PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34576117-0 2021 Acute Glucose Shift Induces the Activation of the NLRP3 Inflammasome in THP-1 Cells. Glucose 6-13 NLR family pyrin domain containing 3 Homo sapiens 50-55 34338149-0 2021 Omarigliptin ameliorated high glucose-induced nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation through activating adenosine monophosphate-activated protein kinase alpha (AMPKalpha) in renal glomerular endothelial cells. Glucose 30-37 NLR family pyrin domain containing 3 Homo sapiens 105-110 34831052-3 2021 One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis. Glucose 131-138 NLR family pyrin domain containing 3 Homo sapiens 38-43 33806797-3 2021 Currently, there is limited evidence that supports the pathological role of NLRP3 inflammasome activation in glucose handling in the skeletal muscle of obese individuals. Glucose 109-116 NLR family pyrin domain containing 3 Homo sapiens 76-81 34576117-1 2021 We aimed to investigate the effect of acute glucose shift on the activation of the NLRP3 inflammasome, IL-1beta secretion, and underlying signaling pathways in THP-1 cells. Glucose 44-51 NLR family pyrin domain containing 3 Homo sapiens 83-88 34576117-4 2021 Both directions of the acute glucose shift increased the activation of the NLRP3 inflammasome, generation of reactive oxygen species (ROS), and expression of phosphorylated p38 MAPK, JNK, and NF-kappaB compared with either constant NG or HG. Glucose 29-36 NLR family pyrin domain containing 3 Homo sapiens 75-80 34576117-5 2021 Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-kappaB. Glucose 84-91 NLR family pyrin domain containing 3 Homo sapiens 139-144 34576117-6 2021 Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells. Glucose 87-94 NLR family pyrin domain containing 3 Homo sapiens 190-195 33546399-10 2021 Finally, studies revealing the role of glucose concentration in the activation of NLRP3 inflammasome are analyzed. Glucose 39-46 NLR family pyrin domain containing 3 Homo sapiens 82-87 34198548-3 2021 Macrophage-specific deletion of Glucose Transporter 1 (GLUT1) significantly reduced tumor burden, which was accompanied by increased Natural Killer and CD8+ T cell activity and suppression of the NLRP3-IL1beta inflammasome axis. Glucose 32-39 NLR family pyrin domain containing 3 Homo sapiens 196-201 35584771-0 2022 Agonism of GPR120 Prevented High Glucose-Induced Apoptosis of Retinal Endothelial Cells through Inhibiting NLRP3 Inflammasome. Glucose 33-40 NLR family pyrin domain containing 3 Homo sapiens 107-112 35182568-10 2022 Epac1 and PKA can inhibit of P2X7, which will reduce NLRP3 inflammasome proteins in REC grown in high glucose. Glucose 102-109 NLR family pyrin domain containing 3 Homo sapiens 53-58 6427534-0 1984 Acute effects of a glucose load on plasma apolipoproteins A-I, A-II, C-II, and C-III in normal and non-insulin-dependent diabetic men. Glucose 19-26 NLR family pyrin domain containing 3 Homo sapiens 63-67 33729569-0 2021 Protective mechanisms of Taiwanese green propolis toward high glucose-induced inflammation via NLRP3 inflammasome signaling pathway in human gingival fibroblasts. Glucose 62-69 NLR family pyrin domain containing 3 Homo sapiens 95-100 33729569-10 2021 RESULTS: High glucose could induce IL-1beta-driven inflammatory responses in HGFs via the activation of NLRP3 inflammasome regulated by TLR2/TLR4 coupled ROS in NF-kappaB-dependent manner. Glucose 14-21 NLR family pyrin domain containing 3 Homo sapiens 104-109 33729569-12 2021 CONCLUSION: Taiwanese green propolis could elicit protective effects against IL-1beta-driven inflammation in high glucose-exposed HGFs through TLR2/TLR4 combined ROS/NF-kappaB/NLRP3 inflammasome pathway. Glucose 114-121 NLR family pyrin domain containing 3 Homo sapiens 176-181 34145545-4 2021 increased plasma glucose, fatty acids, and beta-amyloid are augmented during obesity and activate NLRP3 inflammasome expression. Glucose 17-24 NLR family pyrin domain containing 3 Homo sapiens 98-103 34084773-10 2021 Additionally, high glucose markedly activated NLRP3 inflammasome in RPMCs that was blunted