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Emodin inhibits NLRP3. 25 / 25
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"Taken together, our study showed that emodin inhibited NLRP3 inflammasome activation in vitro and LPS induced endotoxin shock in in vivo model."
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"In vitro , we demonstrated that emodin could inhibit NLRP3 and then inhibit the expression of ASC , CASP1 , GSDMD , IL-1beta , and IL-18 ."
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"These, together with the effects of emodin, similar to C23, suggest that emodin may inhibit the activation of NLRP3 inflammasome by inhibiting the CIRP-induced NF-κB activation in resident macrophages."
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"Studies have shown that emodin can induce circulating neutrophil apoptosis through the Ca -calpain1-caspase12-caspase-3 signaling pathway to protect SAP rats from excessive inflammation (Wang et al. 2016), In addition, emodin suppresses the P2X7/NLRP3 signaling pathway and reactive oxygen species generation to reduce the production of proinflammatory factors (Xia et al. 2019; Zhang et al. 2019)."
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"Emodin was also shown to attenuate activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome that led to decreased cardiomyocyte death in response to ischemia-reperfusion (I/R) injury [23]."
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"Importantly, the administration of either emodin or AYC markedly inhibited AP-associated activation of NLRP3 inflammasome in AMs, which was supported by the downregulated expression levels of NLRP3, ASC, and Caspase1 p10."
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"Emodin has also been reported to reduce intestinal pyroptosis in NEC neonatal rats by inhibiting the NLRP3/IL-1β pathway (56)."
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"In this study, we hypothesized that emodin inhibited NLRP3 inflammasome activation via Nrf2 signaling."
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"17 Emodin‐induced inhibition of NLRP3 inflammasome alleviates the pancreatitis‐associated lung injury."
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"In summary, emodin treatment activates AMPK, suppresses NLRP3 inflammasome response, elevates antioxidant response, inhibits spinal inflammatory reaction and alleviates arthritis pain."
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"These results are in alignment with previous reports that emodin may inhibit the activation of the NLRP3 inflammasome."
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"Moreover, emodin alleviated C. acnes-stimulated pro-inflammatory cytokines production and inactivated the NLRP3 inflammasome."
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"RFAs including rhein/diacerein, emodin, aloe emodin and 1,8-dihydroxyanthraquinone inhibited NLRP3 inflammasome by inhibiting IL-1β (Fig. 1C), the cleavage of pro-caspase-1(Fig. 1E) and the formation of ASC specks (Fig. 1F, G) in mouse BMDMs stimulated by LPS + nigericin, but bad no effect on TNF-α (Fig. 1D)."
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"Furthermore, emodin inhibited the P2X7/NLRP3 signaling pathway followed by the decrease of pro-inflammatory factors, and the latter is beneficial for the recovery of SAP."
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"In summary, emodin treatment blocked the HDAC6/NLRP3 inflammasome signaling, suppresses spinal inflammation and alleviates chronic inflammatory pain."
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"The emodin treatment decreased the NLRP3 and caspase-1 intensity to 1.28 ± 0.13 and 1.13 ± 0.07, respectively (Fig. 3A-D)."
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"RFAs including rhein/diacerein, emodin, aloe emodin and 1,8-dihydroxyanthraquinone inhibited NLRP3 inflammasome by inhibiting IL-1β, but had no effect on TNF-α."
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"RFAs including rhein/diacerein, emodin, aloe emodin and 1,8-dihydroxyanthraquinone inhibited NLRP3 inflammasome."
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"Emodin and rhein inhibited the cascade reaction of NALP3 inflammasome, reduced the related inflammatory cytokines and alleviated tissue damage ( Han JW et al., 2015 ; Ge H et al., 2017 )."
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"Emodin reduces the inflammatory response and pyroptosis in cardiomyocytes by suppressing the activation of the NLRP3 inflammasome (134)."
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"In vitro, we demonstrated that emodin could inhibit NLRP3 and then inhibit the expression of ASC, CASP1, GSDMD, IL-1β, and IL-18."
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"Emodin elicits strong attenuation of NLRP3 inflammosome activation induced by lipopolysaccharide (LPS; a bacterial endotoxin which is often used for hyperactivation of pro-inflammatory signaling in in vivo and in vitro models) in mice, thereby preventing secretion of pro-inflammatory mediators such as IL-1β."
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"In this study, emodin was found to significantly reduce inflammatory and pyroptotic signaling via its actions on multiple effectors by inhibiting the NLRP3 pathway in a methyltransferase-like 3 (METTL-3)-dependent manner."
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"Emodin might inhibit the cold-inducible RNA-binding protein (CIRP)-mediated activation of the NLRP3/IL-1β/CXCL1 signaling in rats, which then ameliorated the SAP-associated ALI (Xu et al., 2021)."
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"Although the detailed mechanisms that link the common molecular pathways to the means by which emodin attenuates NLRP3 inflammasome activation remains to be elucidated, this is the first report providing scientific evidence substantiating the use of emodin in medicine for the treatment of various inflammatory diseases through the regulation of inflammasome activation, which may provide a valuable therapeutic strategy for controlling inflammasome mediated pathological conditions."
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