IndraLab

Statements



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"These results indicated that scutellarin inhibited NLRP3 inflammasome activation in macrophages upon ATP treatment."

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"The results showed that scutellarin dose-dependently reduced caspase-1 activation and decreased mature interleukin-1beta (IL-1beta) release in lipopolysaccharide (LPS)-primed macrophages upon ATP or nigericin stimulation, indicating that scutellarin inhibited NLRP3 inflammasome activation in macrophages."

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"Together with our previous study XREF_BIBR, scutellarin can not only inhibit the NLRP3 inflammasome activation, but also suppress the caspase-11 inflammasome activation (Supporting Information Fig.S6), thereby attenuating bacterial sepsis in mice XREF_BIBR."

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"We demonstrated that scutellarin inhibited NLRP3 inflammasome activation and pyroptosis in macrophages through augmenting PKA signaling, unraveling a novel anti-inflammatory mechanism beyond previously identified inhibitory action on the NF-kappaB and Notch pathways."

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"We found that scutellarin inhibited NLRP3 inflammasome activation by both ATP and nigericin, suggesting that its action may on the downstream components of P2X7 receptor."

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"Our results also showed that scutellarin inhibited the non canonical NLRP3 inflammasome activation downstream of caspase-11 activation in macrophages transfected with LPS."

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"These data indicated that scutellarin suppressed NLRP3 inflammasome activation in macrophages by augmenting PKA signaling, highlighting its potential therapeutic application for treating NLRP3 related inflammatory diseases."

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"Together these results showed that scutellarin treatment inhibited NLRP3 inflammasome activation and pyroptosis in LPS primed murine macrophages upon ATP or nigericin stimulation."

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"Although scutellarin is able to suppress canonical NLRP3 inflammasome activation upon ATP or nigericin stimulation in our previous study XREF_BIBR, it had no overt effect on NLRC4 (stimulated by flagellin) and AIM2 [by poly (dA : dT)] inflammasome activation (Supporting Information Fig.S1)."

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"Together, these results indicated that scutellarin inhibited NLRP3 inflammasome activation and pyroptosis by augmenting PKA signaling in murine macrophages."

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"Our data reveals that scutellarin is able to suppress NLRP3 inflammasome activation thus exhibiting therapeutic effects against NLRP3 related inflammatory diseases."

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"In this study, we found that scutellarin inhibited NLRP3 inflammasome activation and pyroptosis in LPS primed macrophages upon ATP or nigericin stimulation."

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"These results together demonstrate that scutellarin, to certain extent, specifically suppressed both canonical and caspase-11-mediated non canonical NLRP3 inflammasome activation in macrophages."

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"3.2 Scutellarin suppresses non canonical NLRP3 inflammasome activation in macrophages."

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"Altogether, these data indicated that scutellarin inhibited NLRP3 inflammasome activation and pyroptosis in macrophages by augmenting PKA signaling."

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"Different from MCC950, however, scutellarin not only inhibited non canonical NLRP3 inflammasome activation but also suppressed caspase-11 activation and caspase-11-mediated pyroptosis."

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"Scutellarin Suppresses NLRP3 Inflammasome Activation in Macrophages and Protects Mice against Bacterial Sepsis."

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"As previous studies have revealed that scutellarin can inhibit canonical NLRP3 inflammasome activation in macrophages XREF_BIBR, we sought to discern whether scutellarin mediated inhibition of caspase-11 activation is dependent on the NLRP3 and ASC inflammasome pathway."

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"We report that scutellarin partially inhibited the activation of NLRP3 inflammasomes under hypoxic conditions in vitro and in vivo, improved the survival rate of RGCs, and decreased the number of impaired retinal microglia."
| PMC

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"We have previously found that scutellarin can suppress the canonical NLRP3 inflammasome activation, thus alleviating bacterial sepsis in mice XREF_BIBR."

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"In light of the fact that scutellarin can increase cAMP levels (and therefore increases the PKA activity), we proposed that scutellarin might block NLRP3 activation by enhancing PKA signaling."