PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34692754-4 2021 In this study, we obtained a fat-soluble extract from Chlorella (CE) and demonstrated that it reduced NLRP3 inflammasome activation by inhibiting mitochondrial reactive oxygen species and caspase-1 activation. Oxygen 169-175 NLR family pyrin domain containing 3 Homo sapiens 102-107 34108686-5 2021 Conditional deletion of TIM-3 in DCs led to increased accumulation of reactive oxygen species resulting in NLRP3 inflammasome activation. Oxygen 79-85 NLR family pyrin domain containing 3 Homo sapiens 107-112 32058297-4 2020 Generation of reactive oxygen species (ROS) and intracellular calcium mobilization can activate the NLRP3 inflammasome. Oxygen 23-29 NLR family pyrin domain containing 3 Homo sapiens 100-105 32707731-6 2020 Upon NLRP3 inflammasome activation, inhibiting Cbl increased glycolysis-dependent activation of mitochondrial respiration and increased the production of reactive oxygen species, which contributes to NLRP3 inflammasome activation and IL-1beta secretion. Oxygen 163-169 NLR family pyrin domain containing 3 Homo sapiens 200-205 31683435-10 2020 Both in vivo and in vitro, CBNPs exposure significantly increased the expression of NLRP3 inflammasome, accompanied by the increased reactive oxygen species (ROS), decreased miR-96 and increased FOXO3a expressions dose -and time-dependently. Oxygen 142-148 NLR family pyrin domain containing 3 Homo sapiens 84-89 35474599-5 2022 Deactivated AMPK induces metabolic dysregulation, mitochondrial fragmentation, and reactive oxygen species formation, leading to the activation of the NLRP3 inflammasome. Oxygen 92-98 NLR family pyrin domain containing 3 Homo sapiens 151-156 32335773-0 2021 Knockdown of TRIM22 Relieves Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis and Inflammation Through Inhibition of NF-kappaB/NLRP3 Axis. Oxygen 29-35 NLR family pyrin domain containing 3 Homo sapiens 137-142 31993073-5 2020 In atherosclerotic plaques, excessive generation of reactive oxygen species (ROS) activates the NLRP3 inflammasome. Oxygen 61-67 NLR family pyrin domain containing 3 Homo sapiens 96-101 31870428-2 2019 Reactive oxygen species (ROS) play an important role in OA development; they may activate the NLRP3 inflammasome, thereby inducing the secretion of proinflammatory IL-1beta and IL-18, leading to the aggravation of the downstream inflammatory response. Oxygen 9-15 NLR family pyrin domain containing 3 Homo sapiens 94-99 31490096-0 2020 Plumbagin attenuated oxygen-glucose deprivation/reoxygenation-induced injury in human SH-SY5Y cells by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome. Oxygen 21-27 NLR family pyrin domain containing 3 Homo sapiens 141-146 31284572-3 2019 The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. Oxygen 180-186 NLR family pyrin domain containing 3 Homo sapiens 4-9 31577960-5 2019 Then, we will debate the NLRP3 inflammasome putting the focus on its activation through the canonical, non-canonical and alternative pathways and the triggers involved herein namely endoplasmic reticulum stress, mitochondrial dysfunction, reactive oxygen species and amyloid beta peptide. Oxygen 248-254 NLR family pyrin domain containing 3 Homo sapiens 25-30 32042826-10 2019 Candidate genes were identified after adjustment for age, sex and presence of lymphopenia with significantly negative correlations with partial pressure of O2 in an arterial blood (PaO2) and fraction of inspiration O2 (FiO2) ratio, among which NLRP3, SOS1, ELF1 and STAT3 held an increasing expression in ex vivo validation while the others, PSMA5, CLEC4D, CD300A, PRKD2 and PSMA2 showed the opposite alteration from those in vivo. Oxygen 156-158 NLR family