This article reviews the mechanism of the NLRP3 inflammasome and its correlation with immune reconstitution in PLHIV treated with ART.	art	130-133	NLR family pyrin domain containing 3	Homo sapiens	42-47
35310096-4	2022	Modafinil treatment attenuated inflammasome activity and reduced neuronal pyroptosis involving the NLRP3/NLRP1/NLRC4-caspase-1-IL-1beta pathway.	Modafinil	0-9	NLR family pyrin domain containing 3	Homo sapiens	99-104
35227133-0	2022	Cholesterol crystals activate NLRP3 inflammasomes and promote gallstone formation by increasing mucin secretion.	Cholesterol	0-11	NLR family pyrin domain containing 3	Homo sapiens	30-35
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Reactive Oxygen Species	34-57	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Reactive Oxygen Species	59-62	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Acetylcysteine	116-132	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Acetylcysteine	134-137	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Adenosine	143-152	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Adenosine Triphosphate	167-170	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Reactive Oxygen Species	210-213	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Adenosine Triphosphate	52-55	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Adenosine Triphosphate	52-55	NLR family pyrin domain containing 3	Homo sapiens	175-180
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Reactive Oxygen Species	65-68	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Acetylcysteine	89-92	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Acetylcysteine	89-92	NLR family pyrin domain containing 3	Homo sapiens	175-180
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Reactive Oxygen Species	102-105	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Reactive Oxygen Species	102-105	NLR family pyrin domain containing 3	Homo sapiens	175-180
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Reactive Oxygen Species	134-137	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Reactive Oxygen Species	134-137	NLR family pyrin domain containing 3	Homo sapiens	175-180
35434015-9	2022	These results suggest that Nrf2 regulates NQO1 to attenuate ROS, which negatively regulates NLRP3 inflammasome.	Reactive Oxygen Species	60-63	NLR family pyrin domain containing 3	Homo sapiens	92-97
35434015-10	2022	Conclusions: Nrf2/NQO1 was an inhibitor of ROS-induced NLRP3 inflammasome activation in Q-VD-OPH-induced necroptosis following cerebral I/R injury.	Reactive Oxygen Species	43-46	NLR family pyrin domain containing 3	Homo sapiens	55-60
35184679-0	2022	Rapamycin ameliorates chronic intermittent hypoxia and sleep deprivation-induced renal damage via the mammalian target of rapamycin (mTOR)/NOD-like receptor protein 3 (NLRP3) signaling pathway.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	139-166
35184679-0	2022	Rapamycin ameliorates chronic intermittent hypoxia and sleep deprivation-induced renal damage via the mammalian target of rapamycin (mTOR)/NOD-like receptor protein 3 (NLRP3) signaling pathway.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	168-173
35184679-1	2022	Rapamycin inhibits the activation of NOD-like receptor protein 3 (NLRP3) by regulating the mammalian target of rapamycin (mTOR) to treat obstructive sleep apnea-related renal injury.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	37-64
35184679-1	2022	Rapamycin inhibits the activation of NOD-like receptor protein 3 (NLRP3) by regulating the mammalian target of rapamycin (mTOR) to treat obstructive sleep apnea-related renal injury.	Sirolimus	0-9	NLR family pyrin domain containing 3	Homo sapiens	66-71
35309342-10	2022	Stimulation with uric acid in HK-2 cells also resulted in NLRP3 inflammasome activation and pyroptotic cell death, however treatment with 3-MA prevented all these responses.	Uric Acid	17-26	NLR family pyrin domain containing 3	Homo sapiens	58-63
35309342-10	2022	Stimulation with uric acid in HK-2 cells also resulted in NLRP3 inflammasome activation and pyroptotic cell death, however treatment with 3-MA prevented all these responses.	3-methyladenine	138-142	NLR family pyrin domain containing 3	Homo sapiens	58-63
35246004-0	2022	Emodin relieves the inflammation and pyroptosis of lipopolysaccharide-treated 1321N1 cells by regulating methyltransferase-like 3 -mediated NLR family pyrin domain containing 3 expression.	Emodin	0-6	NLR family pyrin domain containing 3	Homo sapiens	140-176
35246004-8	2022	NLRP3 activator, nigericin, was used to overexpress NLRP3.	Nigericin	17-26	NLR family pyrin domain containing 3	Homo sapiens	0-5
35246004-8	2022	NLRP3 activator, nigericin, was used to overexpress NLRP3.	Nigericin	17-26	NLR family pyrin domain containing 3	Homo sapiens	52-57
35246004-11	2022	Emodin treatment decreased the levels of TNF-alpha, IL-1beta, IL-6, NLRP3, SDC-1, GSDMD-N, and Caspase-1, while increasing the levels of IL-10 in LPS-treated 1321N1 cells.	Emodin	0-6	NLR family pyrin domain containing 3	Homo sapiens	68-73
35246004-15	2022	Therefore, emodin inhibits the inflammation and pyroptosis of LPS-treated 1321N1 cells by inactivating METTL3-mediated NLRP3 expression.	Emodin	11-17	NLR family pyrin domain containing 3	Homo sapiens	119-124
35227133-6	2022	Experiments in vitro showed that cholesterol crystals promote MUC5AC secretion; they also increase expression of NLRP3, NLR family CARD domain-containing 4 (NLRC4), apoptosis-associated speck-like protein containing caspase recruitment domain (ASC), and cleaved caspase-1 in biliary epithelial cells.	Cholesterol	33-44	NLR family pyrin domain containing 3	Homo sapiens	113-118
35144130-0	2022	GSDMD-miR-223-NLRP3 axis involved in B(a)P-induced inflammatory injury of alveolar epithelial cells.	Phosphorus	41-42	NLR family pyrin domain containing 3	Homo sapiens	14-19
35144130-15	2022	In conclusion, GSDMD may regulate NLRP3 inflammasome through miR-223, which is involved in B(a)P induced inflammatory damage in A549 cells.	Benzo(a)pyrene	91-96	NLR family pyrin domain containing 3	Homo sapiens	34-39
35124344-2	2022	Further, the study also analyzed the regulatory role of NLRP3 in resistance to gemcitabine among ovarian cancer cells and its underlying interaction mechanisms with Wnt/beta-catenin in vitro.	gemcitabine	79-90	NLR family pyrin domain containing 3	Homo sapiens	56-61
35219847-0	2022	Silica nanoparticles induce pyroptosis and cardiac hypertrophy via ROS/NLRP3/Caspase-1 pathway.	Silicon Dioxide	0-6	NLR family pyrin domain containing 3	Homo sapiens	71-76
35219847-0	2022	Silica nanoparticles induce pyroptosis and cardiac hypertrophy via ROS/NLRP3/Caspase-1 pathway.	ros	67-70	NLR family pyrin domain containing 3	Homo sapiens	71-76
35219847-7	2022	For in vitro study, SiNPs increased the intracellular ROS generation and activated the NLRP3/Caspase-1/GSDMD signaling pathway in cardiomyocytes.	sinps	20-25	NLR family pyrin domain containing 3	Homo sapiens	87-92
