PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34951978-0	2022	Pinocembrin ameliorates acute liver failure via activating the Sirt1/PPARalpha pathway in vitro and in vivo.	pinocembrin	0-11	sirtuin 1	Homo sapiens	63-68
34951978-0	2022	Pinocembrin ameliorates acute liver failure via activating the Sirt1/PPARalpha pathway in vitro and in vivo.	pinocembrin	0-11	peroxisome proliferator activated receptor alpha	Homo sapiens	69-78
34951978-7	2022	Pinocembrin inhibited the hepatocyte apoptosis and pro-inflammatory reaction of peritoneal macrophages by reducing reactive oxygen species (ROS) via the Sirt1/PPARalpha signaling pathway.	pinocembrin	0-11	sirtuin 1	Homo sapiens	153-158
34951978-7	2022	Pinocembrin inhibited the hepatocyte apoptosis and pro-inflammatory reaction of peritoneal macrophages by reducing reactive oxygen species (ROS) via the Sirt1/PPARalpha signaling pathway.	pinocembrin	0-11	peroxisome proliferator activated receptor alpha	Homo sapiens	159-168
34338973-0	2021	Pinocembrin pretreatment counteracts the chlorpyrifos-induced HO-1 downregulation, mitochondrial dysfunction, and inflammation in the SH-SY5Y cells.	pinocembrin	0-11	heme oxygenase 1	Homo sapiens	62-66
34338973-8	2021	Silencing of Nrf2 or inhibition of HO-1 suppressed the PB-induced effects in the CPF-challenged cells.	pinocembrin	55-57	NFE2 like bZIP transcription factor 2	Homo sapiens	13-17
34338973-8	2021	Silencing of Nrf2 or inhibition of HO-1 suppressed the PB-induced effects in the CPF-challenged cells.	pinocembrin	55-57	heme oxygenase 1	Homo sapiens	35-39
34338973-9	2021	Thus, PB promoted beneficial effects by a mechanism dependent on the Nrf2/HO-1/CO + BR axis in the CPF-treated cells.	pinocembrin	6-8	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
34338973-9	2021	Thus, PB promoted beneficial effects by a mechanism dependent on the Nrf2/HO-1/CO + BR axis in the CPF-treated cells.	pinocembrin	6-8	heme oxygenase 1	Homo sapiens	74-78
34488618-0	2021	Pinocembrin ameliorates post-infarct heart failure through activation of Nrf2/HO-1 signaling pathway.	pinocembrin	0-11	NFE2 like bZIP transcription factor 2	Rattus norvegicus	73-77
34488618-0	2021	Pinocembrin ameliorates post-infarct heart failure through activation of Nrf2/HO-1 signaling pathway.	pinocembrin	0-11	heme oxygenase 1	Rattus norvegicus	78-82
34336656-0	2021	Pinocembrin Inhibits the Proliferation and Metastasis of Breast Cancer via Suppression of the PI3K/AKT Signaling Pathway.	pinocembrin	0-11	AKT serine/threonine kinase 1	Homo sapiens	99-102
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	cyclin B1	Homo sapiens	112-120
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	cyclin dependent kinase 1	Homo sapiens	122-126
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	128-133
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	BCL2 apoptosis regulator	Homo sapiens	135-140
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	198-203
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	caspase 3	Homo sapiens	213-221
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	caspase 9	Homo sapiens	231-239
34336656-7	2021	PCB downregulated the expression levels of proteins involved in cell cycle progression and apoptosis, including cyclinB1, Cdc2, PARP1, Bcl-2, and survivin, and upregulated protein levels of cleaved PARP1, cleaved caspase3, cleaved caspase9, and BAX.	pinocembrin	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	245-248
34336656-10	2021	Mechanistically, PCB administration was correlated to suppression of the PI3K/AKT signaling pathway.	pinocembrin	17-20	AKT serine/threonine kinase 1	Homo sapiens	78-81
33752080-6	2021	The cardiac injury evidenced by LDH and CK-MB activities were reduced while the levels of IL-1beta and IL-18 were decreased following PCB treatment compared to DOX-treated mice.	pinocembrin	134-137	interleukin 1 alpha	Mus musculus	90-98
34060409-2	2021	The time-dependent inhibition of CYP3A4 by acacetin, apigenin, chrysin, and pinocembrin was experimentally detected, but not entirely elaborated so far.	pinocembrin	76-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
34986062-8	2022	Up-regulated substance P and Tacr1 were induced after hip fracture, which could be reversed by PCN treatment.	pinocembrin	95-98	tachykinin receptor 1	Rattus norvegicus	29-34
33752080-6	2021	The cardiac injury evidenced by LDH and CK-MB activities were reduced while the levels of IL-1beta and IL-18 were decreased following PCB treatment compared to DOX-treated mice.	pinocembrin	134-137	interleukin 18	Mus musculus	103-108
33752080-7	2021	Mechanically, our present results showed that PCB significantly inhibited DOX-induced cardiomyocyte pyroptosis via activating Nrf2/Sirt3 signal pathway.	pinocembrin	46-49	nuclear factor, erythroid derived 2, like 2	Mus musculus	126-130
33752080-7	2021	Mechanically, our present results showed that PCB significantly inhibited DOX-induced cardiomyocyte pyroptosis via activating Nrf2/Sirt3 signal pathway.	pinocembrin	46-49	sirtuin 3	Rattus norvegicus	131-136
33752080-8	2021	Furthermore, the inhibition of Nrf2 in H9c2 cells abolished the protective role of PCB against DOX-induced cell toxicity, which was at least partly via upregulation of NLRP3-mediated pyroptosis.	pinocembrin	83-86	NFE2 like bZIP transcription factor 2	Rattus norvegicus	31-35
33752080-8	2021	Furthermore, the inhibition of Nrf2 in H9c2 cells abolished the protective role of PCB against DOX-induced cell toxicity, which was at least partly via upregulation of NLRP3-mediated pyroptosis.	pinocembrin	83-86	NLR family, pyrin domain containing 3	Rattus norvegicus	168-173
33859344-3	2021	Recent evidence shows that pinocembrin, a natural flavonoid compound, exerts anti-cerebral ischemia effect and expands the time window of t-PA.	pinocembrin	27-38	plasminogen activator, tissue type	Homo sapiens	138-142
33859344-6	2021	Administration of pinocembrin (10 mg/kg, iv) prior t-PA infusion significantly decreased the infarct volume, ameliorated t-PA-induced HT, and protected blood-brain barrier.	pinocembrin	18-29	plasminogen activator, tissue type	Rattus norvegicus	51-55
33393179-8	2021	Finally, the activity of CYP1A1 and Src in lung tissues from mice supplemented with PCB was noticeably decreased and lower than that in lung tissues from mice supplemented with B(a)P alone.	pinocembrin	84-87	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	25-31
33393179-0	2021	Pinocembrin attenuates benzo(a)pyrene-induced CYP1A1 expression through multiple pathways: An in vitro and in vivo study.	pinocembrin	0-11	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	46-52
33393179-5	2021	The aim of this investigation is to examine the potential ability of a flavonoid pinocembrin (PCB) to alleviate B(a)P toxicity and analyze the underlying molecular mechanisms.	pinocembrin	94-97	prohibitin 2	Mus musculus	112-117
33393179-6	2021	We found that PCB inhibited DNA adduct formation by attenuating CYP1A1 expression through the suppression of the AhR/Src/ERK pathways.	pinocembrin	14-17	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	64-70
33859344-6	2021	Administration of pinocembrin (10 mg/kg, iv) prior t-PA infusion significantly decreased the infarct volume, ameliorated t-PA-induced HT, and protected blood-brain barrier.	pinocembrin	18-29	plasminogen activator, tissue type	Rattus norvegicus	121-125
33393179-8	2021	Finally, the activity of CYP1A1 and Src in lung tissues from mice supplemented with PCB was noticeably decreased and lower than that in lung tissues from mice supplemented with B(a)P alone.	pinocembrin	84-87	Rous sarcoma oncogene	Mus musculus	36-39
33393179-8	2021	Finally, the activity of CYP1A1 and Src in lung tissues from mice supplemented with PCB was noticeably decreased and lower than that in lung tissues from mice supplemented with B(a)P alone.	pinocembrin	84-87	prohibitin 2	Mus musculus	177-182
33781824-0	2021	Pinocembrin alleviates lipopolysaccharide-induced myocardial injury and cardiac dysfunction in rats by inhibiting p38/JNK MAPK pathway.	pinocembrin	0-11	mitogen activated protein kinase 14	Rattus norvegicus	114-117
33393179-6	2021	We found that PCB inhibited DNA adduct formation by attenuating CYP1A1 expression through the suppression of the AhR/Src/ERK pathways.	pinocembrin	14-17	aryl-hydrocarbon receptor	Mus musculus	113-116
33393179-6	2021	We found that PCB inhibited DNA adduct formation by attenuating CYP1A1 expression through the suppression of the AhR/Src/ERK pathways.	pinocembrin	14-17	Rous sarcoma oncogene	Mus musculus	117-120
33393179-6	2021	We found that PCB inhibited DNA adduct formation by attenuating CYP1A1 expression through the suppression of the AhR/Src/ERK pathways.	pinocembrin	14-17	mitogen-activated protein kinase 1	Mus musculus	121-124
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	prohibitin 2	Mus musculus	18-23
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	Rous sarcoma oncogene	Mus musculus	57-60
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	mitogen-activated protein kinase 3	Mus musculus	65-71
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	94-100
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	prohibitin 2	Mus musculus	129-134
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	158-167
33393179-7	2021	PCB mitigated the B(a)P-stimulated DNA damage, inhibited Src and ERK1/2 expression, decreased CYP1A1 expression, and reduced the B(a)P-induced stimulation of NF-kappaB and MAPK signaling in lung epithelial cells.	pinocembrin	0-3	mitogen-activated protein kinase 1	Mus musculus	172-176
33290968-0	2021	Pinocembrin relieves lipopolysaccharide and bleomycin induced lung inflammation via inhibiting TLR4-NF-kappaB-NLRP3 inflammasome signaling pathway.	pinocembrin	0-11	toll-like receptor 4	Mus musculus	95-99
33739886-0	2021	Pinocembrin Reduces Arthritic Symptoms in Mouse Model via Targeting Sox4 Signaling Molecules.	pinocembrin	0-11	SRY (sex determining region Y)-box 4	Mus musculus	68-72