by mPGES-1 inhibition. Glucose 19-26 NLR family pyrin domain containing 3 Homo sapiens 46-51 34997266-10 2022 Furthermore, PQQ abolished mitochondrial dysfunction and the activation of NF-kappaB/IkappaB, and decreased NLRP3 inflammation-mediated pyroptosis in AC16 cells under high-glucose conditions. Glucose 172-179 NLR family pyrin domain containing 3 Homo sapiens 108-113 34058229-0 2021 VDAC1 regulates mitophagy in NLRP3 inflammasome activation in retinal capillary endothelial cells under high-glucose conditions. Glucose 109-116 NLR family pyrin domain containing 3 Homo sapiens 29-34 33404978-0 2021 Telmisartan Inhibits the NLRP3 Inflammasome by Activating the PI3K Pathway in Neural Stem Cells Injured by Oxygen-Glucose Deprivation. Glucose 114-121 NLR family pyrin domain containing 3 Homo sapiens 25-30 33064063-6 2020 Furthermore, inhibition of the Warburg effect by 2-Deoxy-d-glucose reversed the increased expression of NLRP3 induced by Ni-refining fumes. Glucose 59-66 NLR family pyrin domain containing 3 Homo sapiens 104-109 32391974-0 2020 LncRNA MALAT1 promoted high glucose-induced pyroptosis of renal tubular epithelial cell by sponging miR-30c targeting for NLRP3. Glucose 28-35 NLR family pyrin domain containing 3 Homo sapiens 122-127 32439949-0 2020 High glucose mediates NLRP3 inflammasome activation via upregulation of ELF3 expression. Glucose 5-12 NLR family pyrin domain containing 3 Homo sapiens 22-27 32650532-4 2020 Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D. Glucose 125-132 NLR family pyrin domain containing 3 Homo sapiens 143-148 32707731-7 2020 Mechanistically, inhibiting Cbl increased surface expression of glucose transporter 1 (GLUT1) protein through post-transcriptional regulation, which increased cellular glucose uptake and consequently raised glycolytic capacity, and in turn enhanced NLRP3 inflammasome activation. Glucose 64-71 NLR family pyrin domain containing 3 Homo sapiens 249-254 32298723-9 2020 In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression. Glucose 90-97 NLR family pyrin domain containing 3 Homo sapiens 177-182 32298723-9 2020 In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression. Glucose 107-114 NLR family pyrin domain containing 3 Homo sapiens 177-182 32439949-3 2020 We hypothesized that ELF3 modulates MARK4 expression in vascular endothelial cells, thus contributing to high glucose-mediated NLRP3 inflammasome activation. Glucose 110-117 NLR family pyrin domain containing 3 Homo sapiens 127-132 32439949-5 2020 An in vitro study indicated that high glucose increased IL-1beta and IL-18 expression and activated the NLRP3 inflammasome via upregulation of MARK4 in human umbilical vein endothelial cells (HUVECs). Glucose 38-45 NLR family pyrin domain containing 3 Homo sapiens 104-109 31705795-3 2020 The IL-1beta response to excess glucose was mediated by uric acid-induced activation of the NLRP3 inflammasome. Glucose 32-39 NLR family pyrin domain containing 3 Homo sapiens 92-97 32018221-3 2020 Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death. Glucose 28-35 NLR family pyrin domain containing 3 Homo sapiens 103-108 32018221-3 2020 Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death. Glucose 173-180 NLR family pyrin domain containing 3 Homo sapiens 103-108 32420343-6 2020 Our data showed that high glucose induced NLRP3-caspase-1-GSDMD activation and pore formation in a dose- and time-dependent manner (p < 0.05) and resulted in the inflammatory cytokines IL-1beta and IL-18 and lactate dehydrogenase (LDH) release from HRPs (p < 0.05), which are all signs of HRP pyroptosis. Glucose 26-33 NLR family pyrin domain containing 3 Homo sapiens 42-47 32420343-9 2020 Taken together, our results firstly revealed that high glucose induced the loss of retinal pericytes partly via NLRP3-caspase-1-GSDMD-mediated pyroptosis. Glucose 55-62 NLR family pyrin domain containing 3 Homo sapiens 112-117 32329444-0 2020 HDAC6 inhibitor Cay10603 inhibits high glucose-induced oxidative stress, inflammation and apoptosis in retinal pigment epithelial cells via regulating NF-kappaB and NLRP3 inflammasome pathway. Glucose 