35219847-8	2022	Whereas, the NADPH oxidase (NOX) inhibitor VAS2870 had effectively inhibited the ROS level and suppressed the expression of NLRP3, ASC, Pro-Caspase-1, Cleaved-Caspase-1, N-GSDMD, IL-18, Cleaved-IL-1beta, ANP, BNP and beta-MHC.	3-benzyl-7-(2-benzoxazolyl)thio-1,2,3-triazolo(4,5-d)pyrimidine	43-50	NLR family pyrin domain containing 3	Homo sapiens	124-129
35219847-9	2022	Moreover, transfected with si-NLRP3 or adopted with Caspase-1 inhibitor VX-765 in cardiomyocytes showed an inhibitory effect on SiNPs-induced pyroptosis and cardiac hypertrophy.	sinps	128-133	NLR family pyrin domain containing 3	Homo sapiens	30-35
35023144-0	2022	ROS-NLRP3 signaling pathway induces sterile inflammation after thulium laser resection of the prostate.	ros	0-3	NLR family pyrin domain containing 3	Homo sapiens	4-9
35023144-0	2022	ROS-NLRP3 signaling pathway induces sterile inflammation after thulium laser resection of the prostate.	Thulium	63-70	NLR family pyrin domain containing 3	Homo sapiens	4-9
35023144-2	2022	This study mainly focuses on the role of the reactive oxygen species-NLR family, pyrin domain-containing 3 (ROS-NLRP3) signaling pathway in SI after thulium laser resection of the prostate (TmLRP).	reactive	45-53	NLR family pyrin domain containing 3	Homo sapiens	112-117
35023144-2	2022	This study mainly focuses on the role of the reactive oxygen species-NLR family, pyrin domain-containing 3 (ROS-NLRP3) signaling pathway in SI after thulium laser resection of the prostate (TmLRP).	oxygen species	54-68	NLR family pyrin domain containing 3	Homo sapiens	112-117
35023144-2	2022	This study mainly focuses on the role of the reactive oxygen species-NLR family, pyrin domain-containing 3 (ROS-NLRP3) signaling pathway in SI after thulium laser resection of the prostate (TmLRP).	ros	108-111	NLR family pyrin domain containing 3	Homo sapiens	112-117
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	ros	141-144	NLR family pyrin domain containing 3	Homo sapiens	48-53
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	NLR family pyrin domain containing 3	Homo sapiens	48-53
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	NLR family pyrin domain containing 3	Homo sapiens	45-50
35023144-12	2022	Activation of the ROS-NLRP3 signaling pathway induces SI in the wound after prostatectomy.	ros	18-21	NLR family pyrin domain containing 3	Homo sapiens	22-27
35113170-0	2022	Colchicine for COVID-19: targeting NLRP3 inflammasome to blunt hyperinflammation.	Colchicine	0-10	NLR family pyrin domain containing 3	Homo sapiens	35-40
35113170-3	2022	Since colchicine is an anti-inflammatory drug with the ability to block NLRP3 inflammasome oligomerization, this may prevent the release of active IL-1beta and block the detrimental effects of downstream cytokines, i.e. IL-6.	Colchicine	6-16	NLR family pyrin domain containing 3	Homo sapiens	72-77
35113170-5	2022	As colchicine is a nonspecific inhibitor of the NLRP3 inflammasome, compounds specifically blocking this molecule might provide increased advantages in reducing the inflammatory burden and its related clinical manifestations.	Colchicine	3-13	NLR family pyrin domain containing 3	Homo sapiens	48-53
35438288-3	2022	Mefenamic acid which belongs to fenamate group inhibits the NLRP3 inflammasome by inhibiting efflux of chloride ions and influx of calcium ions through blocking VRAC and TRPM2 respectively.	Mefenamic Acid	0-14	NLR family pyrin domain containing 3	Homo sapiens	60-65
35438288-3	2022	Mefenamic acid which belongs to fenamate group inhibits the NLRP3 inflammasome by inhibiting efflux of chloride ions and influx of calcium ions through blocking VRAC and TRPM2 respectively.	Fenamates	32-40	NLR family pyrin domain containing 3	Homo sapiens	60-65
35438288-3	2022	Mefenamic acid which belongs to fenamate group inhibits the NLRP3 inflammasome by inhibiting efflux of chloride ions and influx of calcium ions through blocking VRAC and TRPM2 respectively.	Chlorides	103-111	NLR family pyrin domain containing 3	Homo sapiens	60-65
35438288-3	2022	Mefenamic acid which belongs to fenamate group inhibits the NLRP3 inflammasome by inhibiting efflux of chloride ions and influx of calcium ions through blocking VRAC and TRPM2 respectively.	Calcium	131-138	NLR family pyrin domain containing 3	Homo sapiens	60-65
35438288-4	2022	Thus, Mefenamic acid provides a potentially practical pharmacological approach for treating NLRP3- driven diseases.	Mefenamic Acid	6-20	NLR family pyrin domain containing 3	Homo sapiens	92-97
35124344-3	2022	The current in vitro study detailed that when downregulating NLRP3, it could enhance the gemcitabine sensitivity in GRC cells.	gemcitabine	89-100	NLR family pyrin domain containing 3	Homo sapiens	61-66
35124344-4	2022	In case of gemcitabine-resistant cells, the up-regulation of NLRP3 can increase the drug-resistance through the activation of IL-1beta, EMT and Wnt/beta-catenin signaling pathways.	gemcitabine	11-22	NLR family pyrin domain containing 3	Homo sapiens	61-66
35124344-8	2022	The current study conducted in vitro experiments and the findings infer that the downregulation of NLRP3 can enhance the sensitivity of gemcitabine among GRC cells.	gemcitabine	136-147	NLR family pyrin domain containing 3	Homo sapiens	99-104
35226250-4	2022	We previously showed that arsenic-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation contributed to hepatic IR.	Arsenic	26-33	NLR family pyrin domain containing 3	Homo sapiens	42-69
35059736-12	2022	Furthermore, nicotine exposure increased the expression levels of caspase-1, IL-1beta, IL-18, NLRP3, apoptosis-associated speck-like protein and gasdermin D in 16HBE cells.	Nicotine	13-21	NLR family pyrin domain containing 3	Homo sapiens	94-99
35226250-4	2022	We previously showed that arsenic-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation contributed to hepatic IR.	Arsenic	26-33	NLR family pyrin domain containing 3	Homo sapiens	71-76
35226250-5	2022	However, the regulatory mechanisms underlying the role of arsenic toward the post-transcriptional modification of NLRP3 remain unclear.	Arsenic	58-65	NLR family pyrin domain containing 3	Homo sapiens	114-119
35226250-6	2022	Here, we showed that NLRP3 mRNA stability was enhanced by METTL14-mediated m6A methylation during arsenic-induced hepatic IR.	Arsenic	98-105	NLR family pyrin domain containing 3	Homo sapiens	21-26
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	93-100	NLR family pyrin domain containing 3	Homo sapiens	138-143
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	198-205	NLR family pyrin domain containing 3	Homo sapiens	138-143
35382471-5	2022	BPBA inhibited self- and Cu2+- or Zn2+-induced Abeta aggregation, disaggregated the already formed Abeta aggregates, and reduced the neurotoxicity of Abeta aggregates; it also inhibited the activation of the NLRP3 inflammasome and reduced the release of IL-1beta in vitro and vivo.	2-Bromopyridine-5-boronic acid	0-4	NLR family pyrin domain containing 3	Homo sapiens	208-213