33739886-6	2021	Biochemically, PCB interacts with the transcription factor, SRY-related HMG-box 4 (Sox4), and then modulates its dysregulated expression and the expression of Sox4/Stat3 signaling molecules in AIA mice.	pinocembrin	15-18	SRY (sex determining region Y)-box 4	Mus musculus	60-81
33739886-6	2021	Biochemically, PCB interacts with the transcription factor, SRY-related HMG-box 4 (Sox4), and then modulates its dysregulated expression and the expression of Sox4/Stat3 signaling molecules in AIA mice.	pinocembrin	15-18	SRY (sex determining region Y)-box 4	Mus musculus	83-87
33739886-6	2021	Biochemically, PCB interacts with the transcription factor, SRY-related HMG-box 4 (Sox4), and then modulates its dysregulated expression and the expression of Sox4/Stat3 signaling molecules in AIA mice.	pinocembrin	15-18	SRY (sex determining region Y)-box 4	Mus musculus	159-163
33739886-6	2021	Biochemically, PCB interacts with the transcription factor, SRY-related HMG-box 4 (Sox4), and then modulates its dysregulated expression and the expression of Sox4/Stat3 signaling molecules in AIA mice.	pinocembrin	15-18	signal transducer and activator of transcription 3	Mus musculus	164-169
33739886-8	2021	The possible PCB interaction with Sox4 transcriptional protein was confirmed through molecular docking where three hydrogen bonds were formed at ARG and LYS residues at a stable binding energy of -4.72.	pinocembrin	13-16	SRY (sex determining region Y)-box 4	Mus musculus	34-38
33290968-0	2021	Pinocembrin relieves lipopolysaccharide and bleomycin induced lung inflammation via inhibiting TLR4-NF-kappaB-NLRP3 inflammasome signaling pathway.	pinocembrin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-109
33290968-0	2021	Pinocembrin relieves lipopolysaccharide and bleomycin induced lung inflammation via inhibiting TLR4-NF-kappaB-NLRP3 inflammasome signaling pathway.	pinocembrin	0-11	NLR family, pyrin domain containing 3	Mus musculus	110-115
31947997-10	2020	The study confirms the existence of the link between TPC and color, and it shows that there is a correlation between pinocembrin and galangin, two compounds that are reported to ameliorate insulin resistance.	pinocembrin	117-128	insulin	Homo sapiens	189-196
33176803-0	2020	Pinocembrin ameliorates intermittent hypoxia-induced neuroinflammation through BNIP3-dependent mitophagy in a murine model of sleep apnea.	pinocembrin	0-11	BCL2/adenovirus E1B interacting protein 3	Mus musculus	79-84
33176803-11	2020	Pinocembrin treatment significantly inhibited the formation of NLRP3 inflammasome and infiltration of microglia and enhanced BNIP3-mediated mitophagy in the hippocampus of IH mice.	pinocembrin	0-11	NLR family, pyrin domain containing 3	Mus musculus	63-68
33176803-11	2020	Pinocembrin treatment significantly inhibited the formation of NLRP3 inflammasome and infiltration of microglia and enhanced BNIP3-mediated mitophagy in the hippocampus of IH mice.	pinocembrin	0-11	BCL2/adenovirus E1B interacting protein 3	Mus musculus	125-130
32470335-0	2020	Pinocembrin alleviates glucocorticoid-induced apoptosis by activating autophagy via suppressing the PI3K/Akt/mTOR pathway in osteocytes.	pinocembrin	0-11	thymoma viral proto-oncogene 1	Mus musculus	105-108
32470335-0	2020	Pinocembrin alleviates glucocorticoid-induced apoptosis by activating autophagy via suppressing the PI3K/Akt/mTOR pathway in osteocytes.	pinocembrin	0-11	mechanistic target of rapamycin kinase	Mus musculus	109-113
32460706-12	2020	Moreover, PB activated Nrf2/HO-1 signal pathway but inhibited the phosphorylation of NF-kB.	pinocembrin	10-12	nuclear factor, erythroid derived 2, like 2	Mus musculus	23-27
32460706-12	2020	Moreover, PB activated Nrf2/HO-1 signal pathway but inhibited the phosphorylation of NF-kB.	pinocembrin	10-12	heme oxygenase 1	Mus musculus	28-32
31704291-7	2019	Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-kappaBalpha (IkappaBalpha) and the activation of nuclear factor-kappa B (NF-kappaB)subunit p65.	pinocembrin	13-24	gap junction protein, alpha 1	Rattus norvegicus	84-88
31634778-5	2019	CCK8 assay, cell scratch assay and Annexin V-FITC/PI staining found that when pinocembrin concentration reached 100 muM and the treatment time reached 48 h, pinocembrin could inhibit the cell proliferation and migration and promote the cell apoptosis, and this effect was enhanced with the increase of pinocembrin concentration.	pinocembrin	157-168	annexin A5	Homo sapiens	35-44
31634778-5	2019	CCK8 assay, cell scratch assay and Annexin V-FITC/PI staining found that when pinocembrin concentration reached 100 muM and the treatment time reached 48 h, pinocembrin could inhibit the cell proliferation and migration and promote the cell apoptosis, and this effect was enhanced with the increase of pinocembrin concentration.	pinocembrin	157-168	annexin A5	Homo sapiens	35-44
31704291-6	2019	Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6 in the serum and the left atrial (LA).	pinocembrin	30-41	tumor necrosis factor	Rattus norvegicus	418-445
31704291-6	2019	Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6 in the serum and the left atrial (LA).	pinocembrin	30-41	tumor necrosis factor	Rattus norvegicus	447-456
31704291-7	2019	Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-kappaBalpha (IkappaBalpha) and the activation of nuclear factor-kappa B (NF-kappaB)subunit p65.	pinocembrin	13-24	NFKB inhibitor alpha	Rattus norvegicus	161-173
31814878-0	2019	The Nrf2/HO-1 Axis as Targets for Flavanones: Neuroprotection by Pinocembrin, Naringenin, and Eriodictyol.	pinocembrin	65-76	NFE2 like bZIP transcription factor 2	Homo sapiens	4-8
31704291-6	2019	Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6 in the serum and the left atrial (LA).	pinocembrin	30-41	interleukin 1 beta	Rattus norvegicus	459-481
31704291-6	2019	Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6 in the serum and the left atrial (LA).	pinocembrin	30-41	interleukin 6	Rattus norvegicus	486-490
31814878-0	2019	The Nrf2/HO-1 Axis as Targets for Flavanones: Neuroprotection by Pinocembrin, Naringenin, and Eriodictyol.	pinocembrin	65-76	heme oxygenase 1	Homo sapiens	9-13
29807112-6	2018	Furthermore, we discovered that pinocembrin suppressed autophagy through the activation of PI3K/Akt/mTOR pathway, which serves as a dual mechanism to enhance the pro-death effect of pinocembrin.	pinocembrin	32-43	AKT serine/threonine kinase 1	Homo sapiens	96-99
31035509-0	2019	Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin.	pinocembrin	0-11	insulin	Homo sapiens	97-104
31035509-3	2019	Pinocembrin, the most abundant flavonoid in propolis, has been recently proven to interfere with RAGE activation in Abeta-RAGE-induced toxicity.	pinocembrin	0-11	advanced glycosylation end-product specific receptor	Homo sapiens	97-101
31035509-3	2019	Pinocembrin, the most abundant flavonoid in propolis, has been recently proven to interfere with RAGE activation in Abeta-RAGE-induced toxicity.	pinocembrin	0-11	advanced glycosylation end-product specific receptor	Homo sapiens	122-126
29914794-5	2018	Mechanistically, pinocembrin suppresses activation of the MAPK kinase p38 and NF-kappaB pathways in the context of ox-LDL.	pinocembrin	17-28	mitogen-activated protein kinase 14	Homo sapiens	70-73
29914794-5	2018	Mechanistically, pinocembrin suppresses activation of the MAPK kinase p38 and NF-kappaB pathways in the context of ox-LDL.	pinocembrin	17-28	nuclear factor kappa B subunit 1	Homo sapiens	78-87
30420897-0	2018	Galangin and Pinocembrin from Propolis Ameliorate Insulin Resistance in HepG2 Cells via Regulating Akt/mTOR Signaling.	pinocembrin	13-24	insulin	Homo sapiens	50-57
30420897-0	2018	Galangin and Pinocembrin from Propolis Ameliorate Insulin Resistance in HepG2 Cells via Regulating Akt/mTOR Signaling.	pinocembrin	13-24	AKT serine/threonine kinase 1	Homo sapiens	99-102
30420897-0	2018	Galangin and Pinocembrin from Propolis Ameliorate Insulin Resistance in HepG2 Cells via Regulating Akt/mTOR Signaling.	pinocembrin	13-24	mechanistic target of rapamycin kinase	Homo sapiens	103-107
30420897-4	2018	Galangin and pinocembrin treatments substantially increase glucose consumption and glycogen content by enhancing the activities of hexokinase and pyruvate kinase.	pinocembrin	13-24	hexokinase 1	Homo sapiens	131-141
30420897-7	2018	Most notably, this is the first study to our knowledge to investigate pinocembrin about the alleviation of insulin resistance.	pinocembrin	70-81	insulin	Homo sapiens	107-114
29807112-6	2018	Furthermore, we discovered that pinocembrin suppressed autophagy through the activation of PI3K/Akt/mTOR pathway, which serves as a dual mechanism to enhance the pro-death effect of pinocembrin.	pinocembrin	182-193	mechanistic target of rapamycin kinase	Homo sapiens	100-104
29807112-6	2018	Furthermore, we discovered that pinocembrin suppressed autophagy through the activation of PI3K/Akt/mTOR pathway, which serves as a dual mechanism to enhance the pro-death effect of pinocembrin.	pinocembrin	32-43	mechanistic target of rapamycin kinase	Homo sapiens	100-104
29807112-6	2018	Furthermore, we discovered that pinocembrin suppressed autophagy through the activation of PI3K/Akt/mTOR pathway, which serves as a dual mechanism to enhance the pro-death effect of pinocembrin.	pinocembrin	182-193	AKT serine/threonine kinase 1	Homo sapiens	96-99
29850586-3	2018	In this study, we sought to determine the effect of pinocembrin (PCB; a pleiotropic neuroprotective agent) on t-PA administration-induced BBB damage in a novel rat thromboembolic stroke model.	pinocembrin	52-63	plasminogen activator, tissue type	Rattus norvegicus	110-114
30022020-0	2018	Effects of Pinocembrin Pretreatment on Connexin 43 (Cx43) Protein Expression After Rat Myocardial Ischemia-Reperfusion and Cardiac Arrhythmia.	pinocembrin	11-22	gap junction protein, alpha 1	Rattus norvegicus	39-50
