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

Author:

Liu Tong1,Xia Yujing1,Li Jingjing1,Li Sainan1,Feng Jiao1,Wu Liwei1,Zhang Rong12,Xu Shizan12,Cheng Keran13,Zhou Yuqing13,Zhou Shunfeng13,Dai Weiqi1,Chen Kan1,Wang Fan1,Lu Jie1,Zhou Yingqun1,Guo Chuanyong1

Affiliation:

1. Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China

2. The First Clinical Medical College, Nanjing Medical University, Nanjing 210029, China

3. The First Affiliated Hospital of Soochow University, Suzhou 215006, China

Abstract

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-γwere 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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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