35187677-0	2022	alpha-Mangostin protects lipopolysaccharide-stimulated nucleus pulposus cells against NLRP3 inflammasome-mediated apoptosis via the NF-kappaB pathway.	mangostin	0-15	NLR family pyrin domain containing 3	Homo sapiens	86-91
35187677-11	2022	alpha-Mangostin treatment also inhibited the LPS-induced increase in expression levels of NLRP3, ASC and pro-caspase-1, as well as the production of IL-1beta and IL-18 in NPCs.	mangostin	0-15	NLR family pyrin domain containing 3	Homo sapiens	90-95
35335908-0	2022	Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study.	Aspirin	0-20	NLR family pyrin domain containing 3	Homo sapiens	143-148
35335908-0	2022	Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study.	Atorvastatin	88-100	NLR family pyrin domain containing 3	Homo sapiens	143-148
35335908-4	2022	The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain-like receptor 3 (NLRP3), interleukin-1beta (IL-1beta) miRNA155 expression levels in the frontal cortex of the brain tissue.	Alcohols	47-54	NLR family pyrin domain containing 3	Homo sapiens	129-170
35335908-4	2022	The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain-like receptor 3 (NLRP3), interleukin-1beta (IL-1beta) miRNA155 expression levels in the frontal cortex of the brain tissue.	Alcohols	47-54	NLR family pyrin domain containing 3	Homo sapiens	172-177
35335908-4	2022	The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain-like receptor 3 (NLRP3), interleukin-1beta (IL-1beta) miRNA155 expression levels in the frontal cortex of the brain tissue.	Atorvastatin	58-62	NLR family pyrin domain containing 3	Homo sapiens	129-170
35335908-4	2022	The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain-like receptor 3 (NLRP3), interleukin-1beta (IL-1beta) miRNA155 expression levels in the frontal cortex of the brain tissue.	Atorvastatin	58-62	NLR family pyrin domain containing 3	Homo sapiens	172-177
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	NLR family pyrin domain containing 3	Homo sapiens	63-68
35335908-9	2022	To further investigate these findings, we have performed an extensive molecular docking study to investigate the binding affinity of ASA to the binding pockets of the NLRP3 protein.	Aspirin	133-136	NLR family pyrin domain containing 3	Homo sapiens	167-172
35335908-10	2022	Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions.	Aspirin	27-30	NLR family pyrin domain containing 3	Homo sapiens	86-91
35335908-10	2022	Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions.	Aspirin	27-30	NLR family pyrin domain containing 3	Homo sapiens	137-142
35335908-11	2022	Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.	Aspirin	86-89	NLR family pyrin domain containing 3	Homo sapiens	224-229
35335908-11	2022	Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.	Alcohols	129-136	NLR family pyrin domain containing 3	Homo sapiens	224-229
35188323-8	2022	MtROS reduction inhibited IL-1beta and IL-8 secretions by NLRP3/caspase-1/IL-1beta/IL-8 pathway.	mtros	0-5	NLR family pyrin domain containing 3	Homo sapiens	58-63
35187677-15	2022	Moreover, inhibition of NF-kappaB by PDTC aggravated the inhibitory effects of alpha-mangostin on NLRP3 inflammasome activation and apoptosis in LPS-induced NPCs.	prolinedithiocarbamate	37-41	NLR family pyrin domain containing 3	Homo sapiens	98-103
35187677-15	2022	Moreover, inhibition of NF-kappaB by PDTC aggravated the inhibitory effects of alpha-mangostin on NLRP3 inflammasome activation and apoptosis in LPS-induced NPCs.	mangostin	79-94	NLR family pyrin domain containing 3	Homo sapiens	98-103
35187677-16	2022	These findings suggested that alpha-mangostin exerted a protective effect on NLRP3 inflammasome-mediated apoptosis in LPS-induced NPCs through regulating NF-kappaB signaling.	mangostin	30-45	NLR family pyrin domain containing 3	Homo sapiens	77-82
35382471-7	2022	BPBA exerts an anti-AD effect mainly through dissolving Abeta aggregates and inhibiting NLRP3 inflammasome activation synergistically.	2-Bromopyridine-5-boronic acid	0-4	NLR family pyrin domain containing 3	Homo sapiens	88-93
35172843-0	2022	Dopamine signaling modulates microglial NLRP3 inflammasome activation: implications for Parkinson"s disease.	Dopamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	40-45
35221708-2	2022	Methods: A Dox-controlled system was utilized to induce the expression of the ASC transgene in HEK293 cells while simultaneously overexpressing NLRP3 and CASP1.	Doxorubicin	11-14	NLR family pyrin domain containing 3	Homo sapiens	144-149
35221708-5	2022	The applicability and effectiveness of the CASPorter cell line were tested by co-treatment with Dox and four known CASP1/NLRP3 inhibitors (MCC950, Glyburide, VX-765 and VRT-043198).	Doxorubicin	96-99	NLR family pyrin domain containing 3	Homo sapiens	121-126
35221708-5	2022	The applicability and effectiveness of the CASPorter cell line were tested by co-treatment with Dox and four known CASP1/NLRP3 inhibitors (MCC950, Glyburide, VX-765 and VRT-043198).	Glyburide	147-156	NLR family pyrin domain containing 3	Homo sapiens	121-126
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	9-12	NLR family pyrin domain containing 3	Homo sapiens	184-189
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	9-12	NLR family pyrin domain containing 3	Homo sapiens	205-210
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	249-252	NLR family pyrin domain containing 3	Homo sapiens	184-189
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	249-252	NLR family pyrin domain containing 3	Homo sapiens	205-210
35221708-8	2022	In HEK293-iASC-NLRP3/CASP1-CASPorter cell system, cleavage of the CASP1 consensus site (YVAD) in the CASPorter protein after Dox treatment causing excitation/emission of green fluorescence and the 71% GFP+ cell population increase quantified by FC (78.1% vs 6.90%).	Doxorubicin	125-128	NLR family pyrin domain containing 3	Homo sapiens	15-20
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	0-3	NLR family pyrin domain containing 3	Homo sapiens	30-35
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	0-3	NLR family pyrin domain containing 3	Homo sapiens	122-127
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	83-86	NLR family pyrin domain containing 3	Homo sapiens	30-35
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	83-86	NLR family pyrin domain containing 3	Homo sapiens	122-127
35169962-0	2022	Correction to: Novel biphenyl diester derivative AB-38b inhibits NLRP3 inflammasome through Nrf2 activation in diabetic nephropathy.	biphenyl diester	21-37	NLR family pyrin domain containing 3	Homo sapiens	65-70
35169962-0	2022	Correction to: Novel biphenyl diester derivative AB-38b inhibits NLRP3 inflammasome through Nrf2 activation in diabetic nephropathy.	ab-38b	49-55	NLR family pyrin domain containing 3	Homo sapiens	65-70