30022020-0	2018	Effects of Pinocembrin Pretreatment on Connexin 43 (Cx43) Protein Expression After Rat Myocardial Ischemia-Reperfusion and Cardiac Arrhythmia.	pinocembrin	11-22	gap junction protein, alpha 1	Rattus norvegicus	52-56
28745105-4	2018	This study is aimed at an evaluation of the inhibitory potency of selected food honey flavonoids (namely galangin, myricetin, pinocembrin, pinobanksin, chrysin and fisetin) toward hOATP2B1 and hOATP1A2 as well as at examining their effect on the cellular uptake of the known OATP substrate rosuvastatin.	pinocembrin	126-137	solute carrier organic anion transporter family member 2B1	Homo sapiens	180-188
28745105-4	2018	This study is aimed at an evaluation of the inhibitory potency of selected food honey flavonoids (namely galangin, myricetin, pinocembrin, pinobanksin, chrysin and fisetin) toward hOATP2B1 and hOATP1A2 as well as at examining their effect on the cellular uptake of the known OATP substrate rosuvastatin.	pinocembrin	126-137	solute carrier organic anion transporter family member 1A2	Homo sapiens	181-185
28745105-8	2018	Chrysin, galangin and pinocembrin were found to inhibit both hOATP2B1 and hOATP1A2 in lower or comparable concentrations as the known flavonoid OATP inhibitor quercetin.	pinocembrin	22-33	solute carrier organic anion transporter family member 2B1	Homo sapiens	61-69
28745105-8	2018	Chrysin, galangin and pinocembrin were found to inhibit both hOATP2B1 and hOATP1A2 in lower or comparable concentrations as the known flavonoid OATP inhibitor quercetin.	pinocembrin	22-33	solute carrier organic anion transporter family member 1A2	Homo sapiens	74-82
28745105-8	2018	Chrysin, galangin and pinocembrin were found to inhibit both hOATP2B1 and hOATP1A2 in lower or comparable concentrations as the known flavonoid OATP inhibitor quercetin.	pinocembrin	22-33	solute carrier organic anion transporter family member 1A2	Homo sapiens	62-66
28745105-9	2018	Galangin, chrysin and pinocembrin effectively inhibited rosuvastatin uptake by hOATP2B1 with IC50 ~1-10 muM.	pinocembrin	22-33	solute carrier organic anion transporter family member 2B1	Homo sapiens	79-87
29850586-3	2018	In this study, we sought to determine the effect of pinocembrin (PCB; a pleiotropic neuroprotective agent) on t-PA administration-induced BBB damage in a novel rat thromboembolic stroke model.	pinocembrin	65-68	plasminogen activator, tissue type	Rattus norvegicus	110-114
29850586-4	2018	By assessing the leakage of Evans blue into the ischemic hemisphere, we demonstrated that PCB pretreatment 5 min before t-PA administration significantly reduced BBB damage following 2 hr, 4 hr, 6 hr, and even 8 hr ischemia.	pinocembrin	90-93	plasminogen activator, tissue type	Rattus norvegicus	120-124
29850586-5	2018	Consistently, PCB pretreatment significantly decreased t-PA infusion-resulting brain edema and infarction volume and improved the behavioral outcomes following 6 hr ischemia.	pinocembrin	14-17	plasminogen activator, tissue type	Rattus norvegicus	55-59
29850586-6	2018	Mechanistically, PCB pretreatment inhibited the activation of MMP-2 and MMP-9 and degradation of tight junction proteins (TJPs) occludin and claudin-5 in the ischemic hemisphere.	pinocembrin	17-20	matrix metallopeptidase 2	Rattus norvegicus	62-67
29850586-6	2018	Mechanistically, PCB pretreatment inhibited the activation of MMP-2 and MMP-9 and degradation of tight junction proteins (TJPs) occludin and claudin-5 in the ischemic hemisphere.	pinocembrin	17-20	matrix metallopeptidase 9	Rattus norvegicus	72-77
29850586-6	2018	Mechanistically, PCB pretreatment inhibited the activation of MMP-2 and MMP-9 and degradation of tight junction proteins (TJPs) occludin and claudin-5 in the ischemic hemisphere.	pinocembrin	17-20	occludin	Rattus norvegicus	128-136
29850586-6	2018	Mechanistically, PCB pretreatment inhibited the activation of MMP-2 and MMP-9 and degradation of tight junction proteins (TJPs) occludin and claudin-5 in the ischemic hemisphere.	pinocembrin	17-20	claudin 5	Rattus norvegicus	141-150
29850586-7	2018	Moreover, PCB pretreatment significantly reduced phosphorylation of platelet-derived growth factor receptor alpha (PDGFRalpha) as compared with t-PA alone.	pinocembrin	10-13	platelet derived growth factor receptor alpha	Rattus norvegicus	68-113
29850586-7	2018	Moreover, PCB pretreatment significantly reduced phosphorylation of platelet-derived growth factor receptor alpha (PDGFRalpha) as compared with t-PA alone.	pinocembrin	10-13	plasminogen activator, tissue type	Rattus norvegicus	144-148
29850586-9	2018	In conclusion, we demonstrated that PCB pretreatment shortly before t-PA infusion significantly protects BBB function and improves neurological outcomes following prolonged ischemia beyond the regular 4.5 hr t-PA time window.	pinocembrin	36-39	plasminogen activator, tissue type	Rattus norvegicus	208-212
29850586-10	2018	PCB pretreatment may represent a novel means of increasing the safety and the therapeutic time window of t-PA following ischemic stroke.	pinocembrin	0-3	plasminogen activator, tissue type	Rattus norvegicus	105-109
28084593-0	2018	Pinocembrin Suppresses H2O2-Induced Mitochondrial Dysfunction by a Mechanism Dependent on the Nrf2/HO-1 Axis in SH-SY5Y Cells.	pinocembrin	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	94-98
29469035-1	2018	INTRODUCTION: The present study aimed to elucidate the potential antifibrotic effects of pinocembrin (PIN), a flavanone found abundantly in honey and propolis, by studying its effect on different oxidative stress, inflammatory and fibrosis markers in an experimental model of CCl4-induced liver fibrosis.	pinocembrin	89-100	C-C motif chemokine ligand 4	Rattus norvegicus	276-280
29469035-1	2018	INTRODUCTION: The present study aimed to elucidate the potential antifibrotic effects of pinocembrin (PIN), a flavanone found abundantly in honey and propolis, by studying its effect on different oxidative stress, inflammatory and fibrosis markers in an experimental model of CCl4-induced liver fibrosis.	pinocembrin	102-105	C-C motif chemokine ligand 4	Rattus norvegicus	276-280
29352975-0	2018	Pinocembrin from Penthorum chinense Pursh suppresses hepatic stellate cells activation through a unified SIRT3-TGF-beta-Smad signaling pathway.	pinocembrin	0-11	sirtuin 3	Rattus norvegicus	105-110
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	heme oxygenase 1	Homo sapiens	217-221
28084593-0	2018	Pinocembrin Suppresses H2O2-Induced Mitochondrial Dysfunction by a Mechanism Dependent on the Nrf2/HO-1 Axis in SH-SY5Y Cells.	pinocembrin	0-11	heme oxygenase 1	Homo sapiens	99-103
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	NFE2 like bZIP transcription factor 2	Homo sapiens	259-263
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	336-338	NFE2 like bZIP transcription factor 2	Homo sapiens	204-208
28084593-12	2018	Overall, PB afforded cytoprotection by the Nrf2/HO-1 axis in H2O2-treated SH-SY5Y cells.	pinocembrin	9-11	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
28084593-12	2018	Overall, PB afforded cytoprotection by the Nrf2/HO-1 axis in H2O2-treated SH-SY5Y cells.	pinocembrin	9-11	heme oxygenase 1	Homo sapiens	48-52
28084593-10	2018	Furthermore, PB induced anti-inflammatory effects by abolishing the H2O2-dependent activation of the nuclear factor-kappaB (NF-kappaB) and upregulation of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).	pinocembrin	13-15	interleukin 1 beta	Homo sapiens	155-172
28084593-10	2018	Furthermore, PB induced anti-inflammatory effects by abolishing the H2O2-dependent activation of the nuclear factor-kappaB (NF-kappaB) and upregulation of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).	pinocembrin	13-15	interleukin 1 beta	Homo sapiens	174-182
28084593-10	2018	Furthermore, PB induced anti-inflammatory effects by abolishing the H2O2-dependent activation of the nuclear factor-kappaB (NF-kappaB) and upregulation of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).	pinocembrin	13-15	tumor necrosis factor	Homo sapiens	188-215
28084593-10	2018	Furthermore, PB induced anti-inflammatory effects by abolishing the H2O2-dependent activation of the nuclear factor-kappaB (NF-kappaB) and upregulation of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).	pinocembrin	13-15	tumor necrosis factor	Homo sapiens	217-226
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	heme oxygenase 1	Homo sapiens	78-94
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	heme oxygenase 1	Homo sapiens	96-100
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	NFE2 like bZIP transcription factor 2	Homo sapiens	159-202
28084593-11	2018	The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 muM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB.	pinocembrin	4-6	NFE2 like bZIP transcription factor 2	Homo sapiens	204-208
29055190-0	2017	Pinocembrin attenuates allergic airway inflammation via inhibition of NF-kappaB pathway in mice.	pinocembrin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	70-79
29663896-9	2018	RESULTS: The docking results revealed promising inhibitory potential of Pinocembrin against VEGFR-2 with binding energy of -8.50 kcal/mole as compared to its known inhibitors Sorafenib and YLT192 having binding energy of -6.49 kcal/mole and -8.02 kcal/mol respectively.	pinocembrin	72-83	kinase insert domain receptor	Homo sapiens	92-99
29663896-13	2018	CONCLUSION: Obtained results propose Pinocembrin as a multi-targeted novel lead compound that bears outstanding antiangiogenic potential against VEGFR-2.	pinocembrin	37-48	kinase insert domain receptor	Homo sapiens	145-152
29055190-2	2017	This study aimed to evaluate whether pinocembrin could attenuate ovalbumin (OVA)-induced allergic airway inflammation in mice and to explore the possible mechanism.	pinocembrin	37-48	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	65-74
