IndraLab

Statements



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"In this study, we find that NO donor not only inhibits NLRP3 inflammasome activation in mouse macrophages, but also suppresses human NLRP3 inflammasome activation in human THP-1 cells and primary PBMCs."

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"Furthermore, dopamine, β-hydroxybutyric acid, nitric oxide, and unsaturated fatty acids have also been found to suppress the activity of NLRP3 inflammasome."

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"The dramatic enhancement of both NO and the expression of iNOS in Txnip -/- macrophages suggested that TXNIP may be involved in NO mediated NLRP3 inhibition."

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"Interestingly, nitric oxide seems to stabilize mitochondria against dysfunction and suppress NLRP3 activation by S nitrosylation."

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"Our observation that the human NLRP3 inflammasome is inhibited by NO further suggests a potential therapeutic application of NO in the treatment of inflammatory diseases."

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"Overall, these results suggest that excessive NO produced by Txnip -/- cells could inhibit NLRP3 inflammasome activation."

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"Furthermore, our in vivo results support the hypothesis that excessive NO induced by LPS treatment in Txnip -/- mice inhibited NLRP3 inflammasome activation and then prevented the secretion of IL-1beta."

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"For example, infection of macrophages with B. abortus that are deficient in NO production, which is known to inhibit NLRP3, resulted in higher secretion of IL-1β, but no differences in bacterial load were observed, indicating that B. abortus employs additional mechanisms to ensure survival in macrophages (165)."

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"Furthermore, S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, markedly inhibited NLRP3 inflammasome activation, whereas the AIM2 and NLRC4 inflammasomes were only partially inhibited by SNAP."

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"Similarly, a previous study has found that NO inhibits NLRP3 activation, thereby preventing pyroptosis in endothelial cells (Jiang et al., 2020)."

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"Viral ablation of neuronal nitric oxide synthase type-1 (nNOS-1) ACs reduced surround suppression only in the mesopic range and linearized AII responses to flickering light."

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"On the other hand, it is recently demonstrated that nitric oxide (NO) is able to inhibit the NLRP3 inflammasome-dependent production of IL-1β."

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"On the other hand, it is recently demonstrated that nitric oxide (NO) is able to inhibit the NLRP3 inflammasome-dependent production of IL-1β."

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"Yet, NO has been previously shown to inhibit NLRP3 inflammasome activation through the S nitrosylation of NLRP3 and caspase-1 XREF_BIBR, XREF_BIBR."

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"Of note, NO was found to inhibit the NLRP3 inflammasome-dependent processing of IL1β (Mishra et al., 2013)."

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"IL-1beta levels are regulated by IFN-gamma-induced nitric oxide inhibition of the NLRP3 inflammasome [XREF_BIBR]."

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"Furthermore, pDCs are also not characterized by nitric oxide (NO) synthesis, as they have very low levels of iNOS and, thus, it is unlikely that NO would inhibit NLRP3 through nitrosylation [144]."

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"Altogether, mitophagy is accomplished by SESN2- and ULK1 mediated selective autophagy of perinuclearly clustered mitochondria primed by SESN2-SQSTM1, leading to the suppression of prolonged inflammasome activation.suggesting that perinuclear clustering of damaged mitochondria may not always be required for mitophagy induction in BMDMs in response to LPS and ATP.It has been reported that NOS2 generated NO can suppress the activation of the NLRP3 inflammasome by maintaining mitochondrial homeostasis in macrophages,35 though the mechanism by which NO regulates mitochondrial homeostasis has not been reported."

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"On the contrary, it is known that NLRP3 inflammasome activity is inhibited by type-1 interferon and nitric oxide [XREF_BIBR]."

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"It is interesting to note that NO mediated thiol nitrosylation inhibited assembly and activation of the NLRP3 but not AIM2 inflammasome."

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"It was recently demonstrated that NO was able to inhibit the NLRP3 inflammasome dependent processing of IL-1β via S-nitrosylation ( Mishra et al., 2013 )."

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"Treatment with S-nitroso-N-acetyl penicillamine (SNAP), an NO donor, significantly downregulated TXNIP/NLRP3 inflammasome signaling in RMG, decreased RGC apoptosis, and enhanced tube formation in RMEC."

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"Also study by Mao et al. demonstrated that NO prevented the activation of the NLRP3 inflammasome."

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"In this context, nitric oxide, which is generated in increased amounts by OA chondrocytes in situ, suppresses NLRP3 activation."

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"Endogenous NO downregulates NLRP3 inflammasome activation and stabilizes mitochondria."

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"Recent studies suggest that nitric oxide (NO), Ca 2+ and cyclic AMP negatively regulate the NLRP3 inflammasome but the detailed mechanisms are unclear XREF_BIBR, XREF_BIBR."

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"Recent studies suggest that nitric oxide (NO), Ca 2+ and cyclic AMP negatively regulate the NLRP3 inflammasome but the detailed mechanisms are unclear XREF_BIBR, XREF_BIBR."

