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Lipopolysaccharide inhibits NLRP3. 85 / 85
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"Since there is no effective treatment strategy to reduce ARDS associated lung injury and fibrosis, it could be suggested that pirfenidone could attenuate lung injury based on published data showing that pirfenidone reduces LPS induced acute lung injury and subsequent fibrosis by suppressing NLRP3 inflammasome activation (34)."
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"MNS prevents the oligomerization and activation of the NLRP3 inflammasome, inhibiting LPS induced NLRP3 activation and IL-1beta release from mouse BMDMs with an IC 50 of 2 microMStructures of direct NLRP3 inhibitors that have the potential to be covalent modifiers.NLRP3 inflammasome inhibitors MNS (3,4-methylenedioxy-beta-nitrostyrene) [29], INF39 (ethyl 2-(2-chlorobenzyl) acrylate) [30], INF58 [31] and OLT1177 (dapansutrile) [32] also bind to the ATP binding site."
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"Not surprisingly, resveratrol, the polyphenol present in the skin of grapes, another sirtuin activator, also inhibits NLRP3 inflammasome activation in mice by preserving mitochondrial function, and protects against hepatosteatosis, renal inflammation and LPS induced lung injury [XREF_BIBR - XREF_BIBR]."
eidos
"Combining previous results that demonstrated that the expression of NLRP3 was upregulated by LPS and downregulated by NEAT1 , in the present study , the autophagy inhibitor , Baf A1 ( 200 nM for 4 h of incubation ) , was applied on the cells in the different groups , and western blot analysis of LC3 , p62 , NLRP3 and OPN expression was then performed ."
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"The inhibitory effects of WA in LPS induced upregulation of Tnfa, Il6, Il1b, were lost in Nlrp3 -/- macrophage when WA was used at the lower dose of 0.2 microM, while this effect was still found with WA at the higher dose of 0.5 microM in Nlrp3 -/- macrophage, suggesting that WA has both NLRP3 dependent and NLRP3 independent anti-inflammatory effects."
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"Wierenga et al. found that DHA pre-incubation suppressed silica induced inflammasome activation and release of IL-1beta and IL-1alpha in macrophages and that these suppressive effects were linked to inhibition of LPS induced Nlrp3, Il1b, and Il1a transcription, potentially through the activation of the transcription factor PPARgamma."
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"Both acute and chronic liver injury models were used: lipopolysaccharide (LPS)/adenosine-triphosphate (ATP) to induce in vivo NLRP3 activation, choline-deficient, L-amino acid-defined high-fat diet (CDAA-HFAT), and Western-type diet to induce fibrotic-non-alcoholic steatohepatitis (NASH)."
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"Since there is no effective treatment strategy to reduce ARDS associated lung injury and fibrosis, it could be suggested that pirfenidone could attenuate lung injury based on published data showing that pirfenidone reduces LPS induced acute lung injury and subsequent fibrosis by suppressing NLRP3 inflammasome activation."
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"P. gingivalis activates the double-stranded RNA (dsRNA)-dependent kinase in osteoblastic MC3T3-E1 cells, thereby promoting NLRP3 expression by activating NF-κB, and LPS from P. gingivalis triggers NLRP3 inflammasome-dependent pyroptosis of gingival fibroblasts, which can be alleviated by eldecalcitol (a vitamin D analog) and inhibitors of ROS or NLRP3 (256, 257)."
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"Here, we observed the therapeutic effects of Ori on depression by inhibiting NLRP3 inflammasome via activation of autophagy both in LPS-induced depression mice and LPS-treated astrocytes.Our results showed that Ori treatment alleviated LPS-induced depressive-like behaviors in mice according to sucrose preference, FST and TST assays that have been widely applied as animal models for screening potential antidepressants."
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"Both acute and chronic liver injury models were used: lipopolysaccharide (LPS)/adenosine-triphosphate (ATP) to induce in vivo NLRP3 activation, choline-deficient, L-amino acid-defined high-fat diet (CDAA-HFAT), and Western-type diet to induce fibrotic-non-alcoholic steatohepatitis (NASH)."
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"Our findings have, for the first time, revealed the novel mechanism underlying the inhibitory effect of molecular hydrogen on LPS caused NLRP3 inflammasome activation, highlighting the promising application of this new antioxidant in the treatment of LPS associated inflammatory pathological damage."
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"Recently, in vitro and in vivo studies showed that H 2 S mitigated lipopolysaccharide (LPS)-induced sepsis against oxidative stress and inflammation damage mediated by the NADPH oxidase 4 (Nox4) pathway [XREF_BIBR], inhibiting the vicious cycle of NLRP3 inflammasome and oxidative stress in human retinal pigment epithelial cells [XREF_BIBR] and in hypertensive rats [XREF_BIBR]."
| PMC
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"In vitro, HD inhibited LPS-induced oxidative stress and inflammation in RAW 264.7 cells, which largely depend upon the upregulation of antioxidant defensive Nrf2 pathway, thereby suppressing LPS-activated proinflammatory mediator secretion, NLRP3 inflammasome, and MAPK/NF-κB signaling pathway."
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"NU9056 significantly reduced LPS-induced apoptosis of microglia, the average fluorescence intensity of ROS, and the release of IL-1beta and IL-18, while improving cell viability in vitro.Conclusions: NU9056 might effectively alleviate LPS-induced cognitive impairment and emotional disorder in experimental mice by inhibiting the NLRP3 inflammasome."
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"In vivo, CORM2 treatment prevented NLRP3 activation in an experimental model of LPS driven acute lung injury [XREF_BIBR], while CORM-3 administration resulted in decreased IL-1beta production in mice with streptozotocin induced diabetes [XREF_BIBR] and suppressed NLRP3 activation in cardiac fibroblasts from mice with LPS induced sepsis resulting in improved cardiac function [XREF_BIBR]."