Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3

被引：53

作者：

Li, Sainan ^{[1
]}

Xia, Yujing ^{[1
]}

Chen, Kan ^{[1
]}

Li, Jingjing ^{[1
]}

Liu, Tong ^{[1
]}

Wang, Fan ^{[1
]}

Lu, Jie ^{[1
]}

Zhou, Yingqun ^{[1
]}

Guo, Chuanyong ^{[1
]}

机构：

[1] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Dept Gastroenterol, Shanghai 200072, Peoples R China

来源：

DRUG DESIGN DEVELOPMENT AND THERAPY | 2016年 / 10卷

基金：

中国国家自然科学基金;

关键词：

concanavalin A; hepatitis; EGCG; autophagy; apoptosis; BNIP3; STAT3; JAKs; IL-6; ORAL POLYPHENON E; RAI STAGE 0; CELL-DEATH; BH3-ONLY PROTEINS; URSODEOXYCHOLIC ACID; COMBINATION THERAPY; LIVER-DISEASE; MITOCHONDRIAL; EGCG; GALLATE;

D O I：

10.2147/DDDT.S99420

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

Background: Epigallocatechin-3-gallate (EGCG) is the most effective compound in green tea, and possesses a wide range of beneficial effects, including anti-inflammatory, antioxidant, antiobesity, and anticancer effects. In this study, we investigated the protective effects of EGCG in concanavalin A (ConA)-induced hepatitis in mice and explored the possible mechanisms involved in these effects. Methods: Balb/C mice were injected with ConA (25 mg/kg) to induce acute autoimmune hepatitis, and EGCG (10 or 30 mg/kg) was administered orally twice daily for 10 days before ConA injection. Serum liver enzymes, proinflammatory cytokines, and other marker proteins were determined 2, 8, and 24 hours after the ConA administration. Results: BNIP3 mediated cell apoptosis and autophagy in ConA-induced hepatitis. EGCG decreased the immunoreaction and pathological damage by reducing inflammatory factors, such as TNF-alpha, IL-6, IFN-gamma, and IL-1 beta. EGCG also exhibited an antiapoptotic and antiautophagic effect by inhibiting BNIP3 via the IL-6/JAKs/STAT3 pathway. Conclusion: EGCG attenuated liver injury in ConA-induced hepatitis by downregulating IL-6/JAKs/STAT3/BNIP3-mediated apoptosis and autophagy.

引用

页码：631 / 647

页数：17

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