39-46 NLR family pyrin domain containing 3 Homo sapiens 165-170 31703838-7 2020 Activation of NLRP3 inflammasome exacerbated podocyte autophagy and reduced podocyte nephrin expression, while silencing of NLRP3 efficiently restored podocyte autophagy and ameliorated podocyte injury induced by high glucose. Glucose 218-225 NLR family pyrin domain containing 3 Homo sapiens 124-129 31703838-8 2020 The results showed that NLRP3 was a negative regulator of autophagy and suggested that restoration of podocyte autophagy by inactivation of NLRP3 under high glucose could reduce podocyte injury. Glucose 157-164 NLR family pyrin domain containing 3 Homo sapiens 24-29 31703838-8 2020 The results showed that NLRP3 was a negative regulator of autophagy and suggested that restoration of podocyte autophagy by inactivation of NLRP3 under high glucose could reduce podocyte injury. Glucose 157-164 NLR family pyrin domain containing 3 Homo sapiens 140-145 31938471-0 2020 The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells. Glucose 36-43 NLR family pyrin domain containing 3 Homo sapiens 54-59 31938471-3 2020 Hence, this study was aimed to investigate whether high concentration of glucose (HG), which mimics the hyperglycemia environment, could initiate vascular calcification through NLRP3/IL-1beta inflammasome and the underlying mechanism. Glucose 73-80 NLR family pyrin domain containing 3 Homo sapiens 177-182 32062019-7 2020 Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1beta pathway, which could be reversed by activated Nrf2-HO-1 pathway. Glucose 31-38 NLR family pyrin domain containing 3 Homo sapiens 276-281 31885713-0 2020 Hydrogen sulfide modulates high glucose-induced NLRP3 inflammasome activation in 3T3-L1 adipocytes. Glucose 32-39 NLR family pyrin domain containing 3 Homo sapiens 48-53 31885713-4 2020 The present study aimed to investigate the effect of H2S on high glucose (HG)-induced NLRP3 inflammasome activation in adipocytes. Glucose 65-72 NLR family pyrin domain containing 3 Homo sapiens 86-91 31736762-3 2019 Methods: THP-1-derived macrophages were treated with high glucose to induce NLRP3 inflammasome activation. Glucose 58-65 NLR family pyrin domain containing 3 Homo sapiens 76-81 31736762-9 2019 Conclusion: Rapamycin can ameliorate high glucose-induced NLRP3 inflammasome activation by attenuating the mTOR/NF-kappaB signaling pathway in macrophages. Glucose 42-49 NLR family pyrin domain containing 3 Homo sapiens 58-63 31638409-3 2019 A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-kappaB, NLRP3, caspase 1, interleukin-1beta, inducible nitric oxide synthase, and tumor necrosis factor alpha, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes. Glucose 7-14 NLR family pyrin domain containing 3 Homo sapiens 122-127 31302140-1 2019 Activation of the NLRP3 inflammasome plays an important role in high glucose- induced endothelial dysfunction in patients with type 2 diabetes mellitus (T2DM). Glucose 69-76 NLR family pyrin domain containing 3 Homo sapiens 18-23 31571967-9 2019 Moreover, either high glucose or IL-1beta promoted the expression of adhesion molecules, which were suppressed by NLRP3 knockdown or IL-1beta receptor antagonist. Glucose 22-29 NLR family pyrin domain containing 3 Homo sapiens 114-119 31571967-1 2019 Background: NLRP3 inflammasome can be activated by high glucose and links inflammation and metabolic disease. Glucose 56-63 NLR family pyrin domain containing 3 Homo sapiens 12-17 31571967-8 2019 In vitro, the expression of NLRP3 inflammasome components and the secretion of IL-1beta were augmented by high glucose in HUVECs. Glucose 111-118 NLR family pyrin domain containing 3 Homo sapiens 28-33 31351069-0 2019 The protective effects of orexin a against high glucose-induced activation of NLRP3 inflammasome in human vascular endothelial cells. Glucose 48-55 NLR family pyrin domain containing 3 Homo sapiens 78-83 31351069-5 2019 In the present study, we explored the role of orexin A, an endogenous peptide produced in the hypothalamus, in high glucose-induced activation of the NLRP3 inflammasome, oxidative stress, and expression of