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"It has been demonstrated that NO negatively regulated the activation of the NLRP3 inflammasome by stabilizing mitochondria in macrophages and prevented lipopolysaccharide induced septic shock [XREF_BIBR]."

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"Cutting edge : nitric oxide inhibits the NLRP3 inflammasome."

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"Contrastingly, nitric oxide suppresses NLRP3 inflammasome dependent processing of IL-1beta and controls the immunopathology of tuberculosis infection [XREF_BIBR]."

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"While nitric oxide suppresses NLRP3 activation and protects against LPS-induced septic shock and reduces cytokine production (35)."

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"For instance, NO impairs the activity of the NLRP3 inflammasome, a process that is crucial for the control of tissue damage in mice models for Mycobacterium infection and septic shock [79,97]."

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"Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS induced septic shock."

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"Additionally, nitric oxide (NO) downregulates NLRP3 activation through enhancing the removal of the dysfunctional mitochondria and preventing assembly of the inflammasome [XREF_BIBR, XREF_BIBR]."

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"Additionally, nitric oxide (NO) downregulates NLRP3 activation through enhancing the removal of the dysfunctional mitochondria and preventing assembly of the inflammasome [XREF_BIBR, XREF_BIBR]."

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"Nitric oxide (NO) negatively regulates NLRP3 inflammasome activation through S nitrosylation of NLRP3."

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"Nitric oxide (NO) negatively regulates NLRP3 inflammasome activation through S nitrosylation of NLRP3."

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"Similarly, the addition of NO donor compounds to macrophages or induction of NO by IFN-gamma treatment inhibited NLRP3 activation."

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"Both IFN-gamma-induced NO production and NO donor (SNAP) treatment inhibit canonical and Mycobacterium tuberculosis mediated NLRP3 inflammasome activation through induction of NO induced S nitrosylation of NLRP3."

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"In keeping with this hypothesis, nitrogen oxide (NO) has been reported to induce NLRP3 and caspase-1 nitrosylation and thereby inhibit NLRP3 inflammasome activity (Kim et al., 1998; Mishra et al., 2013)."

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"NO inhibits NLRP3 dependent IL-1 responses."

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"We found that NO negatively regulated the activation of the NLRP3 inflammasome by stabilizing mitochondria in macrophages and prevented LPS induced septic shock in vivo."

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"It was demonstrated that NO suppresses NALP3 inflammasome activation by nitrosylation of NALP3 proteins resulting in decreased synthesis of mature IL-1 beta and IL-18, impaired Th1 immunity and NK cell activation XREF_BIBR."

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"The findings suggest that intravenous Arg supplementation immediately after sepsis restores plasma Arg levels and is beneficial for attenuating septic AKI, partly via NO mediated NLRP3 inflammasome inhibition."

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"Since NO is an inhibitor of caspase-1 [XREF_BIBR], availability of NO may inhibit NLRP3 inflammasome activation and subsequent IL-1beta and IL-18 production."

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"Since Arg plus L-NIL administration also attenuated kidney injury after CLP, the favorable effect of Arg resulting from NO mediated NLRP3 inflammasome inhibition may be partly responsible for attenuating septic AKI."

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"Since the deleterious effects of LPS are associated with the secretion of TNF-α, and NO predominantly by tissue macrophages, significantly lower level of both TNF-α and NO induced by L-LPS in our study further confirms its lower endotoxicity than E-LPS.Leptospira can activate NLRP3 inflammasome in mouse macrophages via signalling through its LPS, lipoproteins and glycoproteins [47]."

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"Interestingly, another small molecule, nitric oxide (NO), attenuates NLRP3 inflammasome activity at the post-translational level by direct S-nitrosylation158.In addition to post-translational and post-transcriptional regulation, a number of molecules can directly or indirectly interact with different components of the NLRP3 inflammasome, through which they impede the assembly of NLRP3 with ASC and caspase-1."

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"Interestingly, another small molecule, nitric oxide (NO), attenuates NLRP3 inflammasome activity at the post-translational level by direct S-nitrosylation158.In addition to post-translational and post-transcriptional regulation, a number of molecules can directly or indirectly interact with different components of the NLRP3 inflammasome, through which they impede the assembly of NLRP3 with ASC and caspase-1."

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"While Mishra et al. report NO induced nitrosylation of NLRP3 blocks activation by preventing assembly of the inflammasome, the study by Mao et al. suggests that NO downregulates NLRP3 activation through enhancing the removal of the dysfunctional mitochondria that activate NLRP3."

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"Nitric oxide (NO) produced by macrophages suppresses the NLRP3 inflammasome through a mechanism that involves direct S-nitrosylation of NLRP3 and caspase-1 [34]."

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"Nitric oxide (NO) produced by macrophages suppresses the NLRP3 inflammasome through a mechanism that involves direct S-nitrosylation of NLRP3 and caspase-1 [34]."

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"Nitric oxide inhibits human NLRP3 inflammasome activation."

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"The findings reported above suggested that exogenous NO donors inhibited NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation."

