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

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...

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Autores principales: Li, Sainan, Xia, Yujing, Chen, Kan, Li, Jingjing, Liu, Tong, Wang, Fan, Lu, Jie, Zhou, Yingqun, Guo, Chuanyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760659/
https://www.ncbi.nlm.nih.gov/pubmed/26929598
http://dx.doi.org/10.2147/DDDT.S99420
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author Li, Sainan
Xia, Yujing
Chen, Kan
Li, Jingjing
Liu, Tong
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
author_facet Li, Sainan
Xia, Yujing
Chen, Kan
Li, Jingjing
Liu, Tong
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
author_sort Li, Sainan
collection PubMed
description 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-α, IL-6, IFN-γ, and IL-1β. 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.
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spelling pubmed-47606592016-02-29 Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3 Li, Sainan Xia, Yujing Chen, Kan Li, Jingjing Liu, Tong Wang, Fan Lu, Jie Zhou, Yingqun Guo, Chuanyong Drug Des Devel Ther Original Research 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-α, IL-6, IFN-γ, and IL-1β. 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. Dove Medical Press 2016-02-15 /pmc/articles/PMC4760659/ /pubmed/26929598 http://dx.doi.org/10.2147/DDDT.S99420 Text en © 2016 Li et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Li, Sainan
Xia, Yujing
Chen, Kan
Li, Jingjing
Liu, Tong
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title_full Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title_fullStr Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title_full_unstemmed Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title_short Epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin A-induced hepatitis by inhibiting BNIP3
title_sort epigallocatechin-3-gallate attenuates apoptosis and autophagy in concanavalin a-induced hepatitis by inhibiting bnip3
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760659/
https://www.ncbi.nlm.nih.gov/pubmed/26929598
http://dx.doi.org/10.2147/DDDT.S99420
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