several key cytokines. Glucose 116-123 NLR family pyrin domain containing 3 Homo sapiens 150-155 31351069-7 2019 We also show that orexin A inhibits high glucose-induced expression of TxNIP, which is crucial to the activation of the NLRP3 inflammasome, as well as that of HMGB1. Glucose 41-48 NLR family pyrin domain containing 3 Homo sapiens 120-125 31302140-3 2019 In the current study, we aimed to investigate whether dulaglutide possesses a protective effect against high glucose- induced activation of the NLRP3 inflammasome. Glucose 109-116 NLR family pyrin domain containing 3 Homo sapiens 144-149 31302140-6 2019 Dulaglutide suppressed high glucose- induced activation of NLRP3 inflammasome by reducing the expression of NLRP3, ASC, and cleaved caspase 1 (P10). Glucose 28-35 NLR family pyrin domain containing 3 Homo sapiens 59-64 31108165-12 2019 Taken together, these results suggest that downregulation of hsa_circ_0068087 ameliorates TLR4/NF-kappaB/NLRP3 inflammasome-mediated inflammation and endothelial cell dysfunction in the high glucose condition by sponging miR-197. Glucose 191-198 NLR family pyrin domain containing 3 Homo sapiens 105-110 31302140-6 2019 Dulaglutide suppressed high glucose- induced activation of NLRP3 inflammasome by reducing the expression of NLRP3, ASC, and cleaved caspase 1 (P10). Glucose 28-35 NLR family pyrin domain containing 3 Homo sapiens 108-113 31178664-6 2019 Furthermore, high glucose increased the mRNA expression levels of NLRP3, ACS, and caspase-1. Glucose 18-25 NLR family pyrin domain containing 3 Homo sapiens 66-71 31354329-3 2019 We and others have shown that high glucose can activate the NOD-like receptor family, pyrin domain containing family member 3 (NLRP3) pathway, leading to increased levels of cleaved caspase 1 and IL-1beta to activate a number of inflammatory pathways in the retina. Glucose 35-42 NLR family pyrin domain containing 3 Homo sapiens 127-132 30660990-7 2019 Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10). Glucose 53-60 NLR family pyrin domain containing 3 Homo sapiens 70-75 30660990-7 2019 Importantly, anagliptin treatment downregulated high glucose- induced NLRP3 inflammasome activation, as evidenced by reducing the expressions of NLRP3, ASC, and cleaved caspase-1 (P10). Glucose 53-60 NLR family pyrin domain containing 3 Homo sapiens 145-150 30906223-0 2019 Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4/NF-kappaB and CaSR. Glucose 33-40 NLR family pyrin domain containing 3 Homo sapiens 49-54 30804327-8 2019 Especially, FADD, but not IL-1beta, secretion following NLRP3 inflammasome activation required extracellular glucose. Glucose 109-116 NLR family pyrin domain containing 3 Homo sapiens 56-61 30906223-10 2019 In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression. Glucose 58-65 NLR family pyrin domain containing 3 Homo sapiens 90-95 30906223-7 2019 The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1beta (IL-1beta), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR. Glucose 29-36 NLR family pyrin domain containing 3 Homo sapiens 119-124 30906223-11 2019 In conclusion, this study suggested that As-IV could inhibit high glucose-induced NLRP3 inflammasome activation and subsequent secretion of proinflammatory cytokines via inhibiting TLR4/NF-kappaB signaling pathway and CaSR, which provides new insights into the anti-inflammatory activity of As-IV. Glucose 66-73 NLR family pyrin domain containing 3 Homo sapiens 82-87 30906223-9 2019 Meanwhile, NPS2143, BAY 11-7082, and INF39 could significantly abolish the high glucose-enhanced NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression in vitro. Glucose 80-87 NLR family pyrin domain containing 3 Homo sapiens 97-102 30307163-2 2018 In this study, we explored the role of NLRP3 inflammasome on high glucose (HG) or transforming growth factor-B1 (TGFB1)-induced EMT in HK-2 cells. Glucose 66-73 NLR family pyrin domain containing 3 Homo sapiens 39-44 30591217-0 2019 Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22. Glucose 40-47 NLR family pyrin domain containing 3 Homo sapiens 104-109 30591217-11 2019 Together, our