29055190-8	2017	Treatment with pinocembrin significantly reduced Th2 cytokines interleukin (IL)-4, IL-5 and IL-13 in BALF, and OVA-specific IgE in serum.	pinocembrin	15-26	interleukin 5	Mus musculus	83-87
29055190-8	2017	Treatment with pinocembrin significantly reduced Th2 cytokines interleukin (IL)-4, IL-5 and IL-13 in BALF, and OVA-specific IgE in serum.	pinocembrin	15-26	interleukin 13	Mus musculus	92-97
29055190-9	2017	Moreover, pinocembrin treatment suppressed phosphorylation of inhibitor-kappaBalpha (IkappaBalpha) and NF-kappaB subunit p65 activation in lung tissue of OVA-sensitized mice.	pinocembrin	10-21	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	85-97
29055190-9	2017	Moreover, pinocembrin treatment suppressed phosphorylation of inhibitor-kappaBalpha (IkappaBalpha) and NF-kappaB subunit p65 activation in lung tissue of OVA-sensitized mice.	pinocembrin	10-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	103-112
29055190-9	2017	Moreover, pinocembrin treatment suppressed phosphorylation of inhibitor-kappaBalpha (IkappaBalpha) and NF-kappaB subunit p65 activation in lung tissue of OVA-sensitized mice.	pinocembrin	10-21	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	121-124
28007523-0	2017	Pinocembrin protects hemorrhagic brain primarily by inhibiting toll-like receptor 4 and reducing M1 phenotype microglia.	pinocembrin	0-11	toll-like receptor 4	Mus musculus	63-83
28821452-0	2017	Pinocembrin, a novel histidine decarboxylase inhibitor with anti-allergic potential in in vitro.	pinocembrin	0-11	histidine decarboxylase	Homo sapiens	21-44
28821452-5	2017	Preliminary studies, using a microbiological model of Klebsiella pneumoniae, provided first evidences that suggest Pinocembrin as a potential thermal stable inhibitor for HDC.	pinocembrin	115-126	histidine decarboxylase	Homo sapiens	171-174
28821452-7	2017	In vitro studies validated the predicted interaction and showed that Pinocembrin inhibits HDC activity and histamine in IgE-sensitized RBL-2H3 in response to dinitrophenol (DNP)-bovine serum albumin (BSA) stimulation.	pinocembrin	69-80	histidine decarboxylase	Homo sapiens	90-93
28821452-10	2017	In conclusion, current study suggests Pinocembrin as a potential HDC inhibitor, and provides the first evidences it is in vitro anti-allergic properties, suggesting Pinocembrin as a new candidate for natural anti-allergic drugs.	pinocembrin	38-49	histidine decarboxylase	Homo sapiens	65-68
27696114-0	2017	Pinocembrin Provides Mitochondrial Protection by the Activation of the Erk1/2-Nrf2 Signaling Pathway in SH-SY5Y Neuroblastoma Cells Exposed to Paraquat.	pinocembrin	0-11	mitogen-activated protein kinase 3	Homo sapiens	71-77
27696114-0	2017	Pinocembrin Provides Mitochondrial Protection by the Activation of the Erk1/2-Nrf2 Signaling Pathway in SH-SY5Y Neuroblastoma Cells Exposed to Paraquat.	pinocembrin	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
27696114-5	2017	PB (25 muM) pretreatment (for 4 h) downregulated the levels of Bcl-2-associated X protein (Bax), blocked the release of cytochrome c to the cytosol, and inhibited the PQ-induced activation of caspase-9 and caspase-3.	pinocembrin	0-2	BCL2 associated X, apoptosis regulator	Homo sapiens	63-89
27696114-5	2017	PB (25 muM) pretreatment (for 4 h) downregulated the levels of Bcl-2-associated X protein (Bax), blocked the release of cytochrome c to the cytosol, and inhibited the PQ-induced activation of caspase-9 and caspase-3.	pinocembrin	0-2	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
27696114-5	2017	PB (25 muM) pretreatment (for 4 h) downregulated the levels of Bcl-2-associated X protein (Bax), blocked the release of cytochrome c to the cytosol, and inhibited the PQ-induced activation of caspase-9 and caspase-3.	pinocembrin	0-2	cytochrome c, somatic	Homo sapiens	120-132
27696114-5	2017	PB (25 muM) pretreatment (for 4 h) downregulated the levels of Bcl-2-associated X protein (Bax), blocked the release of cytochrome c to the cytosol, and inhibited the PQ-induced activation of caspase-9 and caspase-3.	pinocembrin	0-2	caspase 9	Homo sapiens	192-201
27696114-5	2017	PB (25 muM) pretreatment (for 4 h) downregulated the levels of Bcl-2-associated X protein (Bax), blocked the release of cytochrome c to the cytosol, and inhibited the PQ-induced activation of caspase-9 and caspase-3.	pinocembrin	0-2	caspase 3	Homo sapiens	206-215
27696114-10	2017	PB afforded mitochondrial protection by activating the extracellular signal-regulated kinase/nuclear factor erythroid 2-related factor 2 (Erk1/2-Nrf2) axis, since inhibition of Erk1/2 or silencing of Nrf2 abrogated these effects.	pinocembrin	0-2	mitogen-activated protein kinase 3	Homo sapiens	138-144
27696114-10	2017	PB afforded mitochondrial protection by activating the extracellular signal-regulated kinase/nuclear factor erythroid 2-related factor 2 (Erk1/2-Nrf2) axis, since inhibition of Erk1/2 or silencing of Nrf2 abrogated these effects.	pinocembrin	0-2	NFE2 like bZIP transcription factor 2	Homo sapiens	145-149
27696114-10	2017	PB afforded mitochondrial protection by activating the extracellular signal-regulated kinase/nuclear factor erythroid 2-related factor 2 (Erk1/2-Nrf2) axis, since inhibition of Erk1/2 or silencing of Nrf2 abrogated these effects.	pinocembrin	0-2	mitogen-activated protein kinase 3	Homo sapiens	177-183
27696114-10	2017	PB afforded mitochondrial protection by activating the extracellular signal-regulated kinase/nuclear factor erythroid 2-related factor 2 (Erk1/2-Nrf2) axis, since inhibition of Erk1/2 or silencing of Nrf2 abrogated these effects.	pinocembrin	0-2	NFE2 like bZIP transcription factor 2	Homo sapiens	200-204
27696114-11	2017	Therefore, PB exerted mitochondrial and cellular protection by an Erk1/2-Nrf2-dependent mechanism.	pinocembrin	11-13	mitogen-activated protein kinase 3	Homo sapiens	66-72
27696114-11	2017	Therefore, PB exerted mitochondrial and cellular protection by an Erk1/2-Nrf2-dependent mechanism.	pinocembrin	11-13	NFE2 like bZIP transcription factor 2	Homo sapiens	73-77
28000163-0	2017	Pinocembrin Attenuates Mitochondrial Dysfunction in Human Neuroblastoma SH-SY5Y Cells Exposed to Methylglyoxal: Role for the Erk1/2-Nrf2 Signaling Pathway.	pinocembrin	0-11	mitogen-activated protein kinase 3	Homo sapiens	125-131
28000163-0	2017	Pinocembrin Attenuates Mitochondrial Dysfunction in Human Neuroblastoma SH-SY5Y Cells Exposed to Methylglyoxal: Role for the Erk1/2-Nrf2 Signaling Pathway.	pinocembrin	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	132-136
28000163-2	2017	The antioxidant capacity of PB is associated with the activation of the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway.	pinocembrin	28-30	NFE2 like bZIP transcription factor 2	Homo sapiens	72-115
28000163-2	2017	The antioxidant capacity of PB is associated with the activation of the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway.	pinocembrin	28-30	NFE2 like bZIP transcription factor 2	Homo sapiens	146-150
28000163-6	2017	PB (25 microM) provided mitochondrial protection (decreased lipid peroxidation, protein carbonylation, and protein nitration in mitochondrial membranes; decreased mitochondrial free radical production; enhanced the content of GSH in mitochondria; rescued mitochondrial membrane potential-MMP) and blocked MG-triggered cell death by a mechanism dependent on the activation of the extracellular-related kinase (Erk1/2) and consequent upregulation of Nrf2.	pinocembrin	0-2	mitogen-activated protein kinase 3	Homo sapiens	409-415
28000163-6	2017	PB (25 microM) provided mitochondrial protection (decreased lipid peroxidation, protein carbonylation, and protein nitration in mitochondrial membranes; decreased mitochondrial free radical production; enhanced the content of GSH in mitochondria; rescued mitochondrial membrane potential-MMP) and blocked MG-triggered cell death by a mechanism dependent on the activation of the extracellular-related kinase (Erk1/2) and consequent upregulation of Nrf2.	pinocembrin	0-2	NFE2 like bZIP transcription factor 2	Homo sapiens	448-452
28000163-7	2017	PB increased the levels of GPx, GR, HO-1, and mitochondrial GSH.	pinocembrin	0-2	glutathione-disulfide reductase	Homo sapiens	32-34
28000163-8	2017	The PB-induced effects were suppressed by silencing of Nrf2 with siRNA.	pinocembrin	4-6	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
28000163-9	2017	Therefore, PB activated the Erk1/2-Nrf2 signaling pathway resulting in mitochondrial protection in SH-SY5Y cells exposed to MG.	pinocembrin	11-13	mitogen-activated protein kinase 3	Homo sapiens	28-34
28000163-9	2017	Therefore, PB activated the Erk1/2-Nrf2 signaling pathway resulting in mitochondrial protection in SH-SY5Y cells exposed to MG.	pinocembrin	11-13	NFE2 like bZIP transcription factor 2	Homo sapiens	35-39
28007523-5	2017	The optimal dose of pinocembrin (5mg/kg) suppressed microglial activation as evidenced by decreases in CD68-positive microglia and reduced proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6.	pinocembrin	20-31	CD68 antigen	Mus musculus	103-107
28007523-5	2017	The optimal dose of pinocembrin (5mg/kg) suppressed microglial activation as evidenced by decreases in CD68-positive microglia and reduced proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6.	pinocembrin	20-31	tumor necrosis factor	Mus musculus	165-198
28007523-5	2017	The optimal dose of pinocembrin (5mg/kg) suppressed microglial activation as evidenced by decreases in CD68-positive microglia and reduced proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6.	pinocembrin	20-31	interleukin 1 beta	Mus musculus	200-222
28007523-5	2017	The optimal dose of pinocembrin (5mg/kg) suppressed microglial activation as evidenced by decreases in CD68-positive microglia and reduced proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6.	pinocembrin	20-31	interleukin 6	Mus musculus	228-232
27538638-0	2016	Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells.	pinocembrin	52-63	NFE2 like bZIP transcription factor 2	Homo sapiens	72-76