35172843-5	2022	Dopamine blocks microglial NLRP3 inflammasome activation in the MPTP model, but its effects in this framework, highly relevant to PD, remain unexplored in primary human microglia and in other in vivo parkinsonism models.	Dopamine	0-8	NLR family pyrin domain containing 3	Homo sapiens	27-32
35172843-5	2022	Dopamine blocks microglial NLRP3 inflammasome activation in the MPTP model, but its effects in this framework, highly relevant to PD, remain unexplored in primary human microglia and in other in vivo parkinsonism models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	64-68	NLR family pyrin domain containing 3	Homo sapiens	27-32
35172843-6	2022	METHODS: Biochemical techniques including quantification of IL-1beta secretion and confocal microscopy were employed to gain insight into dopamine signaling-mediated inhibition of the NLRP3 inflammasome mechanism in primary human microglia and the SYN120 transgenic mouse model.	Dopamine	138-146	NLR family pyrin domain containing 3	Homo sapiens	184-189
35172843-9	2022	RESULTS: We show in primary human microglia that dopamine, L-DOPA, and high extracellular K+, but not norepinephrine and epinephrine, block canonical, non-canonical, and alpha-syn-mediated NLRP3 inflammasome-driven IL-1beta secretion.	Dopamine	49-57	NLR family pyrin domain containing 3	Homo sapiens	189-194
35172843-9	2022	RESULTS: We show in primary human microglia that dopamine, L-DOPA, and high extracellular K+, but not norepinephrine and epinephrine, block canonical, non-canonical, and alpha-syn-mediated NLRP3 inflammasome-driven IL-1beta secretion.	Levodopa	59-65	NLR family pyrin domain containing 3	Homo sapiens	189-194
35172843-13	2022	CONCLUSIONS: Dopamine inhibits canonical, non-canonical, and alpha-syn-mediated activation of the NLRP3 inflammasome in primary human microglia, as does high extracellular K+.	Dopamine	13-21	NLR family pyrin domain containing 3	Homo sapiens	98-103
35172843-14	2022	We suggest that dopamine serves as an endogenous repressor of the K+ efflux-dependent microglial NLRP3 inflammasome activation that contributes to dopaminergic neurodegeneration in PD, and that this reciprocation may account for the specific vulnerability of these neurons to disease pathology.	Dopamine	16-24	NLR family pyrin domain containing 3	Homo sapiens	97-102
35222388-9	2022	Mechanistically, 1,2-diol blocks the NLRP3 inflammasome activation by disrupting NLRP3-NEK7 interaction and the subsequent NLRP3 inflammasome assembly and activation.	MLS002693268	17-25	NLR family pyrin domain containing 3	Homo sapiens	81-86
35222388-0	2022	A 4-Benzene-Indol Derivative Alleviates LPS-Induced Acute Lung Injury Through Inhibiting the NLRP3 Inflammasome.	4-benzene-indol	2-17	NLR family pyrin domain containing 3	Homo sapiens	93-98
35222388-9	2022	Mechanistically, 1,2-diol blocks the NLRP3 inflammasome activation by disrupting NLRP3-NEK7 interaction and the subsequent NLRP3 inflammasome assembly and activation.	MLS002693268	17-25	NLR family pyrin domain containing 3	Homo sapiens	123-128
35222388-8	2022	The results showed that 4-benzene-indol derivative could not only suppress the activation of NLRP3 inflammasome both in vitro and alleviate LPS-induced ALI in vivo but also suppress the NLRP3 inflammasome in human myeloid leukemia mononuclear cells (THP-1) cell lines.	4-benzene-indol	24-39	NLR family pyrin domain containing 3	Homo sapiens	93-98
35222388-10	2022	To summarize, this research indicated that the newly-discovered 4-benzene-indol derivative targets NLRP3 inflammasome signaling, which consequently alleviates sepsis-related ALI.	4-benzene-indol	64-79	NLR family pyrin domain containing 3	Homo sapiens	99-104
35222388-8	2022	The results showed that 4-benzene-indol derivative could not only suppress the activation of NLRP3 inflammasome both in vitro and alleviate LPS-induced ALI in vivo but also suppress the NLRP3 inflammasome in human myeloid leukemia mononuclear cells (THP-1) cell lines.	4-benzene-indol	24-39	NLR family pyrin domain containing 3	Homo sapiens	186-191
35211530-8	2022	In vitro studies demonstrated that exogenous C18-ceramide promoted macrophage inflammation and matrix metalloprotein (MMP) expression through the NLRP3-caspase 1 pathway.	C18-CERAMIDE	45-57	NLR family pyrin domain containing 3	Homo sapiens	146-151
35222388-9	2022	Mechanistically, 1,2-diol blocks the NLRP3 inflammasome activation by disrupting NLRP3-NEK7 interaction and the subsequent NLRP3 inflammasome assembly and activation.	MLS002693268	17-25	NLR family pyrin domain containing 3	Homo sapiens	37-42
35211530-10	2022	Conclusions: Our findings demonstrated that ceramide metabolism disturbance might play a vital role in TAD development by aggravating aortic inflammation through the NLRP3 pathway, possibly providing a new target for pharmacological therapy and a potential biomarker of TAD.	Ceramides	44-52	NLR family pyrin domain containing 3	Homo sapiens	166-171
35132157-6	2022	In contrast, conditioned medium from UPEC-infected NLRP3 knockdown cells significantly decreased the phagocytosis of CFT073 and significantly increased the ROS production from neutrophils.	ros	156-159	NLR family pyrin domain containing 3	Homo sapiens	51-56
35143820-0	2022	Quinolinic acid, a tryptophan metabolite of the skin microbiota, negatively regulates the NLRP3 inflammasome through the aryl hydrocarbon receptor in psoriasis.	Quinolinic Acid	0-15	NLR family pyrin domain containing 3	Homo sapiens	90-95
35143820-0	2022	Quinolinic acid, a tryptophan metabolite of the skin microbiota, negatively regulates the NLRP3 inflammasome through the aryl hydrocarbon receptor in psoriasis.	Tryptophan	19-29	NLR family pyrin domain containing 3	Homo sapiens	90-95
35143820-5	2022	In vitro and in vivo, applying QA significantly alleviated skin inflammation in an aryl hydrocarbon receptor (AhR)-dependent manner, resulting in the inhibition of the NLRP3 inflammasome activation.	Quinolinic Acid	31-33	NLR family pyrin domain containing 3	Homo sapiens	168-173
35143820-7	2022	Collectively, our data suggest that QA, a skin microbiota-derived metabolite, negatively regulates AhR-NLRP3 inflammasome signaling activation in patients with psoriasis, providing an insight into the correlation between microbiota metabolism and the host skin in individuals with psoriasis.	Quinolinic Acid	36-38	NLR family pyrin domain containing 3	Homo sapiens	103-108
34993560-11	2022	CONCLUSIONS: In summary, TMZ alleviated pyroptosis induced by myocardial I/R injury through the TLR4/MyD88/NF-kappaB/NLRP3 inflammasome pathway.	Trimetazidine	25-28	NLR family pyrin domain containing 3	Homo sapiens	117-122
35110683-5	2022	gp78 or Insig-1 deficiency in myeloid cells led to exacerbated NLRP3 inflammasome-dependent inflammation in vivo, including lipopolysaccharide-induced systemic inflammation and alum-induced peritonitis.	aluminum sulfate	177-181	NLR family pyrin domain containing 3	Homo sapiens	63-68