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"Nitric oxide (NO) has been reported to negatively regulate NLRP3 inflammasome mediated caspase-1 activation [XREF_BIBR]."

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"However, little is known regarding the regulatory mechanism of ginsenoside 20(S)-Rg3 and 20(R)-Rg3 for NO-mediated NLRP3 inflammasome inhibition.In this study, we found that ginsenosides 20(R)-Rg3 and[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Nitric oxide (NO) has been reported to negatively regulate NLRP3 inflammasome mediated caspase-1 activation [XREF_BIBR]."

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"Also, NO inhibits the NLRP3 inflammasome activation in macrophages, which may involve S nitrosylation of NLRP3 and caspase-1 77."

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"The suppression of both NO production and iNOS expression by 20(R)-Rg3 and 20(S)-Rg3 might be involved in NO-mediated NLRP3 inhibition."

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"Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS induced septicshock."

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"Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS induced septic shock."

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"It has been reported that NO has a relationship with NO-mediated NLRP3 inflammasome inhibition via the S-nitrosylation of the NLRP3 inflammasome [14–17] ."

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"However, little is known regarding the regulatory mechanism of ginsenoside 20(S)-Rg3 and 20(R)-Rg3 for NO-mediated NLRP3 inflammasome inhibition."

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"These results collectively confirm that the endogenous NO produced by iNOS negatively regulates NLRP3 inflammasome activation in macrophages."

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"However, other studies have shown that nitric oxide may actually inhibit the triggering of the keystone NLRP3 inflammasome; suggesting a co-dependant oxidation relationship for the purpose of maintain[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Furthermore, NO suppresses NLRP3 inflammasome activation, which is a multi protein complex that triggers the maturation of the pro inflammatory cytokines IL-1beta and IL-18."

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"10-hydroxydecanoic acid, another NSAIDs isolated from royal jelly, can decrease nitric oxide synthase (NOS) and NO levels, and inhibit NLRP3 inflammasome over-activation via the downregulation of p53 [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"5 Interestingly, interferon (IFN) and the nitric oxide synthase-2-mediated NO pathways were shown to inhibit NLRP3 activation and thereby prevent tuberculosis associated pathology."

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"5 Interestingly, interferon (IFN) and the nitric oxide synthase-2-mediated NO pathways were shown to inhibit NLRP3 activation and thereby prevent tuberculosis associated pathology."

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"120 showed that a similar NO dependent mechanism suppresses NLRP3 activation during LPS challenge to protect against septic shock."

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"In addition, T cell derived IFNgamma has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis 71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity."

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"It has been reported that NO prevents NLRP3 activation and protects against LPS induced septic shock."

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"NO thus specifically inhibits NLRP3 inflammasome activation but not the TLR and NF-kappaB signaling pathways."

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"NO inhibits the assembly of the NLRP3 inflammasome."

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"In addition, T cell derived IFNgamma has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis 71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity."

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"Thus, in both macrophages and transfected 293T cells NO specifically inhibited the assembly and activity of the NLRP3 inflammasome complex."

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"The addition of an NO donor (SNAP) inhibited the NLRP3 dependent maturation of IL-1beta in these transfected cells, but had no effect on the AIM2 inflammasome, implying that this compound might directly modulate the assembly or activity of the NLRP3 inflammasome (XREF_FIG)."

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"In this study, we found that NO not only inhibits NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation, but also inhibits NLRC4- and AIM-2-mediated IL-1beta secretion and caspase-1 activation (XREF_SUPPLEMENTARY), but to a much less extent (3-fold decrease for NLRC4 and AIM-2, 40-fold decrease for NLRP3)."

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"However, little is known about the regulatory mechanism for NO mediated NLRP3 inflammasome inhibition and the potential role for TXNIP in this progression."

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"In addition, we also observed increased NO production in Txnip -/- cells, which suppressed NLRP3 inflammasome activation, indicating a critical role for TXNIP in the activation of the NLRP3 inflammasome during endotoxic shock."

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"In relation with the immune response, interferon-gamma generates NO production, that in turn, negatively regulates the formation of NLRP3 inflammasome by suppressing the nitrosylation reaction and/or caspase 1 activation [12]."

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"Firstly, the ability of IFN-gamma or NO to specifically inhibit the NLRP3 inflammasome and not other caspase-1 containing complexes indicates that caspase-1 is unlikely to be a functional nitrosylation target in this context."

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"An experimental study reported that NO inhibits NLRP3 activation that may be responsible for the underlying mechanisms in occurrence of the diseases that are related to ischemia-reperfusion injury [16]."

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"These observations establish a mechanism whereby IFN-gamma-induced NO inhibits NLRP3 dependent IL-1 responses."

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"Using an iNOS inhibitor, iNOS specific siRNA and iNOS deficient macrophages, we found that the endogenous NO derived from iNOS negatively regulates NLRP3 inflammasome activation at the late stage of LPS priming."

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"NLRP3 is also negatively regulated by NO mediated S nitrosylation."