文献类型：期刊文献

英文题名：RETRACTED: Cyanidin 3-O-β-Glucoside Ameliorates Ethanol-Induced Acute Liver Injury by Attenuating Oxidative Stress and Apoptosis: The Role of SIRT1/FOXO1 Signaling (Retracted article. See vol. 40, pg 2023, 2016)

作者：Liu, Juncheng[1];Zhou, Jun[2];Wu, Zhonghua[3];Wang, Xiaoyu[4];Liu, Liqiong[5];Yao, Chonghua[6]

第一作者：Liu, Juncheng

通信作者：Liu, LQ[1];Yao, CH[2]

机构：[1]Gansu Univ Tradit Chinese Med, Clin Med Coll, Lanzhou, Peoples R China;[2]Cent S Univ, Xiangya Hosp 2, Ctr Minimally Invas Surg, Changsha, Hunan, Peoples R China;[3]Shanghai Univ Tradit Chinese Med, Expt Ctr Sci & Technol, Shanghai, Peoples R China;[4]Shanghai Univ Tradit Chinese Med, Sch Pharm, Shanghai, Peoples R China;[5]Indiana Univ Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA;[6]Shanghai Univ Tradit Chinese Med, Shanghai Municipal Hosp Tradit Chinese Med, Dept Rheumatism, Shanghai, Peoples R China

第一机构：甘肃中医药大学临床医学院

通信机构：[1]corresponding author), 950 W Walnut St R2-302, Indianapolis, IN 46202 USA;[2]corresponding author), 274 M ZhiJiang Rd, Shanghai 200074, Peoples R China.

年份：2016

卷号：40

期号：3

起止页码：457

外文期刊名：ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000372023000003)】；

语种：英文

外文关键词：Endoplasmic Reticulum Stress; Silent Mating Type Information Regulation 2 Homolog 1 (SIRT1); Cyanidin 3-O-beta-Glucoside; Reactive Oxygen Species; Forkhead Fox-O-1 (FOXO1)

摘要：BackgroundThe aim of this study was to examine the effects of Cyanidin 3-O--glucoside (C3G) on ethanol (EtOH)-induced acute liver injury in mice as well as in cultured hepatic cells exposed to EtOH, with a focus on the involvement of Silent Mating Type Information Regulation 2 Homolog 1 (SIRT1)/Forkhead fox-O-1 (FOXO1) signaling pathway, and to explore the underlying molecular mechanisms. MethodsC57BL/6 adolescent male mice were given EtOH via intraperitoneal injection for 2 consecutive days, and the changes in the livers were detected via hematoxylin-eosin staining. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured by biochemical methods. Protein expression of SIRT1, FOXO1, acetylated FOXO1 (ac-FOXO1), GRP78, p-eukaryotic initiation factor-2 (eIF2), and apoptosis (p-JNK, p-c-Jun, and Bax) parameters was determined by Western blot. Reactive oxygen species (ROS) was detected by flow cytometry. Human hepatocytes Chang cell line was used to assay cell apoptosis by Annexin V and propidium iodide.In addition, mRNA levels of SIRT1, tumor necrosis factor alpha (TNF-), interleukin 6 (IL-6), and monocyte chemoattractant protein 1 in liver tissues were detected by real-time polymerase chain reaction. ResultsThis study demonstrated that C3G (10mg/kg) administration diminished EtOH-induced acute liver injury compared to control group, as evidenced by the significant decreases in ALT and AST levels. Pretreatment with C3G exerted anti-inflammatory effects as indicated by the decreased TNF- and IL-6 levels, as well as decreased inflammatory foci and ballooning cells in liver tissue. The lessened hepatic injury was associated with enhancedSIRT1protein expression and activity by C3Gin vitro and in vivo. C3G treatment also provoked significant attenuation of endoplasmic reticulum stress parameters (GRP78, p-eIF2), which was consistent with reduced levels of both p-c-Jun and Bax. Interestingly, EX527 inhibitor did not affect the protective function of C3G on alcohol-induced cell apoptosis. Moreover, alcohol exposure increased ROS level and decreased ac-FOXO1, while C3G intervention reversed this abnormality, and this may be related to SIRT1activity by C3G. ConclusionsAnthocyanin C3G has significant potency in antioxidant, anti-inflammatory, and anti-apoptotic effects on hepatocytes exposed to EtOH by modulating the SIRT1/FOXO1 signaling pathway. Our findings illustrate a novel and definitive therapeutic action of C3G and represent an economically feasible therapeutic intervention to treat alcoholic liver disease.