35051765-0	2022	Deoxynivalenol aggravates the immunosuppression in piglets and PAMs under the condition of PEDV infection through inhibiting TLR4/NLRP3 signaling pathway.	deoxynivalenol	0-14	NLR family pyrin domain containing 3	Homo sapiens	130-135
35051765-9	2022	Furthermore, DON significantly suppressed the expressions of TLR4/NLRP3 in vivo and in vitro.	deoxynivalenol	13-16	NLR family pyrin domain containing 3	Homo sapiens	66-71
35051765-11	2022	Our findings suggest that DON could aggravate host immunosuppression under the condition of PEDV infection through inhibiting TLR4/NLRP3 signaling pathway, and provide novel theoretical insights into the further studies on the immunotoxicity of DON contamination and PEDV-induced immunosuppression.	deoxynivalenol	26-29	NLR family pyrin domain containing 3	Homo sapiens	131-136
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	triptolide	88-98	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	triptolide	88-98	NLR family pyrin domain containing 3	Homo sapiens	211-216
35039992-0	2022	Phenols and terpenoids: natural products as inhibitors of NLRP3 inflammasome in cardiovascular diseases.	Phenols	0-7	NLR family pyrin domain containing 3	Homo sapiens	58-63
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	Terpenes	102-112	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	Terpenes	102-112	NLR family pyrin domain containing 3	Homo sapiens	211-216
35039992-0	2022	Phenols and terpenoids: natural products as inhibitors of NLRP3 inflammasome in cardiovascular diseases.	Terpenes	12-22	NLR family pyrin domain containing 3	Homo sapiens	58-63
35039992-5	2022	Phenols and terpenoids are naturally natural products that have many anti-inflammatory effects in CVDs by modulating the NLRP3 inflammatory pathway.	Phenols	0-7	NLR family pyrin domain containing 3	Homo sapiens	121-126
35039992-5	2022	Phenols and terpenoids are naturally natural products that have many anti-inflammatory effects in CVDs by modulating the NLRP3 inflammatory pathway.	Terpenes	12-22	NLR family pyrin domain containing 3	Homo sapiens	121-126
35039992-6	2022	Thus, 20 natural products from phenols and terpenoids for the treatment of cardiovascular disease based on the inhibition of NLRP3 inflammasome were summarized and screened.	Terpenes	43-53	NLR family pyrin domain containing 3	Homo sapiens	125-130
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	salvianolic acid B	23-41	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	salvianolic acid B	23-41	NLR family pyrin domain containing 3	Homo sapiens	211-216
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	Ellagic Acid	46-58	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	Ellagic Acid	46-58	NLR family pyrin domain containing 3	Homo sapiens	211-216
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	Phenols	62-69	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	oridonin	75-83	NLR family pyrin domain containing 3	Homo sapiens	148-153
35039992-7	2022	Docking results showed salvianolic acid B and ellagic acid in phenols, and oridonin and triptolide in terpenoids had a better binding activity with NLRP3, which can provide theoretical support for finding novel NLRP3 inflammasome inhibitors or lead compounds in the future.	oridonin	75-83	NLR family pyrin domain containing 3	Homo sapiens	211-216
35098371-0	2022	PARP-1 regulates inflammasome activity by poly-ADP-ribosylation of NLRP3 and interaction with TXNIP in primary macrophages.	poly-adp	42-50	NLR family pyrin domain containing 3	Homo sapiens	67-72
35098371-7	2022	PARP-1 can translocate to cytosol upon ATP stimulation and trigger the PARylation modification on NLRP3, leading to NLRP3 inflammasome assembly.	Adenosine Triphosphate	39-42	NLR family pyrin domain containing 3	Homo sapiens	116-121
35098371-9	2022	Overall, PARP-1 positively regulates NLRP3 inflammasome activation via increasing ROS production and interaction with TXNIP and NLRP3, leading to PARylation of NLRP3.	ros	82-85	NLR family pyrin domain containing 3	Homo sapiens	37-42
35098371-9	2022	Overall, PARP-1 positively regulates NLRP3 inflammasome activation via increasing ROS production and interaction with TXNIP and NLRP3, leading to PARylation of NLRP3.	ros	82-85	NLR family pyrin domain containing 3	Homo sapiens	160-165
35136484-6	2022	In addition, upregulated PPARgamma inhibited the expression of the TXNIP/NLRP3 signaling pathway by reducing ROS-induced injury in the liver during sepsis, which further reduced NLRP3-mediated pyroptosis and the inflammatory response.	Reactive Oxygen Species	109-112	NLR family pyrin domain containing 3	Homo sapiens	73-78
35081900-5	2022	One of the most important tasks remains in the ATPase nucleotide-binding oligomerization domain nucleotide-binding domain leucine-rich repeat-containing receptors protein 3 (NLRP3), in which the blocking of its oligomerization is related to the functional inhibition of inflammasomes.	Leucine	122-129	NLR family pyrin domain containing 3	Homo sapiens	174-179
35136484-6	2022	In addition, upregulated PPARgamma inhibited the expression of the TXNIP/NLRP3 signaling pathway by reducing ROS-induced injury in the liver during sepsis, which further reduced NLRP3-mediated pyroptosis and the inflammatory response.	Reactive Oxygen Species	109-112	NLR family pyrin domain containing 3	Homo sapiens	178-183
35130615-0	2022	NLRP3 inflammasome activation is involved in manganese-induced immunotoxicity.	Manganese	45-54	NLR family pyrin domain containing 3	Homo sapiens	0-5
35154136-0	2022	Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.	ros	8-11	NLR family pyrin domain containing 3	Homo sapiens	20-25
35154136-0	2022	Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.	Calcium Oxalate	70-85	NLR family pyrin domain containing 3	Homo sapiens	20-25
35154136-3	2022	An increasing amount of research have confirmed that inflammation mediated by the cell-crystal reaction can lead to inflammatory injury of renal cells, promote the intracellular expression of NADPH oxidase, induce extensive production of reactive oxygen species, activate NLRP3 inflammasome, discharge a great number of inflammatory factors, trigger inflammatory cascading reactions, promote the aggregation, nucleation and growth process of calcium salt crystals, and ultimately lead to the development of intrarenal crystals and even stones.	calcium salt)	442-454	NLR family pyrin domain containing 3	Homo sapiens	272-277
35046517-9	2022	At the molecular level, colchicine reduces proinflammatory cytokine release and inhibits NF-kappaB signaling and NLRP3 inflammasome activation.	Colchicine	24-34	NLR family pyrin domain containing 3	Homo sapiens	113-118