27538638-0	2016	Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells.	pinocembrin	52-63	heme oxygenase 1	Homo sapiens	77-81
27538638-5	2016	Exposure of SH-SY5Y cells to 25muM Abeta25-35 for 24h caused viability loss, apoptotic increase and reactive oxygen species (ROS) increase, pre-treatment with PCB for 4h significantly reduced the viability loss, apoptotic rate and attenuated Abeta-mediated ROS production.	pinocembrin	159-162	amyloid beta precursor protein	Homo sapiens	35-40
27538638-6	2016	PCB strikingly inhibited Abeta25-35-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio.	pinocembrin	0-3	BCL2 apoptosis regulator	Homo sapiens	120-125
27538638-6	2016	PCB strikingly inhibited Abeta25-35-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio.	pinocembrin	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	126-129
27538638-7	2016	In addition, PCB suppressed the release of cytochrome c and the cleavage of caspase-3.	pinocembrin	13-16	cytochrome c, somatic	Homo sapiens	43-55
27538638-7	2016	In addition, PCB suppressed the release of cytochrome c and the cleavage of caspase-3.	pinocembrin	13-16	caspase 3	Homo sapiens	76-85
27538638-8	2016	PCB treatment also resulted in an increase in Nrf2 protein levels and subsequent induction of heme oxygenase-1(HO-1) expression in SH-SY5Y cells.	pinocembrin	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	46-50
27538638-8	2016	PCB treatment also resulted in an increase in Nrf2 protein levels and subsequent induction of heme oxygenase-1(HO-1) expression in SH-SY5Y cells.	pinocembrin	0-3	heme oxygenase 1	Homo sapiens	94-115
27538638-9	2016	RNA interference-mediated knockdown of Nrf2 expression suppressed the PCB-induced HO-1 expression.	pinocembrin	70-73	NFE2 like bZIP transcription factor 2	Homo sapiens	39-43
27538638-9	2016	RNA interference-mediated knockdown of Nrf2 expression suppressed the PCB-induced HO-1 expression.	pinocembrin	70-73	heme oxygenase 1	Homo sapiens	82-86
27538638-10	2016	Notably, we found that the HO-1 inhibitor zinc protoporphyrin IX (ZnPP) markedly diminished the neuroprotective effect of PCB against Abeta-mediated neurotoxicity.	pinocembrin	122-125	heme oxygenase 1	Homo sapiens	27-31
27538638-11	2016	Taken together, these results indicated that PCB protects SH-SY5Y cells from Abeta25-35-induced neurotoxicity through activation of Nrf2/HO-1 pathways.	pinocembrin	45-48	NFE2 like bZIP transcription factor 2	Homo sapiens	132-136
27538638-11	2016	Taken together, these results indicated that PCB protects SH-SY5Y cells from Abeta25-35-induced neurotoxicity through activation of Nrf2/HO-1 pathways.	pinocembrin	45-48	heme oxygenase 1	Homo sapiens	137-141
27245556-11	2016	Pinocembrin pretreatment improved renal function and renal Oat3 function and reduced oxidative stress and apoptotic conditions.	pinocembrin	0-11	solute carrier family 22 member 8	Rattus norvegicus	59-63
25377066-0	2015	Pinocembrin attenuates 6-OHDA-induced neuronal cell death through Nrf2/ARE pathway in SH-SY5Y cells.	pinocembrin	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	66-70
26655464-0	2016	Pinocembrin attenuates MPP(+)-induced neurotoxicity by the induction of heme oxygenase-1 through ERK1/2 pathway.	pinocembrin	0-11	heme oxygenase 1	Homo sapiens	72-88
26655464-0	2016	Pinocembrin attenuates MPP(+)-induced neurotoxicity by the induction of heme oxygenase-1 through ERK1/2 pathway.	pinocembrin	0-11	mitogen-activated protein kinase 3	Homo sapiens	97-103
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	47-49	heme oxygenase 1	Homo sapiens	60-76
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	47-49	heme oxygenase 1	Homo sapiens	78-82
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	47-49	heme oxygenase 1	Homo sapiens	185-189
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	247-249	heme oxygenase 1	Homo sapiens	60-76
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	247-249	heme oxygenase 1	Homo sapiens	78-82
26655464-3	2016	In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP(+)-induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB.	pinocembrin	247-249	heme oxygenase 1	Homo sapiens	185-189
26655464-4	2016	PB induced the phosphorylation of ERK1/2, and its cytoprotective effect was abolished by ERK1/2 inhibitors.	pinocembrin	0-2	mitogen-activated protein kinase 3	Homo sapiens	34-40
26655464-4	2016	PB induced the phosphorylation of ERK1/2, and its cytoprotective effect was abolished by ERK1/2 inhibitors.	pinocembrin	0-2	mitogen-activated protein kinase 3	Homo sapiens	89-95
26655464-6	2016	Taken together, the results suggest that PB enhances HO-1 expression to suppress MPP(+)-induced oxidative damage via ERK1/2 signaling pathways.	pinocembrin	41-43	heme oxygenase 1	Homo sapiens	53-57
26655464-6	2016	Taken together, the results suggest that PB enhances HO-1 expression to suppress MPP(+)-induced oxidative damage via ERK1/2 signaling pathways.	pinocembrin	41-43	mitogen-activated protein kinase 3	Homo sapiens	117-123
26655464-7	2016	These results revealed the mechanisms of PB enhances HO-1 expression, and contribute to shed some light on the mechanisms whereby PB inhibits the MPP(+)-induced neurotoxicity.	pinocembrin	41-43	heme oxygenase 1	Homo sapiens	53-57
27119082-0	2016	Polyphenols from Chilean Propolis and Pinocembrin Reduce MMP-9 Gene Expression and Activity in Activated Macrophages.	pinocembrin	38-49	matrix metallopeptidase 9	Mus musculus	57-62
27119082-11	2016	However, the effect showed by ethanolic extract of propolis was higher than the effect of pinocembrin, suggesting that MMP-9 inhibition results from a joint contribution between the components of the extract.	pinocembrin	90-101	matrix metallopeptidase 9	Mus musculus	119-124
26049009-0	2015	Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-kappaB pathway.	pinocembrin	0-11	thymoma viral proto-oncogene 1	Mus musculus	134-137
26049009-0	2015	Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-kappaB pathway.	pinocembrin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	138-147
26049009-3	2015	The results showed that pinocembrin dose-dependently inhibited LPS-induced inflammatory mediators TNF-alpha, IL-1beta, NO and PGE2 production.	pinocembrin	24-35	tumor necrosis factor	Mus musculus	98-107
26049009-3	2015	The results showed that pinocembrin dose-dependently inhibited LPS-induced inflammatory mediators TNF-alpha, IL-1beta, NO and PGE2 production.	pinocembrin	24-35	interleukin 1 beta	Mus musculus	109-117
26049009-4	2015	Pinocembrin also inhibited LPS-induced iNOS and COX-2 expression.	pinocembrin	0-11	nitric oxide synthase 2, inducible	Mus musculus	39-43
26049009-4	2015	Pinocembrin also inhibited LPS-induced iNOS and COX-2 expression.	pinocembrin	0-11	cytochrome c oxidase II, mitochondrial	Mus musculus	48-53
26049009-5	2015	Moreover, pinocembrin inhibited LPS-induced PI3K, Akt phosphorylation, and NF-kappaB activation, which were required for inflammatory mediators production.	pinocembrin	10-21	thymoma viral proto-oncogene 1	Mus musculus	50-53
26049009-5	2015	Moreover, pinocembrin inhibited LPS-induced PI3K, Akt phosphorylation, and NF-kappaB activation, which were required for inflammatory mediators production.	pinocembrin	10-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
26049009-6	2015	Furthermore, treatment of pinocembrin induced nuclear translocation of Nrf2 and expression of HO-1.	pinocembrin	26-37	nuclear factor, erythroid derived 2, like 2	Mus musculus	71-75
26049009-6	2015	Furthermore, treatment of pinocembrin induced nuclear translocation of Nrf2 and expression of HO-1.	pinocembrin	26-37	heme oxygenase 1	Mus musculus	94-98
26049009-7	2015	In conclusion, our data indicated that pinocembrin inhibited LPS-induced inflammatory mediators production by suppressing PI3K/Akt/NF-kappaB signaling pathway.	pinocembrin	39-50	thymoma viral proto-oncogene 1	Mus musculus	127-130
26049009-7	2015	In conclusion, our data indicated that pinocembrin inhibited LPS-induced inflammatory mediators production by suppressing PI3K/Akt/NF-kappaB signaling pathway.	pinocembrin	39-50	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	131-140
26319563-8	2015	In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05).	pinocembrin	7-18	BCL2 associated X, apoptosis regulator	Rattus norvegicus	61-64
26319563-8	2015	In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05).	pinocembrin	7-18	BCL2, apoptosis regulator	Rattus norvegicus	65-70
26319563-8	2015	In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05).	pinocembrin	7-18	gap junction protein, alpha 1	Rattus norvegicus	121-132
26319563-8	2015	In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05).	pinocembrin	7-18	gap junction protein, alpha 1	Rattus norvegicus	142-146
26319563-8	2015	In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05).	pinocembrin	7-18	gap junction protein, alpha 1	Rattus norvegicus	157-161
26319563-10	2015	These benefits may be due to pinocembrin"s antiapoptotic and anti-oxidative stress effects and its ability to increase the phosphorylation of Cx43 in ischemic myocardium.	pinocembrin	29-40	gap junction protein, alpha 1	Rattus norvegicus	142-146
25907027-5	2015	The IC50 values of eriodictyol, naringenin, and pinocembrin were 17.4 +- 0.40, 30.2 +- 0.61, and 44.9 +- 0.57 muM, respectively.	pinocembrin	48-59	latexin	Homo sapiens	110-113
25377066-4	2015	Results indicate that pretreatment with PB for 4 h significantly reduced the 6-OHDA-induced cell viability loss, apoptotic rate and decreased Bcl-2/Bax ratio.	pinocembrin	40-42	BCL2 apoptosis regulator	Homo sapiens	142-147
25377066-4	2015	Results indicate that pretreatment with PB for 4 h significantly reduced the 6-OHDA-induced cell viability loss, apoptotic rate and decreased Bcl-2/Bax ratio.	pinocembrin	40-42	BCL2 associated X, apoptosis regulator	Homo sapiens	148-151
