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Lipopolysaccharide inhibits NLRP3. 137 / 137
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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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"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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"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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"These findings showed that Aβ42 activates Syk to inactivate AMPK and activate Akt, with this series of signaling pathways inducing mitochondrial damage and oxidative stress through mitochondrial hyperfission, which strongly activates the NLRP3 inflammasome in microglia.2.4
LPS-induced activation of the NLRP3 inflammasome is attenuated by flufenamic acid."
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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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"Based on these results, we speculated that PSP might exhibit a protective effect against SALI through regulating NLRP3/GSDMD signals.In summary, as shown in Figure 7, our experiments demonstrate a potential protective role of PSP against SALI induced by LPS, which may contribute to inhibiting NLRP3/GSDMD signals."
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"), a prenylflavonoid extracted from the hop plants (Humulus lupulus) (0, 18, 35, and 70 μmol/kg, i.p., for 30 min), showed a protective effect against oxidative stress and inflammatory damage by regulation of the Nrf2 pathway through AMPK/GSK3β activation, and suppression of LPS-activated Txnip / NLRP3 inflammation and the NF-κB signaling pathway (64)."
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"IF analysis (Fig. 4b, f) also confirmed that LPS/ATP co-stimulation led to a significant increase of NLRP3 fluorescent spots in cells (P < 0.01), whereas intervention with PLD significantly reduced the formation and expression of NLRP3 fluorescent spots (P < 0.01); 5.0 μM PLD was more effective than 2.5 μM PLD (P < 0.05)."
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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]."
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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"In conclusion, we identified PPARα as a direct target of FMN, and our data firstly indicated that FMN ameliorates LPS-induced depression-like behaviors through rebalancing microglia M1/M2 polarization and inhibiting NLRP3 inflammasome, with involvement of activating PPARα-mediated autophagy (Fig. 9)."
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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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"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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"This revealed that stigmasterol‐treated LPS‐induced Schwann cell‐conditioned medium could inhibit the activation of CSF/P38MAPK/NFKB signaling pathway, thereby reducing the activation of RAW264.7 macrophages.3.8
Stigmasterol-treated LPS-induced Schwann cell-conditioned medium inhibits NLRP3 inflammasome in macrophages."
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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]."
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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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"Furthermore, oleic acid, reduces the secretion of IL-1b by bone marrow-derived macrophages upon previous stimulation with either LPS or palmitate, supporting that mono-unsaturated FAs can also prevent the over-activation of the NLRP3 inflammasome via the activation of the AMPK pathway [60] (Table 1)."
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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)."