35078487-3	2022	METHODS: Using a mouse model of high-fat diet (HFD) feeding and a cellular model of HepG2 cells challenged by lipopolysaccharide (LPS) and palmitic acid (PA), the possible molecular mechanisms were exploited in the aspects of NF-kappaB/NLRP3 inflammasome and mTORC1-SREBPs signaling pathways by examining the relevant gene/protein expressions.	Palmitic Acid	139-152	NLR family pyrin domain containing 3	Homo sapiens	236-241
35163148-8	2022	We found that sENG increased the gene expression of VEGF-A, pro-inflammatory cytokines/inflammasome mediators (TNF-alpha, IL-6, NLRP3, ASC, Caspase-1, and IL-1beta), and proteolytic enzyme (MMP-9) in BV2 microglia.	seng	14-18	NLR family pyrin domain containing 3	Homo sapiens	128-133
35040439-7	2022	These roles include inhibition of succinate dehydrogenase (which controls levels of succinate, a metabolite with multiple roles in inflammation), inhibition of glycolysis at multiple levels (which will limit inflammation), activation of the antiinflammatory transcription factors Nrf2 and ATF3, and inhibition of the NLRP3 inflammasome.	Succinic Acid	84-93	NLR family pyrin domain containing 3	Homo sapiens	317-322
35082510-6	2022	Studies have shown that a variety of active components found in Glycyrrhiza, such as licochalcone A, echinatin, isoliquiritigenin, and glycyrrhizin, produce a wide range of anti-inflammatory effects by discouraging NLRP3 inflammasome activation.	licochalcone A	85-99	NLR family pyrin domain containing 3	Homo sapiens	215-220
35082510-6	2022	Studies have shown that a variety of active components found in Glycyrrhiza, such as licochalcone A, echinatin, isoliquiritigenin, and glycyrrhizin, produce a wide range of anti-inflammatory effects by discouraging NLRP3 inflammasome activation.	echinatin	101-110	NLR family pyrin domain containing 3	Homo sapiens	215-220
35082510-6	2022	Studies have shown that a variety of active components found in Glycyrrhiza, such as licochalcone A, echinatin, isoliquiritigenin, and glycyrrhizin, produce a wide range of anti-inflammatory effects by discouraging NLRP3 inflammasome activation.	isoliquiritigenin	112-129	NLR family pyrin domain containing 3	Homo sapiens	215-220
35082510-6	2022	Studies have shown that a variety of active components found in Glycyrrhiza, such as licochalcone A, echinatin, isoliquiritigenin, and glycyrrhizin, produce a wide range of anti-inflammatory effects by discouraging NLRP3 inflammasome activation.	Glycyrrhizic Acid	135-147	NLR family pyrin domain containing 3	Homo sapiens	215-220
35095532-0	2021	Piperlongumine Is an NLRP3 Inhibitor With Anti-inflammatory Activity.	piperlonguminine	0-14	NLR family pyrin domain containing 3	Homo sapiens	21-26
35111001-4	2021	In addition, elamipretide has been shown to attenuate neural oxidative stress (hydrogen peroxide, lipid peroxidation, and ROS), neuroinflammation (TNF, IL-6, COX-2, iNOS, NLRP3, cleaved caspase-1, IL-1beta, and IL-18), and toxic protein accumulation (Abeta).	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	13-25	NLR family pyrin domain containing 3	Homo sapiens	171-176
34841901-9	2022	FUTURE DIRECTIONS: Among strategies to inhibit the NLRP3 inflammasome, Glyburide, Metformin, PPAR agonists and the DPP-4 inhibitor saxagliptin appear to be closest to clinical translation, as these drugs are already FDA approved for other indications.	Glyburide	71-80	NLR family pyrin domain containing 3	Homo sapiens	51-56
34841901-9	2022	FUTURE DIRECTIONS: Among strategies to inhibit the NLRP3 inflammasome, Glyburide, Metformin, PPAR agonists and the DPP-4 inhibitor saxagliptin appear to be closest to clinical translation, as these drugs are already FDA approved for other indications.	Metformin	82-91	NLR family pyrin domain containing 3	Homo sapiens	51-56
35022542-0	2022	Sapidolide A alleviates acetaminophen-induced acute liver injury by inhibiting NLRP3 inflammasome activation in macrophages.	Sapidolide A	0-12	NLR family pyrin domain containing 3	Homo sapiens	79-84
35022542-8	2022	In general, the results reported herein revealed that SA exerts anti-inflammatory effects by regulating NLRP3 inflammasome activation in macrophages, which suggests that SA has great a potential for use in the treatment of AILI patients.	sa	54-56	NLR family pyrin domain containing 3	Homo sapiens	104-109
35022542-8	2022	In general, the results reported herein revealed that SA exerts anti-inflammatory effects by regulating NLRP3 inflammasome activation in macrophages, which suggests that SA has great a potential for use in the treatment of AILI patients.	sa	170-172	NLR family pyrin domain containing 3	Homo sapiens	104-109
35038351-5	2022	METHODS: Peripheral blood CD14+ monocytes from asthmatic patients (n=83) and healthy controls (n=46) were stimulated with LPS/ATP to induce NLRP3 activation with or without the autophagy inducer, rapamycin.	Adenosine Triphosphate	126-129	NLR family pyrin domain containing 3	Homo sapiens	140-145
35038351-5	2022	METHODS: Peripheral blood CD14+ monocytes from asthmatic patients (n=83) and healthy controls (n=46) were stimulated with LPS/ATP to induce NLRP3 activation with or without the autophagy inducer, rapamycin.	Sirolimus	196-205	NLR family pyrin domain containing 3	Homo sapiens	140-145
35022393-2	2022	Calcium activates the NLRP3-inflammasome via the calcium-sensing receptor in monocytes/macrophages primed by lipopolysaccharide, and this effect is mediated by the uptake of calciprotein particles (CPPs) formed out of calcium, phosphate, and fetuin-A.	Calcium	0-7	NLR family pyrin domain containing 3	Homo sapiens	22-27
35022393-2	2022	Calcium activates the NLRP3-inflammasome via the calcium-sensing receptor in monocytes/macrophages primed by lipopolysaccharide, and this effect is mediated by the uptake of calciprotein particles (CPPs) formed out of calcium, phosphate, and fetuin-A.	Calcium	218-225	NLR family pyrin domain containing 3	Homo sapiens	22-27
35022393-2	2022	Calcium activates the NLRP3-inflammasome via the calcium-sensing receptor in monocytes/macrophages primed by lipopolysaccharide, and this effect is mediated by the uptake of calciprotein particles (CPPs) formed out of calcium, phosphate, and fetuin-A.	Phosphates	227-236	NLR family pyrin domain containing 3	Homo sapiens	22-27
35095532-4	2021	In this study, we have found that PL is a natural inhibitor of Nod-like receptor family pyrin domain-containing protein-3 (NLRP3) inflammasome, an intracellular multi-protein complex that orchestrates host immune responses to infections or sterile inflammations.	piperlonguminine	34-36	NLR family pyrin domain containing 3	Homo sapiens	63-121
35095532-4	2021	In this study, we have found that PL is a natural inhibitor of Nod-like receptor family pyrin domain-containing protein-3 (NLRP3) inflammasome, an intracellular multi-protein complex that orchestrates host immune responses to infections or sterile inflammations.	piperlonguminine	34-36	NLR family pyrin domain containing 3	Homo sapiens	123-128
