IndraLab

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"Since inflammasomes are involved in IL-1beta secretion, we investigated whether IL-1beta suppression was mediated by inflammasomes, and found that EGCG treatment led to downregulation of the inflammasome component, NLRP1, and reduced caspase-1 activation."
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"For instance, Tsai et al. [46] observed that the flavonoid gallocatechin gallate (EGCG) attenuated lupus nephritis in mice by inhibiting caspase-1 activation through decreased NLRP3 mRNA expression, reducing IL-1β and IL-18 production."
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"In HMC-1 cell line, EGCG suppressed NF- κB activity by inhibiting caspase-1, a special caspase family protein which is responsible for the maturation of IL-1β and IL-18 and activating NF-κB signaling pathway."
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"We further examined the impact of EGCG on NLRP3 inflammasome activation and found that EGCG decreased both gene and protein expression of key signaling proteins in the TXNIP/NLRP3/IL‐1β axis, including TXNIP, ASC, NLRP3, caspase1, and IL‐1β (Figure 4B–D)."
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"EGCG dose-dependently blocked NLRP3-dependent caspase-1 activation and IL-1β maturation( Fig. 2 A, 2B)."
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"Furthermore, EGCG inhibited the activation of caspase-1 in HMC-1 cells."
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"177 In one study, EGCG resulted in NFkappaB inhibition, which was associated with reduced melanoma cell interleukin-1beta (IL-1beta) secretion, downregulation of the inflammasome component, nuclear localization leucine-rich-repeat protein 1 (NLRP1), and decreased caspase-1 activation."
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"In this study, we showed that EGCG prevented the activation of PI3 Kinase, MAP Kinase, caspase-1, and NF-κB signaling pathways in RANKL-simulated HMC-1 cells."
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"EGCG suppressed LPS-induced priming and inflammasome activation (caspase-1 cleavage) in both human and mouse macrophages."
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"Epigallocatechin gallate (EGCG), a tea catechin, reduced both histamine degranulation and cytokine release (TSLP, IL-1β, IL-6, IL-8) in receptor activator of NF-κB ligand (RANKL)-stimulated HMC-1 cells by targeting PI3K, MAPK, caspase-1, and NF-κB signaling cascades [57]."
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"In this study, we found that NO treatment resulted in caspase-1 activation and IL-1beta production, while EGCG inhibited the observed NO induced increase in IL-1beta production and caspase-1 activation, suggesting that the caspase-1 pathway is a potential therapeutic target for preventing NO induced ototoxic damage."
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"After stimulating HMC-1 cells with RANKL, activity of caspase-1 was significantly promoted, whereas treatment with EGCG (10 μg/ml) effectively prevented the caspase-1 activation up to 118% ( Fig. 2 A,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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