pyrin domain containing 3 Homo sapiens 244-249 32042826-10 2019 Candidate genes were identified after adjustment for age, sex and presence of lymphopenia with significantly negative correlations with partial pressure of O2 in an arterial blood (PaO2) and fraction of inspiration O2 (FiO2) ratio, among which NLRP3, SOS1, ELF1 and STAT3 held an increasing expression in ex vivo validation while the others, PSMA5, CLEC4D, CD300A, PRKD2 and PSMA2 showed the opposite alteration from those in vivo. Oxygen 183-185 NLR family pyrin domain containing 3 Homo sapiens 244-249 31606392-7 2019 During activation of NLRP3, the mitochondrial membrane potential (MMP) decreased, the opening rate of mitochondrial permeability transition pore (MPTP) increased, and the content of reactive oxygen species (ROS) increased. Oxygen 191-197 NLR family pyrin domain containing 3 Homo sapiens 21-26 31819864-0 2019 Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And TXNIP. Oxygen 114-120 NLR family pyrin domain containing 3 Homo sapiens 56-61 31485604-10 2019 In conclusion, to the best of our knowledge, the results of the present study demonstrated for the first time that overexpression of miRNA-200a-3p promoted inflammation in sepsis-induced brain injury through reactive oxygen species-induced NLRP3. Oxygen 217-223 NLR family pyrin domain containing 3 Homo sapiens 240-245 31687078-3 2019 ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation. Oxygen 179-185 NLR family pyrin domain containing 3 Homo sapiens 35-40 29950247-2 2018 The recent studies showed that all of S100A9/TLR4, S100A9/CD33 and Nox/ROS signaling pathways can activate oxygen-sensitivity NLRP3 inflammasome and then induce the pyroptosis of hematopoeitic stem cells (HSC) / hematopeitic pregenitor cells (HPC), resulting in ineffective hematopoiesis in patients with MDS. Oxygen 107-113 NLR family pyrin domain containing 3 Homo sapiens 126-131 29257274-7 2018 In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion. Oxygen 73-79 NLR family pyrin domain containing 3 Homo sapiens 183-188 29067455-0 2017 Hyperbaric oxygen alleviates the activation of NLRP-3-inflammasomes in traumatic brain injury. Oxygen 11-17 NLR family pyrin domain containing 3 Homo sapiens 47-53 29067455-2 2017 In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP-3 inflammasome pathway following TBI. Oxygen 73-79 NLR family pyrin domain containing 3 Homo sapiens 101-107 27826011-5 2016 Hyperglycaemia, hyperlipidaemia and hyperuricaemia can activate the NLRP3 inflammasome, which then mediates the occurrence and development of DN through the K+ channel model, the lysosomal damage model and the active oxygen cluster model. Oxygen 217-223 NLR family pyrin domain containing 3 Homo sapiens 68-73 27058421-3 2016 Here we report that hypoxia (1% O2) treatment of PrECs, prostate cell lines, and a macrophage cell line (THP-1) increased the levels of NLRP3, AIM2, and pro-IL-1beta. Oxygen 32-34 NLR family pyrin domain containing 3 Homo sapiens 136-141 26512962-7 2015 This evidence suggests that both potassium efflux and calcium influx are necessary for mitochondrial reactive oxygen generation upstream of NLRP3 inflammasome assembly and pyroptotic cell death. Oxygen 110-116 NLR family pyrin domain containing 3 Homo sapiens 140-145 26512962-8 2015 We propose a model wherein potassium efflux is necessary for calcium influx, resulting in mitochondrial reactive oxygen generation to trigger the NLRP3 inflammasome. Oxygen 113-119 NLR family pyrin domain containing 3 Homo sapiens 146-151 30415294-7 2018 Cell culture in 0.2% O2 induced expression of NLRP3 and pro-IL-1beta genes but not of the pro-IL-18 gene. Oxygen 21-23 NLR family pyrin domain containing 3 Homo sapiens 46-51