35095532-5	2021	PL blocks NLRP3 activity by disrupting the assembly of NLRP3 inflammasome including the association between NLRP3 and NEK7 and subsequent NLRP3 oligomerization.	piperlonguminine	0-2	NLR family pyrin domain containing 3	Homo sapiens	10-15
35095532-5	2021	PL blocks NLRP3 activity by disrupting the assembly of NLRP3 inflammasome including the association between NLRP3 and NEK7 and subsequent NLRP3 oligomerization.	piperlonguminine	0-2	NLR family pyrin domain containing 3	Homo sapiens	55-60
35095532-5	2021	PL blocks NLRP3 activity by disrupting the assembly of NLRP3 inflammasome including the association between NLRP3 and NEK7 and subsequent NLRP3 oligomerization.	piperlonguminine	0-2	NLR family pyrin domain containing 3	Homo sapiens	108-113
35095532-5	2021	PL blocks NLRP3 activity by disrupting the assembly of NLRP3 inflammasome including the association between NLRP3 and NEK7 and subsequent NLRP3 oligomerization.	piperlonguminine	0-2	NLR family pyrin domain containing 3	Homo sapiens	138-143
35095532-6	2021	Furthermore, PL suppressed lipopolysaccharide-induced endotoxemia and MSU-induced peritonitis in vivo, which are NLRP3-dependent inflammation.	piperlonguminine	13-15	NLR family pyrin domain containing 3	Homo sapiens	113-118
35095532-7	2021	Thus, our study identified PL as an inhibitor of NLRP3 inflammasome and indicated the potential application of PL in NLRP3-relevant diseases.	piperlonguminine	27-29	NLR family pyrin domain containing 3	Homo sapiens	49-54
34874326-0	2022	PEG-PEI/siROCK2 inhibits Abeta42-induced microglial inflammation via NLRP3/caspase 1 pathway.	poly(ethylene glycol)-co-poly(ethyleneimine)	0-7	NLR family pyrin domain containing 3	Homo sapiens	69-74
35013104-8	2022	In vivo blocking Nlrp3 inflammasome activation prevents IVDD progression induced by Kindlin-2 loss and abnormal mechanical stress.	ivdd	56-60	NLR family pyrin domain containing 3	Homo sapiens	17-22
35000611-4	2022	Recently it has been established that CCH can activate the inflammasome signaling pathways, involving NLRP3 and AIM2 inflammasomes that critically regulate IL-1beta production.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	38-41	NLR family pyrin domain containing 3	Homo sapiens	102-107
35052628-3	2022	This review focuses on the potential applications of CA and CS for Alzheimer"s disease (AD), Parkinson"s disease (PD), and coronavirus disease 2019 (COVID-19), in part via inhibition of the NLRP3 inflammasome.	carnosol	60-62	NLR family pyrin domain containing 3	Homo sapiens	190-195
35052789-0	2022	Macrophages Modulate Hepatic Injury Involving NLRP3 Inflammasome: The Example of Efavirenz.	efavirenz	81-90	NLR family pyrin domain containing 3	Homo sapiens	46-51
35052789-2	2022	Efavirenz, an anti-HIV drug, induces deleterious actions in hepatocytes that could underlie induction of the NLRP3 inflammasome, an important regulator of inflammatory responses during liver injury.	efavirenz	0-9	NLR family pyrin domain containing 3	Homo sapiens	109-114
35052789-5	2022	Efavirenz triggered inflammation in hepatocytes, in a process that involved NF-kappaB and the NLRP3 inflammasome, and activated hepatic stellate cells (HSCs), thereby enhancing expression of inflammatory and fibrogenic markers.	efavirenz	0-9	NLR family pyrin domain containing 3	Homo sapiens	94-99
35052789-8	2022	Efavirenz elicits a cell-specific activation of the NLRP3 inflammasome in hepatocytes and HSCs, but macrophages appear to counteract efavirenz-induced liver injury.	efavirenz	0-9	NLR family pyrin domain containing 3	Homo sapiens	52-57
34983566-0	2022	Skin damage induced by zinc oxide nanoparticles combined with UVB is mediated by activating cell pyroptosis via the NLRP3 inflammasome-autophagy-exosomal pathway.	Zinc Oxide	23-33	NLR family pyrin domain containing 3	Homo sapiens	116-121
34874326-0	2022	PEG-PEI/siROCK2 inhibits Abeta42-induced microglial inflammation via NLRP3/caspase 1 pathway.	sirock2	8-15	NLR family pyrin domain containing 3	Homo sapiens	69-74
34983566-9	2022	Topical application of pterostilbene attenuates NLRP3 inflammasome activation and pyroptosis by decreasing ROS generation and mitochondrial ROS (mtROS) levels.	pterostilbene	23-36	NLR family pyrin domain containing 3	Homo sapiens	48-53
34983566-10	2022	In addition to its antioxidant effect, PT also reversed autophagy abnormalities by restoring normal autophagic flux and decreasing NLRP3 inflammasome-loaded exosome release.	pterostilbene	39-41	NLR family pyrin domain containing 3	Homo sapiens	131-136
34874326-12	2022	In addition, we found that PPSR suppressed the Abeta-induced NLRP3/caspase 1 pathway in primary microglial cells.	UNII-042A8N37WH	47-52	NLR family pyrin domain containing 3	Homo sapiens	61-66
35127957-6	2022	Piperine also regulates multiple signaling pathways such as Akt/mTOR/MMP-9, 5"-AMP-activated protein kinase-activated NLR family pyrin domain containing-3 inflammasome, voltage-gated K+ current, PKCalpha/ERK1/2, NF-kappaB/AP-1/MMP-9, Wnt/beta-catenin, JNK/P38 MAPK, and gut microbiota.	piperine	0-8	NLR family pyrin domain containing 3	Homo sapiens	118-154
34982235-11	2022	Thus, it indicated the role of Th1 response acting through the NLRP3 pathway which might have been helpful in the recovery of AVH patients.	2-(beta-D-glucosyl)benzothiazole	31-34	NLR family pyrin domain containing 3	Homo sapiens	63-68
34964706-4	2022	Mirtazapine prevented isoflurane-induced production of the pro-inflammatory factors interleukin (IL)-1beta and IL-18 by inhibiting the activation of the nod-like receptor family protein 3 (NLRP3) inflammasome in BV2 microglia.	Mirtazapine	0-11	NLR family pyrin domain containing 3	Homo sapiens	153-187
34964706-4	2022	Mirtazapine prevented isoflurane-induced production of the pro-inflammatory factors interleukin (IL)-1beta and IL-18 by inhibiting the activation of the nod-like receptor family protein 3 (NLRP3) inflammasome in BV2 microglia.	Mirtazapine	0-11	NLR family pyrin domain containing 3	Homo sapiens	189-194
34964706-4	2022	Mirtazapine prevented isoflurane-induced production of the pro-inflammatory factors interleukin (IL)-1beta and IL-18 by inhibiting the activation of the nod-like receptor family protein 3 (NLRP3) inflammasome in BV2 microglia.	Isoflurane	22-32	NLR family pyrin domain containing 3	Homo sapiens	189-194
35062292-3	2022	It has been suggested that in the presence of stress molecules such as nigericin, the trans-Golgi network (TGN) disperses into small puncta-like structures where NLRP3 is recruited and activated.	Nigericin	71-80	NLR family pyrin domain containing 3	Homo sapiens	162-167
35047512-3	2021	NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3), a tripartite protein, contains three functional domains a central nucleotide-binding and oligomerization domain (NACHT), an N-terminal pyrin domain (PYD), and a leucine-rich repeat domain (LRR).	Leucine	228-235	NLR family pyrin domain containing 3	Homo sapiens	0-57
