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Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway

Objective. Shikonin possesses anti-inflammatory effects. However, its function in concanavalin A-induced acute liver injury remains uncertain. The aim of the present study was to investigate the functions of shikonin and its mechanism of protection on ConA-induced acute liver injury. Materials and M...

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Autores principales: Liu, Tong, Xia, Yujing, Li, Jingjing, Li, Sainan, Feng, Jiao, Wu, Liwei, Zhang, Rong, Xu, Shizan, Cheng, Keran, Zhou, Yuqing, Zhou, Shunfeng, Dai, Weiqi, Chen, Kan, Wang, Fan, Lu, Jie, Zhou, Yingqun, Guo, Chuanyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884842/
https://www.ncbi.nlm.nih.gov/pubmed/27293314
http://dx.doi.org/10.1155/2016/2748367
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author Liu, Tong
Xia, Yujing
Li, Jingjing
Li, Sainan
Feng, Jiao
Wu, Liwei
Zhang, Rong
Xu, Shizan
Cheng, Keran
Zhou, Yuqing
Zhou, Shunfeng
Dai, Weiqi
Chen, Kan
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
author_facet Liu, Tong
Xia, Yujing
Li, Jingjing
Li, Sainan
Feng, Jiao
Wu, Liwei
Zhang, Rong
Xu, Shizan
Cheng, Keran
Zhou, Yuqing
Zhou, Shunfeng
Dai, Weiqi
Chen, Kan
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
author_sort Liu, Tong
collection PubMed
description Objective. Shikonin possesses anti-inflammatory effects. However, its function in concanavalin A-induced acute liver injury remains uncertain. The aim of the present study was to investigate the functions of shikonin and its mechanism of protection on ConA-induced acute liver injury. Materials and Methods. Balb/C mice were exposed to ConA (20 mg/kg) via tail vein injection to establish acute liver injury; shikonin (7.5 mg/kg and 12.5 mg/kg) was intraperitoneally administered 2 h before the ConA injection. The serum liver enzyme levels and the inflammatory cytokine levels were determined at 3, 6, and 24 h after ConA injection. Results. After the injection of ConA, inflammatory cytokines IL-1β, TNF-α, and IFN-γ were significantly increased. Shikonin significantly ameliorated liver injury and histopathological changes and suppressed the release of inflammatory cytokines. The expressions of Bcl-2 and Bax were markedly affected by shikonin pretreatment. LC3, Beclin-1, and p-JNK expression levels were decreased in the shikonin-pretreated groups compared with the ConA-treated groups. Shikonin attenuated ConA-induced liver injury by reducing apoptosis and autophagy through the inhibition of the JNK pathway. Conclusion. Our results indicated that shikonin pretreatment attenuates ConA-induced acute liver injury by inhibiting apoptosis and autophagy through the suppression of the JNK pathway.
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spelling pubmed-48848422016-06-12 Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway Liu, Tong Xia, Yujing Li, Jingjing Li, Sainan Feng, Jiao Wu, Liwei Zhang, Rong Xu, Shizan Cheng, Keran Zhou, Yuqing Zhou, Shunfeng Dai, Weiqi Chen, Kan Wang, Fan Lu, Jie Zhou, Yingqun Guo, Chuanyong Mediators Inflamm Research Article Objective. Shikonin possesses anti-inflammatory effects. However, its function in concanavalin A-induced acute liver injury remains uncertain. The aim of the present study was to investigate the functions of shikonin and its mechanism of protection on ConA-induced acute liver injury. Materials and Methods. Balb/C mice were exposed to ConA (20 mg/kg) via tail vein injection to establish acute liver injury; shikonin (7.5 mg/kg and 12.5 mg/kg) was intraperitoneally administered 2 h before the ConA injection. The serum liver enzyme levels and the inflammatory cytokine levels were determined at 3, 6, and 24 h after ConA injection. Results. After the injection of ConA, inflammatory cytokines IL-1β, TNF-α, and IFN-γ were significantly increased. Shikonin significantly ameliorated liver injury and histopathological changes and suppressed the release of inflammatory cytokines. The expressions of Bcl-2 and Bax were markedly affected by shikonin pretreatment. LC3, Beclin-1, and p-JNK expression levels were decreased in the shikonin-pretreated groups compared with the ConA-treated groups. Shikonin attenuated ConA-induced liver injury by reducing apoptosis and autophagy through the inhibition of the JNK pathway. Conclusion. Our results indicated that shikonin pretreatment attenuates ConA-induced acute liver injury by inhibiting apoptosis and autophagy through the suppression of the JNK pathway. Hindawi Publishing Corporation 2016 2016-05-16 /pmc/articles/PMC4884842/ /pubmed/27293314 http://dx.doi.org/10.1155/2016/2748367 Text en Copyright © 2016 Tong Liu et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liu, Tong
Xia, Yujing
Li, Jingjing
Li, Sainan
Feng, Jiao
Wu, Liwei
Zhang, Rong
Xu, Shizan
Cheng, Keran
Zhou, Yuqing
Zhou, Shunfeng
Dai, Weiqi
Chen, Kan
Wang, Fan
Lu, Jie
Zhou, Yingqun
Guo, Chuanyong
Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title_full Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title_fullStr Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title_full_unstemmed Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title_short Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway
title_sort shikonin attenuates concanavalin a-induced acute liver injury in mice via inhibition of the jnk pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884842/
https://www.ncbi.nlm.nih.gov/pubmed/27293314
http://dx.doi.org/10.1155/2016/2748367
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