results suggest that lncRNA MALAT1 promotes high glucose-induced pyroptosis of endothelial cells partly by affecting NLRP3 expression through competitively binding miR-22. Glucose 63-70 NLR family pyrin domain containing 3 Homo sapiens 131-136 30471618-2 2019 Our previous study has demonstrated that in human peritoneal mesothelial cells (HPMCs), exposure to high glucose-based peritoneal dialysis (PD) solutions induced mitochondrial reactive oxygen species (ROS) production, activation of NLRP3 inflammasome and IL-1beta expression. Glucose 105-112 NLR family pyrin domain containing 3 Homo sapiens 232-237 30471618-3 2019 This study aimed to investigate the effect of high glucose-based PD fluids on the TXNIP expression and the underlying mechanisms by which TXNIP-NLRP3 interaction mediates the inflammatory injury to HPMCs in high glucose-based PD fluids conditions. Glucose 51-58 NLR family pyrin domain containing 3 Homo sapiens 144-149 30471618-3 2019 This study aimed to investigate the effect of high glucose-based PD fluids on the TXNIP expression and the underlying mechanisms by which TXNIP-NLRP3 interaction mediates the inflammatory injury to HPMCs in high glucose-based PD fluids conditions. Glucose 212-219 NLR family pyrin domain containing 3 Homo sapiens 144-149 30471618-8 2019 We also found that ROS generation induced by high glucose-based PD solutions disrupts the TRX1-TXNIP association, while promoting the binding of TXNIP to NLRP3 in HPMCs. Glucose 50-57 NLR family pyrin domain containing 3 Homo sapiens 154-159 30471618-9 2019 Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1beta expression. Glucose 81-88 NLR family pyrin domain containing 3 Homo sapiens 121-126 30119194-13 2018 The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells. Glucose 117-124 NLR family pyrin domain containing 3 Homo sapiens 95-100 30307163-0 2018 Knockdown of NLRP3 alleviates high glucose or TGFB1-induced EMT in human renal tubular cells Tubular injury is one of the crucial determinants of progressive renal failure in diabetic nephropathy (DN), while epithelial-to-mesenchymal transition (EMT) of tubular cells contributes to the accumulation of matrix protein in the diabetic kidney. Glucose 35-42 NLR family pyrin domain containing 3 Homo sapiens 13-18 29682582-0 2018 Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway. Glucose 68-75 NLR family pyrin domain containing 3 Homo sapiens 112-117 29263464-14 2017 CONCLUSION: Long-term application of high glucose-based peritoneal dialysis fluids can trigger the consistent activation of NLRP3-IL-1beta in peritoneal mesothelial cells. Glucose 42-49 NLR family pyrin domain containing 3 Homo sapiens 124-129 29263464-0 2017 [Effect of high glucose-based peritoneal dialysis fluids on NLRP3-IL-1beta in human peritoneal mesothelial cells]. Glucose 16-23 NLR family pyrin domain containing 3 Homo sapiens 60-65 28726778-5 2017 Moreover, in high-glucose-stimulated HRECs, increased production of the NLRP3 inflammasome activation and severe apoptosis were rescued with Mcc950 treatment. Glucose 18-25 NLR family pyrin domain containing 3 Homo sapiens 72-77 29263464-1 2017 OBJECTIVE: To explore the effect of high glucose-based peritoneal dialysis fluids on NLRP3-IL-1beta in human peritoneal mesothelial cells. Glucose 41-48 NLR family pyrin domain containing 3 Homo sapiens 85-90 28849014-0 2017 Zinc inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells. Glucose 19-26 NLR family pyrin domain containing 3 Homo sapiens 35-40 28972154-3 2017 We hypothesized that raising glucose above the physiological level of 5.5 mm would stimulate leukocytes to produce MPs and activate the nucleotide-binding domain, leucine-rich repeat pyrin domain-containing 3 (NLRP3) inflammasome. Glucose 29-36 NLR family pyrin domain containing 3 Homo sapiens 210-215 28798291-4 2017 RESULTS After six hours, 12 hours, and 24 hours of high glucose stimulation, the secretion of IL-1beta in human glomerular mesangial cells, compared to unstimulated cells, was 1.85-fold, 3.04-fold, and 4.14-fold; the expression of NLRP3 increased by 2.20-fold, 4.62-fold, and 8.32-fold; and