25377066-6	2015	Moreover, we have revealed the PB treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes of heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthetase (gamma-GCS) in SH-SY5Y cells.	pinocembrin	31-33	NFE2 like bZIP transcription factor 2	Homo sapiens	71-105
25377066-6	2015	Moreover, we have revealed the PB treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes of heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthetase (gamma-GCS) in SH-SY5Y cells.	pinocembrin	31-33	NFE2 like bZIP transcription factor 2	Homo sapiens	107-111
25377066-6	2015	Moreover, we have revealed the PB treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes of heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthetase (gamma-GCS) in SH-SY5Y cells.	pinocembrin	31-33	heme oxygenase 1	Homo sapiens	209-225
25377066-6	2015	Moreover, we have revealed the PB treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes of heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthetase (gamma-GCS) in SH-SY5Y cells.	pinocembrin	31-33	glutamate-cysteine ligase catalytic subunit	Homo sapiens	237-270
25377066-6	2015	Moreover, we have revealed the PB treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes of heme oxygenase-1 (HO-1) and gamma-glutamylcysteine synthetase (gamma-GCS) in SH-SY5Y cells.	pinocembrin	31-33	glutamate-cysteine ligase catalytic subunit	Homo sapiens	272-281
25377066-7	2015	Treatment of SH-SY5Y cells with Nrf2 small interference RNA abolished PB-induced HO-1 and gamma-GCS expression and its protective effects.	pinocembrin	70-72	NFE2 like bZIP transcription factor 2	Homo sapiens	32-36
25377066-7	2015	Treatment of SH-SY5Y cells with Nrf2 small interference RNA abolished PB-induced HO-1 and gamma-GCS expression and its protective effects.	pinocembrin	70-72	glutamate-cysteine ligase catalytic subunit	Homo sapiens	90-99
25377066-8	2015	Taken together, these findings suggest that PB can protect the SH-SY5Y cells from 6-OHDA-induced oxidative cell death via Nrf2/ARE pathway.	pinocembrin	44-46	NFE2 like bZIP transcription factor 2	Homo sapiens	122-126
25187841-8	2014	Pinocembrin treatment was found to alleviate the cognitive impairments, decrease the neurological scores, diminish neuronal loss in the hippocampus and reduce the number of GFAP-positive cells in the hippocampal CA1 region of the TGCI rats.	pinocembrin	0-11	glial fibrillary acidic protein	Rattus norvegicus	173-177
25644385-5	2015	In this study, we found that PB inhibits the expression of MMP-1, MMP-3, and MMP-13 at both mRNA levels and protein levels in human chondrocytes.	pinocembrin	29-31	matrix metallopeptidase 1	Homo sapiens	59-64
25644385-5	2015	In this study, we found that PB inhibits the expression of MMP-1, MMP-3, and MMP-13 at both mRNA levels and protein levels in human chondrocytes.	pinocembrin	29-31	matrix metallopeptidase 3	Homo sapiens	66-71
25644385-5	2015	In this study, we found that PB inhibits the expression of MMP-1, MMP-3, and MMP-13 at both mRNA levels and protein levels in human chondrocytes.	pinocembrin	29-31	matrix metallopeptidase 13	Homo sapiens	77-83
25644385-6	2015	Importantly, the results of luciferase reporter assay indicated that tumor necrosis factor-alpha (TNF-alpha) induced the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) was inhibited by the treatment with PB.	pinocembrin	246-248	tumor necrosis factor	Homo sapiens	69-96
25644385-6	2015	Importantly, the results of luciferase reporter assay indicated that tumor necrosis factor-alpha (TNF-alpha) induced the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) was inhibited by the treatment with PB.	pinocembrin	246-248	tumor necrosis factor	Homo sapiens	98-107
25644385-7	2015	It is also shown that TNF-alpha-induced p65 nuclear translocation was blocked by the treatment with PB.	pinocembrin	100-102	tumor necrosis factor	Homo sapiens	22-31
25644385-7	2015	It is also shown that TNF-alpha-induced p65 nuclear translocation was blocked by the treatment with PB.	pinocembrin	100-102	RELA proto-oncogene, NF-kB subunit	Homo sapiens	40-43
25644385-8	2015	Mechanistically, PB treatment significantly inhibited TNF-alpha-induced phosphorylation and degradation of the NF-kappaB inhibitor IkappaBalpha in human chondrocytes.	pinocembrin	17-19	tumor necrosis factor	Homo sapiens	54-63
25644385-8	2015	Mechanistically, PB treatment significantly inhibited TNF-alpha-induced phosphorylation and degradation of the NF-kappaB inhibitor IkappaBalpha in human chondrocytes.	pinocembrin	17-19	NFKB inhibitor alpha	Homo sapiens	131-143
25187841-8	2014	Pinocembrin treatment was found to alleviate the cognitive impairments, decrease the neurological scores, diminish neuronal loss in the hippocampus and reduce the number of GFAP-positive cells in the hippocampal CA1 region of the TGCI rats.	pinocembrin	0-11	carbonic anhydrase 1	Rattus norvegicus	212-215
24395092-5	2014	We found that pretreatment of SH-SY5Y cells with PB significantly reduced the MPP(+)-induced loss of cell viability, the generation of intracellular ROS, apoptotic rate, and the cleavage of caspase-3.	pinocembrin	49-51	caspase 3	Homo sapiens	190-199
25271424-8	2014	Pinocembrin-treatment could also reduce the number of TUNEL-positive and Caspase-3-positive neurons, and upregulate the expression of LC3B and Beclin1 in penumbra area.	pinocembrin	0-11	caspase 3	Homo sapiens	73-82
25271424-8	2014	Pinocembrin-treatment could also reduce the number of TUNEL-positive and Caspase-3-positive neurons, and upregulate the expression of LC3B and Beclin1 in penumbra area.	pinocembrin	0-11	microtubule associated protein 1 light chain 3 beta	Homo sapiens	134-138
25271424-8	2014	Pinocembrin-treatment could also reduce the number of TUNEL-positive and Caspase-3-positive neurons, and upregulate the expression of LC3B and Beclin1 in penumbra area.	pinocembrin	0-11	beclin 1	Homo sapiens	143-150
25949790-0	2014	Pinocembrin suppresses TGF-beta1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	0-11	transforming growth factor beta 1	Homo sapiens	23-32
25949790-0	2014	Pinocembrin suppresses TGF-beta1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	0-11	protein tyrosine kinase 2	Homo sapiens	167-170
25949790-0	2014	Pinocembrin suppresses TGF-beta1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	0-11	mitogen-activated protein kinase 14	Homo sapiens	171-179
25949790-2	2014	In this study, we investigated the antimetastatic effect of pinocembrin on TGF-beta1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells.	pinocembrin	60-71	transforming growth factor beta 1	Homo sapiens	75-84
25949790-3	2014	RESULTS: Firstly, the results showed that pinocembrin significantly suppresses the TGF-beta1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration.	pinocembrin	42-53	transforming growth factor beta 1	Homo sapiens	83-92
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	protein tyrosine kinase 2	Homo sapiens	66-87
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	protein tyrosine kinase 2	Homo sapiens	89-92
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	mitogen-activated protein kinase 14	Homo sapiens	98-106
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	matrix metallopeptidase 2	Homo sapiens	203-231
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	matrix metallopeptidase 2	Homo sapiens	233-241
25949790-5	2014	Molecular data also showed pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38alpha signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-beta1.	pinocembrin	27-38	transforming growth factor beta 1	Homo sapiens	254-263
25949790-6	2014	Next, pinocembrin also strongly inhibited the degradation of inhibitor of kappaBalpha (IkappaBalpha) and the nuclear levels of nuclear factor kappa B (NF-kappaB).	pinocembrin	6-17	NFKB inhibitor alpha	Homo sapiens	87-99
25949790-6	2014	Next, pinocembrin also strongly inhibited the degradation of inhibitor of kappaBalpha (IkappaBalpha) and the nuclear levels of nuclear factor kappa B (NF-kappaB).	pinocembrin	6-17	nuclear factor kappa B subunit 1	Homo sapiens	127-149
25949790-6	2014	Next, pinocembrin also strongly inhibited the degradation of inhibitor of kappaBalpha (IkappaBalpha) and the nuclear levels of nuclear factor kappa B (NF-kappaB).	pinocembrin	6-17	nuclear factor kappa B subunit 1	Homo sapiens	151-160
25949790-7	2014	Also, a dose-dependent inhibition on the binding ability of NF-kappaB was further observed under pinocembrin treatment.	pinocembrin	97-108	nuclear factor kappa B subunit 1	Homo sapiens	60-69
25949790-8	2014	CONCLUSIONS: Presented results indicated that pinocembrin inhibits TGF-beta1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	46-57	transforming growth factor beta 1	Homo sapiens	67-76
25949790-8	2014	CONCLUSIONS: Presented results indicated that pinocembrin inhibits TGF-beta1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	46-57	protein tyrosine kinase 2	Homo sapiens	195-198
25949790-8	2014	CONCLUSIONS: Presented results indicated that pinocembrin inhibits TGF-beta1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the alphavbeta3 integrin/FAK/p38alpha signaling pathway.	pinocembrin	46-57	mitogen-activated protein kinase 14	Homo sapiens	199-207
24395092-6	2014	PB strikingly inhibited MPP(+)-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio, and the release of cytochrome c.	pinocembrin	0-2	BCL2 apoptosis regulator	Homo sapiens	115-120
24395092-6	2014	PB strikingly inhibited MPP(+)-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio, and the release of cytochrome c.	pinocembrin	0-2	BCL2 associated X, apoptosis regulator	Homo sapiens	121-124
24395092-6	2014	PB strikingly inhibited MPP(+)-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio, and the release of cytochrome c.	pinocembrin	0-2	cytochrome c, somatic	Homo sapiens	151-163
23611777-0	2013	Pinocembrin inhibits angiotensin II-induced vasoconstriction via suppression of the increase of [Ca2+]i and ERK1/2 activation through blocking AT(1)R in the rat aorta.	pinocembrin	0-11	angiotensinogen	Rattus norvegicus	21-35