35047512-3	2021	NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3), a tripartite protein, contains three functional domains a central nucleotide-binding and oligomerization domain (NACHT), an N-terminal pyrin domain (PYD), and a leucine-rich repeat domain (LRR).	Leucine	228-235	NLR family pyrin domain containing 3	Homo sapiens	59-64
34918381-0	2022	SGLT2 inhibitor counteracts NLRP3 inflammasome via tubular metabolite itaconate in fibrosis kidney.	itaconic acid	70-79	NLR family pyrin domain containing 3	Homo sapiens	28-33
34918381-6	2022	Notably, NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation was strikingly blocked by dapagliflozin.	dapagliflozin	117-130	NLR family pyrin domain containing 3	Homo sapiens	9-58
34918381-6	2022	Notably, NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation was strikingly blocked by dapagliflozin.	dapagliflozin	117-130	NLR family pyrin domain containing 3	Homo sapiens	60-65
35081536-0	2022	Mechanism of miRNA-141-3p in calcium oxalate-induced renal tubular epithelial cell injury via NLRP3-mediated pyroptosis.	mirna-141-3p	13-25	NLR family pyrin domain containing 3	Homo sapiens	94-99
35081536-0	2022	Mechanism of miRNA-141-3p in calcium oxalate-induced renal tubular epithelial cell injury via NLRP3-mediated pyroptosis.	Calcium Oxalate	29-44	NLR family pyrin domain containing 3	Homo sapiens	94-99
35081536-9	2022	The binding of miR-141-3p and NLRP3 was validated using a dual-luciferase assay.	-141-3p	18-25	NLR family pyrin domain containing 3	Homo sapiens	30-35
35081536-10	2022	The role of NLRP3 in the protection of miR-141-3p on RTEC injury was verified using functional rescue experiments.	mir-141-3p	39-49	NLR family pyrin domain containing 3	Homo sapiens	12-17
35237974-5	2022	Importantly, activation of the nucleotide oligomerization domain leucine-rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome activates the caspase-1 protease and results in the generation and release of potent pro-inflammatory cytokines, IL-1beta and IL-18.	Leucine	65-72	NLR family pyrin domain containing 3	Homo sapiens	124-129
35081536-15	2022	miR-141-3p bound to NLRP3 and thereby repressed NLRP3 expression.	mir-141-3p	0-10	NLR family pyrin domain containing 3	Homo sapiens	20-25
35081536-15	2022	miR-141-3p bound to NLRP3 and thereby repressed NLRP3 expression.	mir-141-3p	0-10	NLR family pyrin domain containing 3	Homo sapiens	48-53
35081536-17	2022	CONCLUSION: miR-141-3p repressed NLRP3-mediated pyroptosis by suppressing NLRP3 expression, thus protecting CaOx crystals-induced RTEC injury.	mir-141-3p	12-22	NLR family pyrin domain containing 3	Homo sapiens	33-38
35081536-17	2022	CONCLUSION: miR-141-3p repressed NLRP3-mediated pyroptosis by suppressing NLRP3 expression, thus protecting CaOx crystals-induced RTEC injury.	mir-141-3p	12-22	NLR family pyrin domain containing 3	Homo sapiens	74-79
35559886-2	2022	More and more research has indicated that fine particulate matter (PM2.5) plays a critical role in causing pulmonary inflammation or fibrosis, which potentially is ascribed to the activation of nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome.	Leucine	224-231	NLR family pyrin domain containing 3	Homo sapiens	255-260
35559886-5	2022	It was found that aggregated size and PAHs could activate the NLRP3 inflammasome through lysosome rupture and potassium efflux, respectively.	Potassium	110-119	NLR family pyrin domain containing 3	Homo sapiens	62-67
35559886-6	2022	Metal ion, PAHs and surface ROS could also activate the NLRP3 inflammasome through mitochondrial ROS production.	Metals	0-5	NLR family pyrin domain containing 3	Homo sapiens	56-61
35559886-6	2022	Metal ion, PAHs and surface ROS could also activate the NLRP3 inflammasome through mitochondrial ROS production.	Reactive Oxygen Species	28-31	NLR family pyrin domain containing 3	Homo sapiens	56-61
35559886-6	2022	Metal ion, PAHs and surface ROS could also activate the NLRP3 inflammasome through mitochondrial ROS production.	Reactive Oxygen Species	97-100	NLR family pyrin domain containing 3	Homo sapiens	56-61
35264201-7	2022	Mechanistically, the ketone body beta-hydroxybutyrate (BHB) deactivated the activation of NLRP3 inflammasome triggered by CoCrMo alloy particles.	3-Hydroxybutyric Acid	33-53	NLR family pyrin domain containing 3	Homo sapiens	90-95
35264201-7	2022	Mechanistically, the ketone body beta-hydroxybutyrate (BHB) deactivated the activation of NLRP3 inflammasome triggered by CoCrMo alloy particles.	3-Hydroxybutyric Acid	55-58	NLR family pyrin domain containing 3	Homo sapiens	90-95
35212949-3	2022	In this chapter, we present a method to monitor NLRP3 or pyrin inflammasome activation in human monocytes upon extracellular ATP or Clostridium difficile toxin B treatment, respectively, by detecting intracellular oligomers of ASC by flow cytometry.	Adenosine Triphosphate	125-128	NLR family pyrin domain containing 3	Homo sapiens	48-53
35212954-2	2022	Specifically, mitochondrial dysfunction can induce NLRP3 inflammasome activation, where loss of mitochondrial potential leads to production of reactive oxygen species (ROS) and release of Ca2+, which in turn trigger inflammasome assembly.	Reactive Oxygen Species	143-166	NLR family pyrin domain containing 3	Homo sapiens	51-56
35212954-2	2022	Specifically, mitochondrial dysfunction can induce NLRP3 inflammasome activation, where loss of mitochondrial potential leads to production of reactive oxygen species (ROS) and release of Ca2+, which in turn trigger inflammasome assembly.	Reactive Oxygen Species	168-171	NLR family pyrin domain containing 3	Homo sapiens	51-56
35212957-1	2022	Potassium ion (K+) efflux is often considered as an upstream signaling event of NLRP3 activation.	Potassium	0-9	NLR family pyrin domain containing 3	Homo sapiens	80-85
35212958-2	2022	NLRP3 (the NOD, LRR, and pyrin domain-containing protein 3), which initiates the formation of an NLRP3 inflammasome complex, is regulated posttranslationally by phosphorylation at several Ser and Tyr residues.	Serine	188-191	NLR family pyrin domain containing 3	Homo sapiens	0-5
35212958-2	2022	NLRP3 (the NOD, LRR, and pyrin domain-containing protein 3), which initiates the formation of an NLRP3 inflammasome complex, is regulated posttranslationally by phosphorylation at several Ser and Tyr residues.	Tyrosine	196-199	NLR family pyrin domain containing 3	Homo sapiens	0-5
35212958-2	2022	NLRP3 (the NOD, LRR, and pyrin domain-containing protein 3), which initiates the formation of an NLRP3 inflammasome complex, is regulated posttranslationally by phosphorylation at several Ser and Tyr residues.	Tyrosine	196-199	NLR family pyrin domain containing 3	Homo sapiens	97-102
35212958-7	2022	This method can also be adapted to detect modified Ser or Thr residues and is an ideal screening assay to map phospho residues in NLRP3 or other proteins.	Threonine	58-61	NLR family pyrin domain containing 3	Homo sapiens	130-135