the expression of caspase-1 was increased by 1.60-fold, 2.72-fold, and 3.67-fold. Glucose 56-63 NLR family pyrin domain containing 3 Homo sapiens 231-236 28726778-6 2017 Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway. Glucose 107-114 NLR family pyrin domain containing 3 Homo sapiens 180-185 28726778-6 2017 Additionally, the inhibitory effect of Mcc950 was mimicked through downregulation of NEK7 by siRNA in high-glucose-induced HRECs and Mcc950 treatment remarkably inhibited Nek7 and NLRP3 interactions by co-immunoprecipitation, suggesting that Mcc950 may be a potentially protective agent against inflammation, likely via downregulation of the Nek7-NLRP3 pathway. Glucose 107-114 NLR family pyrin domain containing 3 Homo sapiens 347-352 28854426-0 2017 Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages. Glucose 121-128 NLR family pyrin domain containing 3 Homo sapiens 50-55 28854426-2 2017 We hypothesized that stimulation with high glucose following a pro-inflammatory signal would lead to autophagy inhibition, reactive oxygen species (ROS) production and eventually to the activation of the Nod-like receptor protein (NLRP) -3. Glucose 43-50 NLR family pyrin domain containing 3 Homo sapiens 204-239 28854426-9 2017 Our data showed that high glucose inhibited autophagy, induced ROS production, and activated NLRP3 inflammasome and cytokine secretion in THP-1-derived macrophages. Glucose 26-33 NLR family pyrin domain containing 3 Homo sapiens 93-98 28854426-10 2017 To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion. Glucose 14-21 NLR family pyrin domain containing 3 Homo sapiens 30-35 28854426-10 2017 To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion. Glucose 14-21 NLR family pyrin domain containing 3 Homo sapiens 132-137 28854426-10 2017 To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion. Glucose 14-21 NLR family pyrin domain containing 3 Homo sapiens 132-137 28854426-12 2017 Autophagy inhibition and ROS generation play an essential role in high glucose-induced NLRP3 inflammasome activation and cytokine secretion in macrophages. Glucose 71-78 NLR family pyrin domain containing 3 Homo sapiens 87-92 27731349-0 2016 TRPM2 regulates TXNIP-mediated NLRP3 inflammasome activation via interaction with p47 phox under high glucose in human monocytic cells. Glucose 102-109 NLR family pyrin domain containing 3 Homo sapiens 31-36 28164132-0 2017 NLRP3 Inflammasome Expression and Signaling in Human Diabetic Wounds and in High Glucose Induced Macrophages. Glucose 81-88 NLR family pyrin domain containing 3 Homo sapiens 0-5 28164132-2 2017 To investigate the contribution and mechanism of NLRP3 inflammasome expression in human wounds in diabetes mellitus and in high glucose induced macrophages. Glucose 128-135 NLR family pyrin domain containing 3 Homo sapiens 49-54 28164132-5 2017 We also examined whether high glucose induces NLRP3 inflammasome expression in cultures THP-1-derived macrophages and the influence on IL-1beta expression. Glucose 30-37 NLR family pyrin domain containing 3 Homo sapiens 46-51 28164132-8 2017 High glucose induced a significant increase in NLRP3 inflammasome and IL-1beta expression in THP-1-derived macrophages. Glucose 5-12 NLR family pyrin domain containing 3 Homo sapiens 47-52 28164132-12 2017 The higher expression of NLRP3, caspase1, and secretion of IL-1beta, signaling, and activation might contribute to the hyperinflammation in the human diabetic wound and in high glucose induced macrophages. Glucose 177-184 NLR family pyrin domain containing 3 Homo sapiens 25-30 28083517-4 2016 Methods:P. gingivalis strain CCUG25226 was used to study the mechanisms underlying the regulation of HGF NLRP3 expression by the infection of high-glucose-treated P. gingivalis (HGPg). Glucose 147-154 NLR family pyrin domain containing 3 Homo sapiens 105-110 27731349-3 2016 Here, we identified that HG (30 mM glucose for 48 h) induced the activation of the NLRP3-ASC inflammasome, leading to caspase-1 activation, and IL-1beta and IL-18 secretion in human monocytic cell lines. Glucose 35-42 NLR family pyrin domain containing 3 Homo sapiens 83-88 