24468471-4	2014	Here, we report that a 3-month treatment with pinocembrin prevents the cognition decline in APP/PS1 transgenic mice without altering Abeta burden and oxidative stress.	pinocembrin	46-57	presenilin 1	Mus musculus	96-99
25157358-9	2014	Together, the suppression of MAPK and the NF-kappaB signaling pathways play a significant role in the anti-inflammation of pinocembrin in hBMECs subjected to fAbeta(1-40).	pinocembrin	123-134	nuclear factor kappa B subunit 1	Homo sapiens	42-51
23611777-8	2013	Moreover, the increase in the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and myosin light chain 2 (MLC2) induced by AngII was blocked by pinocembrin.	pinocembrin	160-171	angiotensinogen	Rattus norvegicus	139-144
23697399-4	2014	The results showed that there was a lower production of TNFalpha, IL-6, and IL-1beta in the serum of LPS-challenged mice that had been pre-treated with pinocembrin.	pinocembrin	152-163	tumor necrosis factor	Mus musculus	56-64
23697399-4	2014	The results showed that there was a lower production of TNFalpha, IL-6, and IL-1beta in the serum of LPS-challenged mice that had been pre-treated with pinocembrin.	pinocembrin	152-163	interleukin 6	Mus musculus	66-70
23697399-4	2014	The results showed that there was a lower production of TNFalpha, IL-6, and IL-1beta in the serum of LPS-challenged mice that had been pre-treated with pinocembrin.	pinocembrin	152-163	interleukin 1 beta	Mus musculus	76-84
23611777-9	2013	These results demonstrate that pinocembrin inhibits AngII-induced rat aortic ring contraction, and these inhibitory effects may be related to the reduction of the AngII-induced increase in [Ca(2+)]i and ERK1/2 activation via blocking AT1R.	pinocembrin	31-42	angiotensinogen	Rattus norvegicus	52-57
23611777-9	2013	These results demonstrate that pinocembrin inhibits AngII-induced rat aortic ring contraction, and these inhibitory effects may be related to the reduction of the AngII-induced increase in [Ca(2+)]i and ERK1/2 activation via blocking AT1R.	pinocembrin	31-42	angiotensinogen	Rattus norvegicus	163-168
23611777-9	2013	These results demonstrate that pinocembrin inhibits AngII-induced rat aortic ring contraction, and these inhibitory effects may be related to the reduction of the AngII-induced increase in [Ca(2+)]i and ERK1/2 activation via blocking AT1R.	pinocembrin	31-42	mitogen activated protein kinase 3	Rattus norvegicus	203-209
23611777-0	2013	Pinocembrin inhibits angiotensin II-induced vasoconstriction via suppression of the increase of [Ca2+]i and ERK1/2 activation through blocking AT(1)R in the rat aorta.	pinocembrin	0-11	mitogen activated protein kinase 3	Rattus norvegicus	108-114
23611777-9	2013	These results demonstrate that pinocembrin inhibits AngII-induced rat aortic ring contraction, and these inhibitory effects may be related to the reduction of the AngII-induced increase in [Ca(2+)]i and ERK1/2 activation via blocking AT1R.	pinocembrin	31-42	angiotensin II receptor, type 1a	Rattus norvegicus	234-238
23611777-0	2013	Pinocembrin inhibits angiotensin II-induced vasoconstriction via suppression of the increase of [Ca2+]i and ERK1/2 activation through blocking AT(1)R in the rat aorta.	pinocembrin	0-11	angiotensin II receptor, type 1a	Rattus norvegicus	143-149
23611777-4	2013	Pinocembrin was observed to inhibit AngII-induced vasoconstriction in rat aortic rings with either intact or denuded endothelium.	pinocembrin	0-11	angiotensinogen	Rattus norvegicus	36-41
23611777-6	2013	In a docking model, pinocembrin showed effective binding at the active site of AT1R.	pinocembrin	20-31	angiotensin II receptor, type 1a	Rattus norvegicus	79-83
23611777-7	2013	Pinocembrin was shown to inhibit both AngII-induced Ca(2+) release from internal stores and Ca(2+) influx.	pinocembrin	0-11	angiotensinogen	Rattus norvegicus	38-43
23611777-8	2013	Moreover, the increase in the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and myosin light chain 2 (MLC2) induced by AngII was blocked by pinocembrin.	pinocembrin	160-171	mitogen activated protein kinase 3	Rattus norvegicus	88-94
23611777-8	2013	Moreover, the increase in the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and myosin light chain 2 (MLC2) induced by AngII was blocked by pinocembrin.	pinocembrin	160-171	myosin light chain 2	Rattus norvegicus	100-120
23611777-8	2013	Moreover, the increase in the phosphorylation of extracellular signal-regulated kinase (ERK1/2) and myosin light chain 2 (MLC2) induced by AngII was blocked by pinocembrin.	pinocembrin	160-171	myosin light chain 2	Rattus norvegicus	122-126
22263589-0	2012	Uptake characteristics of pinocembrin and its effect on p-glycoprotein at the blood-brain barrier in in vitro cell experiments.	pinocembrin	26-37	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	56-70
23725831-0	2013	Pinocembrin protects rats against cerebral ischemic damage through soluble epoxide hydrolase and epoxyeicosatrienoic acids.	pinocembrin	0-11	epoxide hydrolase 2	Rattus norvegicus	67-92
23725831-1	2013	AIM: To investigate the relationship between cerebroprotection of pinocembrin and epoxyeicosatrienoic acids (EETs) and their regulating enzyme soluble epoxide hydrolase (sEH).	pinocembrin	66-77	epoxide hydrolase 2	Rattus norvegicus	143-168
23725831-1	2013	AIM: To investigate the relationship between cerebroprotection of pinocembrin and epoxyeicosatrienoic acids (EETs) and their regulating enzyme soluble epoxide hydrolase (sEH).	pinocembrin	66-77	epoxide hydrolase 2	Rattus norvegicus	170-173
23725831-7	2013	In an assay for hydrolase activity, pinocembrin significantly lowered brain sEH activity of MCAO rats and inhibited recombinant human sEH activity in a concentration-dependent manner (IC50, 2.58 mumol L(-1)).	pinocembrin	36-47	epoxide hydrolase 2	Rattus norvegicus	76-79
23725831-7	2013	In an assay for hydrolase activity, pinocembrin significantly lowered brain sEH activity of MCAO rats and inhibited recombinant human sEH activity in a concentration-dependent manner (IC50, 2.58 mumol L(-1)).	pinocembrin	36-47	epoxide hydrolase 2	Homo sapiens	134-137
23328619-8	2013	Two active components of propolis, caffeic acid phenethyl ester (CAPE) and pinocembrin (PIN), only had partial effects on TGF-beta1-induced EMT in A549 cells.	pinocembrin	75-86	transforming growth factor beta 1	Homo sapiens	122-131
23216643-0	2012	Inhibitory effect of the combination therapy of simvastatin and pinocembrin on atherosclerosis in ApoE-deficient mice.	pinocembrin	64-75	apolipoprotein E	Mus musculus	98-102
23216643-1	2012	UNLABELLED: The present study was performed to investigate the effects of the combination therapy of pinocembrin and simvastatin on the atherosclerotic lesions development in the ApoE-/- mice.	pinocembrin	101-112	apolipoprotein E	Mus musculus	179-183
23216643-6	2012	RESULTS: The combination treatment with simvastatin and pinocembrin resulted in significantly decreased levels of serum total cholesterol, triglycerides and low-density lipoprotein cholesterol, augmented NO levels and SOD activity, inhibited ET and VEGF expression.	pinocembrin	56-67	vascular endothelial growth factor A	Mus musculus	249-253
23216643-10	2012	CONCLUSION: The combination of simvastatin and pinocembrin synergistically inhibited atherosclerotic lesion development in ApoE-/- mice with hyperlipidemia, which is partially dependent on the protective of vascular endothelium.	pinocembrin	47-58	apolipoprotein E	Mus musculus	123-127
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	mitogen-activated protein kinase 14	Mus musculus	196-203
22713932-6	2012	Additionally, TNF-alpha, IL-1beta and IL-6 concentrations decreased significantly while the concentration of IL-10 was significantly increased after pinocembrin pretreatment.	pinocembrin	149-160	interleukin 10	Mus musculus	109-114
22713932-7	2012	Our results also showed that pinocembrin attenuated LPS-induced lung injury through suppression of IkappaBalpha, JNK and p38MAPK activation.	pinocembrin	29-40	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	99-111
22713932-7	2012	Our results also showed that pinocembrin attenuated LPS-induced lung injury through suppression of IkappaBalpha, JNK and p38MAPK activation.	pinocembrin	29-40	mitogen-activated protein kinase 8	Mus musculus	113-116
22713932-7	2012	Our results also showed that pinocembrin attenuated LPS-induced lung injury through suppression of IkappaBalpha, JNK and p38MAPK activation.	pinocembrin	29-40	mitogen-activated protein kinase 14	Mus musculus	121-128
23725838-0	2013	Rho kinase inhibition activity of pinocembrin in rat aortic rings contracted by angiotensin II.	pinocembrin	34-45	angiotensinogen	Rattus norvegicus	80-94
23725838-4	2013	RESULTS: Pinocembrin produced a relaxant effect on endothelium-denuded aortic rings contracted by Ang II (100 nmol L(-1)) in a dose-dependent manner.	pinocembrin	9-20	angiotensinogen	Rattus norvegicus	98-104
23725838-5	2013	In endothelium-denuded aortic rings stimulated by Ang II, pretreatment with pinocembrin (25 and 100 mumol L(-1)) for 20 min significantly attenuated MYPT1 phosphorylation and ROCK1 protein levels.	pinocembrin	76-87	angiotensinogen	Rattus norvegicus	50-56
23725838-5	2013	In endothelium-denuded aortic rings stimulated by Ang II, pretreatment with pinocembrin (25 and 100 mumol L(-1)) for 20 min significantly attenuated MYPT1 phosphorylation and ROCK1 protein levels.	pinocembrin	76-87	protein phosphatase 1, regulatory subunit 12A	Rattus norvegicus	149-154
23725838-5	2013	In endothelium-denuded aortic rings stimulated by Ang II, pretreatment with pinocembrin (25 and 100 mumol L(-1)) for 20 min significantly attenuated MYPT1 phosphorylation and ROCK1 protein levels.	pinocembrin	76-87	Rho-associated coiled-coil containing protein kinase 1	Rattus norvegicus	175-180
