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Reactive oxygen species inhibits NLRP3. 105 / 105
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103
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"Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS)."
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"Indeed, ROS is identified as a potent endogenous ligand for NLRP3, since the early reports has demonstrated that the inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-induced ROS inhibited NLRP3 activation in macrophages treated with ATP (Cruz et al., 2007); meanwhile, the absence of the p22phox subunit within NADPH oxidase substantially attenuated IL-1β production when macrophages exposed with asbestos (Dostert et al., 2008)."
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"We reported previously that high glucose and lipopolysaccharide activate ROS-TXNIP-NLRP3 inflammasome signaling in GMCs, but ROS inhibitor N-acetylcysteine (NAC) could not completely inhibit the activation of NLRP3 inflammasome induced by high glucose, suggesting that there may be other pathways by which high glucose primes ROS-NLRP3 inflammasome signaling [XREF_BIBR]."
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"It has been demonstrated that a low level of ROS positive regulate the priming signal of the NLRP3 inflammasome and promote NLRP3 inflammasome activation; however, Erttmann and Gekara demonstrated that a high level of ROS release by Streptococcus pneumonia increased the oxidative levels of the inflammasome components ASC and caspases and inhibited the NLRP3 inflammasome."
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"Thus, our findings suggest that moderate ROS levels act as triggers for the NLRP3 inflammasome in line with the known role of mitochondrial ROS released from stressed mitochondria (Latz et al., 2013; Zhou et al., 2011), while excessive ROS levels display an opposite effect and inhibit NLRP3 activation."
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"Finally, RSV and Japanese encephalitis virus (JEV) have both been found to induce NLRP3 activation through K + efflux from the cell and ROS production as treatment with K + buffered medium or the ROS inhibitors APDC or diphenyleneiodonium chloride (DPI) inhibited NLRP3 inflammasome activation."
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"Therefore, to analyze the ROS regulation of NLRP3 inflammasome in brain I/R injury, we chose 250 mg/kg of NAC and 500 nmol of ATP as the optimum dose and concentration, respectively, for further study.We analyzed ROS levels in OE-Nrf2 and sh Nrf2 of rat MCAO models and determined the role of ROS in Nrf2-induced NLRP3 inflammasome inhibition."
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"The administration of a non-specific ROS scavenger, PBN, markedly alleviated mechanical allodynia and inhibited the activation of NLRP3 inflammasome in DRGs and sciatic nerve of the paclitaxel-induced neuropathic pain model.Chemotherapy-induced pain is the most common treatment-limiting complication encountered by cancer patients receiving taxane-, vinca alkaloid-, or platin-based chemotherapy."
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"Cells were pretreated for 1h prior to stimulation with 1 microM MCC950 or 25 microg/ml glybenclamide to inhibit NLRP3 activation, 10 microM DPI to inhibit cellular reactive oxygen species (ROS) production, 100 microM cathepsin inhibitor Ca-047-Me or indicated amounts of the pan-caspase inhibitor z-VAD-fmk."
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"The administration of a non-specific reactive oxygen species scavenger, phenyl-N-tert-butylnitrone, markedly alleviated mechanical allodynia and inhibited the activation of NLRP3 inflammasome in L4-6 dorsal root ganglia and sciatic nerve of the paclitaxel-induced neuropathic pain model."
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"Pathophysiological changes mediated by mitochondria including the imbalance in mitochondrial dynamics and the release of cytochrome c, mitochondrial DNA or reactive oxygen species (ROS) can either activate or inhibit the NLRP3 inflammasome [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"As mitochondria and ROS are critical for NLRP3 inflammasome activation [69,70], we showed that melatonin blocked morphine-induced NLRP3 inflammasome in vitro and in vivo by decreasing the generation of ROS level and CTSB release, which were reported to activate NLRP3 [53,54,66,71,72] and suppress morphine antinociceptive tolerance [73]."
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"Methods : Vascular reactivity, reactive oxygen species (ROS) generation, calcium (Ca 2+) influx and caspase-1 and IL-1beta activation were determined in mesenteric resistance arteries from normoglicemic and streptozotocin induced diabetic C57BL/6 and NLRP3 knockout (Nlrp3 -/-) mice."