26095630-7 2015 After 24 h of incubation with different concentrations of glucose, our results showed a significant increase in NLRP3 expression. Glucose 58-65 NLR family pyrin domain containing 3 Homo sapiens 112-117 26881256-0 2016 High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells. Glucose 5-12 NLR family pyrin domain containing 3 Homo sapiens 42-47 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Glucose 86-93 NLR family pyrin domain containing 3 Homo sapiens 38-43 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Glucose 86-93 NLR family pyrin domain containing 3 Homo sapiens 257-262 26881256-6 2016 Simultaneously, the mRNA and protein levels of TXNIP, NLRP3, procaspase-1, and IL-1beta were significantly induced by high glucose concentration and lipopolysaccharide in a dose-dependent and time-dependent manner in vitro. Glucose 123-130 NLR family pyrin domain containing 3 Homo sapiens 54-59 26881256-8 2016 Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1beta inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy. Glucose 37-44 NLR family pyrin domain containing 3 Homo sapiens 88-93 26825654-2 2016 Here, we investigated the effect of glucose-based PD solutions on mitochondrial reactive oxygen species (ROS) and nod-like receptor 3 (NLRP3) inflammasome activation in human PMCs (HPMCs). Glucose 36-43 NLR family pyrin domain containing 3 Homo sapiens 114-133 26825654-3 2016 Exposure of HPMCs to high glucose-based PD solutions resulted in ROS production, which can trigger NLRP3 activation, leading to IL-1beta secretion. Glucose 26-33 NLR family pyrin domain containing 3 Homo sapiens 99-104 25394884-6 2015 Excess glucose-induced trophoblast IL-1beta production was inhibited by disabling the Nalp3/ASC inflammasome. Glucose 7-14 NLR family pyrin domain containing 3 Homo sapiens 86-91 25879284-6 2015 The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age. Glucose 194-201 NLR family pyrin domain containing 3 Homo sapiens 4-9 26102024-0 2015 Inhibition of autophagy induces IL-1beta release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress. Glucose 126-133 NLR family pyrin domain containing 3 Homo sapiens 85-90 25325516-8 2015 The expression of NLRP3 was significantly upregulated in HGECs when stimulated in vitro by LPS or high glucose (P = 0.00). Glucose 103-110 NLR family pyrin domain containing 3 Homo sapiens 18-23 25325516-9 2015 The simultaneous stimulation of LPS and high glucose contributed to significant upregulation of NLRP3 expression versus LPS or high glucose alone (P = 0.00). Glucose 45-52 NLR family pyrin domain containing 3 Homo sapiens 96-101 25325516-9 2015 The simultaneous stimulation of LPS and high glucose contributed to significant upregulation of NLRP3 expression versus LPS or high glucose alone (P = 0.00). Glucose 132-139 NLR family pyrin domain containing 3 Homo sapiens 96-101 25017793-3 2014 In our study, we confirmed that high glucose (HG) concentrations induced NALP3 inflammasome activation both in vivo and in vitro. Glucose 37-44 NLR family pyrin domain containing 3 Homo sapiens 73-78 25868270-6 2014 This article reviews the activation and regulation of NL-RP3 inflammasome, and the effect of NLRP3 inflammasome on glucose metabolism and its targeted therapy in diabetes. Glucose 115-122 NLR family pyrin domain containing 3 Homo sapiens 93-98 24422572-6 2014 The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease. Glucose 108-115 NLR family pyrin domain containing 3 Homo sapiens 132-137 23434541-8 2013 In vitro culture experiments showed NLRP3 protein expression, cleavage of caspase-1 and IL-1beta, and release of IL-1beta, IL-18 and ATP in HK-2 cells significantly increased after high glucose stimulation. Glucose 186-193 NLR family pyrin domain containing 3 Homo sapiens 36-41 23434541-11 2013 Taken together, these results suggest that ATP-P2X4 signaling mediates high glucose-induced activation of the NLRP3 inflammasome, regulates IL-1 family cytokine secretion, and causes the development of tubulointerstitial inflammation in DN. Glucose 76-83 NLR family pyrin domain containing 3 Homo sapiens 110-115