23725838-7	2013	CONCLUSION: These findings indicate that pinocembrin inhibits vasoconstriction induced by Ang II in rat endothelium-denuded aortic rings, and the mechanism at least in part, is due to the blockade of the RhoA/ROCK pathway.	pinocembrin	41-52	angiotensinogen	Rattus norvegicus	90-96
23725838-7	2013	CONCLUSION: These findings indicate that pinocembrin inhibits vasoconstriction induced by Ang II in rat endothelium-denuded aortic rings, and the mechanism at least in part, is due to the blockade of the RhoA/ROCK pathway.	pinocembrin	41-52	Rho-associated coiled-coil containing protein kinase 1	Rattus norvegicus	209-213
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	tumor necrosis factor	Mus musculus	92-101
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	interleukin 1 beta	Mus musculus	103-111
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	interleukin 6	Mus musculus	113-117
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	interleukin 10	Mus musculus	122-127
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	166-178
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	mitogen-activated protein kinase 3	Mus musculus	180-186
22713932-3	2012	We found that in vitro pretreatment with pinocembrin remarkably regulated the production of TNF-alpha, IL-1beta, IL-6 and IL-10 via inhibiting the phosphorylation of IkappaBalpha, ERK1/2, JNK and p38MAPK.	pinocembrin	41-52	mitogen-activated protein kinase 8	Mus musculus	188-191
22901204-6	2012	Interestingly, pinocembrin slightly increased the number of GST-P positive foci when given prior to diethylnitrosamine injection.	pinocembrin	15-26	glutathione S-transferase pi 1	Rattus norvegicus	60-65
22263589-1	2012	One purpose of the present study was to investigate the uptake characteristics of pinocembrin (PCB) and its effect on p-glycoprotein (P-gp) at the blood-brain barrier (BBB).	pinocembrin	82-93	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	134-138
22263589-1	2012	One purpose of the present study was to investigate the uptake characteristics of pinocembrin (PCB) and its effect on p-glycoprotein (P-gp) at the blood-brain barrier (BBB).	pinocembrin	95-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	118-132
22263589-1	2012	One purpose of the present study was to investigate the uptake characteristics of pinocembrin (PCB) and its effect on p-glycoprotein (P-gp) at the blood-brain barrier (BBB).	pinocembrin	95-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	134-138
22263589-5	2012	Meanwhile, the protein level of P-gp after incubation with PCB was detected by Western blot assay.	pinocembrin	59-62	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	32-36
22263589-1	2012	One purpose of the present study was to investigate the uptake characteristics of pinocembrin (PCB) and its effect on p-glycoprotein (P-gp) at the blood-brain barrier (BBB).	pinocembrin	82-93	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	118-132
18625218-0	2008	Pinocembrin prevents glutamate-induced apoptosis in SH-SY5Y neuronal cells via decrease of bax/bcl-2 ratio.	pinocembrin	0-11	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
19719119-3	2009	In silico structure-based virtual ligand screening using our model resulted in the identification of pinocembrin and 5-hydroxy-7-methoxyflavone, which promoted nuclear translocation and transcriptional activation of AhR and AhR-dependent induction of endogenous target genes.	pinocembrin	101-112	aryl hydrocarbon receptor	Homo sapiens	216-219
19719119-3	2009	In silico structure-based virtual ligand screening using our model resulted in the identification of pinocembrin and 5-hydroxy-7-methoxyflavone, which promoted nuclear translocation and transcriptional activation of AhR and AhR-dependent induction of endogenous target genes.	pinocembrin	101-112	aryl hydrocarbon receptor	Homo sapiens	224-227
21262238-8	2011	It was found that treatment with pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner.	pinocembrin	33-44	myeloperoxidase	Rattus norvegicus	127-130
19685877-6	2009	Furthermore, EEAP, apigenin, curcumin, and pinocembrin decreased LPS-mediated induction of protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.	pinocembrin	43-54	nitric oxide synthase 2, inducible	Mus musculus	122-153
19685877-6	2009	Furthermore, EEAP, apigenin, curcumin, and pinocembrin decreased LPS-mediated induction of protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.	pinocembrin	43-54	nitric oxide synthase 2, inducible	Mus musculus	155-159
19685877-6	2009	Furthermore, EEAP, apigenin, curcumin, and pinocembrin decreased LPS-mediated induction of protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.	pinocembrin	43-54	prostaglandin-endoperoxide synthase 2	Mus musculus	165-181
19685877-6	2009	Furthermore, EEAP, apigenin, curcumin, and pinocembrin decreased LPS-mediated induction of protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.	pinocembrin	43-54	prostaglandin-endoperoxide synthase 2	Mus musculus	183-188
18625218-0	2008	Pinocembrin prevents glutamate-induced apoptosis in SH-SY5Y neuronal cells via decrease of bax/bcl-2 ratio.	pinocembrin	0-11	BCL2 apoptosis regulator	Homo sapiens	95-100
18625218-8	2008	Western blotting results indicated that pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax-Bcl-2 ratio, which is in consistent with the gene expression result.	pinocembrin	40-51	BCL2 associated X, apoptosis regulator	Homo sapiens	88-91
18625218-8	2008	Western blotting results indicated that pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax-Bcl-2 ratio, which is in consistent with the gene expression result.	pinocembrin	40-51	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142
18625218-8	2008	Western blotting results indicated that pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax-Bcl-2 ratio, which is in consistent with the gene expression result.	pinocembrin	40-51	BCL2 apoptosis regulator	Homo sapiens	143-148
18625218-10	2008	Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.	pinocembrin	22-33	tumor protein p53	Homo sapiens	116-119
18625218-10	2008	Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.	pinocembrin	22-33	BCL2 associated X, apoptosis regulator	Homo sapiens	137-140
18625218-10	2008	Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.	pinocembrin	22-33	BCL2 apoptosis regulator	Homo sapiens	141-146
18625218-10	2008	Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.	pinocembrin	22-33	cytochrome c, somatic	Homo sapiens	173-185
18495093-7	2008	Neuronal survival rates were increased, LDH release was decreased and both neurite length and apoptosis were alleviated when pinocembrin was present during reoxygenation, and this protection was associated with the reduction of reactive oxygen species, nitric oxide and neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), and an increase of glutathione.	pinocembrin	125-136	nitric oxide synthase 1	Rattus norvegicus	270-300
18495093-7	2008	Neuronal survival rates were increased, LDH release was decreased and both neurite length and apoptosis were alleviated when pinocembrin was present during reoxygenation, and this protection was associated with the reduction of reactive oxygen species, nitric oxide and neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), and an increase of glutathione.	pinocembrin	125-136	nitric oxide synthase 1	Rattus norvegicus	302-306
18495093-7	2008	Neuronal survival rates were increased, LDH release was decreased and both neurite length and apoptosis were alleviated when pinocembrin was present during reoxygenation, and this protection was associated with the reduction of reactive oxygen species, nitric oxide and neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), and an increase of glutathione.	pinocembrin	125-136	nitric oxide synthase 2	Rattus norvegicus	312-325
18495093-7	2008	Neuronal survival rates were increased, LDH release was decreased and both neurite length and apoptosis were alleviated when pinocembrin was present during reoxygenation, and this protection was associated with the reduction of reactive oxygen species, nitric oxide and neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), and an increase of glutathione.	pinocembrin	125-136	nitric oxide synthase 2	Rattus norvegicus	327-331
18295389-4	2008	We also found that administration of pinocembrin (PIN), one of the major components of propolis, inhibited tTG activation and significantly prevented the development of thioacetamide (TAA)-induced liver cirrhosis.	pinocembrin	37-48	transglutaminase 2	Homo sapiens	107-110
9287415-2	1997	All of the flavanones tested as well as a flavan, epicatechin, protected L-929 cells from TNF-induced cell death of the flavanones tested, hesperetin, isosakuranetin, and pinocembrin failed to modify TNF cytotoxicity, but the 3",4"-dihydroxyflavanones, eriodictyol and taxifolin, showed a protective effect.	pinocembrin	171-182	tumor necrosis factor	Mus musculus	90-93
17186548-0	2007	Pinocembrin triggers Bax-dependent mitochondrial apoptosis in colon cancer cells.	pinocembrin	0-11	BCL2 associated X, apoptosis regulator	Homo sapiens	21-24
17186548-7	2007	Overexpression of proapoptotic Bax protein sensitized the colon cancer cells to pinocembrin-induced apoptosis and Bax knockout cells were resistant to pinocembrin-induced apoptosis.	pinocembrin	80-91	BCL2 associated X, apoptosis regulator	Homo sapiens	31-34
17186548-7	2007	Overexpression of proapoptotic Bax protein sensitized the colon cancer cells to pinocembrin-induced apoptosis and Bax knockout cells were resistant to pinocembrin-induced apoptosis.	pinocembrin	151-162	BCL2 associated X, apoptosis regulator	Homo sapiens	31-34
17186548-7	2007	Overexpression of proapoptotic Bax protein sensitized the colon cancer cells to pinocembrin-induced apoptosis and Bax knockout cells were resistant to pinocembrin-induced apoptosis.	pinocembrin	151-162	BCL2 associated X, apoptosis regulator	Homo sapiens	114-117