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- W1982348992 abstract "Historically, consumption of Green tea (Camellia sinensis) has been associated with health benefits against multiple diseases including cancer, atherosclerosis and cardiovascular disorders. Emerging evidence has suggested a pathogenic role for HMGB1, a newly identified “late” mediator of lethal systemic inflammation, in the aforementioned diseases. Here we demonstrated that a major ingredient of Green tea, EGCG, was internalized into HMGB1-containing LC3-positive cytoplasmic vesicles (likely autophagosomes) in macrophages, and induced HMGB1 aggregation in a time-dependent manner. Furthermore, EGCG stimulated LC3-II production and autophagosome formation, and inhibited LPS-induced HMGB1 up-regulation and extracellular release. The EGCG-mediated HMGB1 inhibitory effects were diminished by inhibition of class III phosphatidylinositol-3 kinase (with 3-methyladenine) or knockdown of an essential autophagy-regulating protein, beclin-1. Moreover, the EGCG-mediated protection against lethal sepsis was partly impaired by co-administration of an autophagy inhibitor, chloroquine. Taken together, the present study has suggested a possibility that EGCG inhibits HMGB1 release by stimulating its autophagic degradation." @default.
- W1982348992 created "2016-06-24" @default.
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- W1982348992 date "2011-05-01" @default.
- W1982348992 modified "2023-09-26" @default.
- W1982348992 title "EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages" @default.
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- W1982348992 doi "https://doi.org/10.1016/j.bcp.2011.02.015" @default.
- W1982348992 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3072446" @default.
- W1982348992 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21371444" @default.
- W1982348992 hasPublicationYear "2011" @default.
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