时间：6月29日星期二16:00-17:30    

Time：4:00-5:30 PM，Tues.，June 29，2021

地点：西湖大学云栖校区3号楼312会议室

Venue: Room 312, 3F, Building 3,  Yunqi Campus

主持人：西湖大学生命科学学院研究员 李旭

Host：Dr. Xu Li, School of Life Sciences

主讲嘉宾/Speaker:

Dr. Xiaobin Dou

Professor and Dean of the School of Life Sciences, Zhejiang Chinese Medicine University

Dr. Dou is a professor and Dean of the School of Life Sciences, Zhejiang Chinese Medicine University, and director of the Lipid Metabolism Laboratory of the National Administration of Traditional Chinese Medicine. His research is focused on deciphering the molecular mechanism in metabolic diseases for its prevention and treatment by traditional medicine. He has published over 80 papers in the journals including Hepatology and Journal of Hepatology.

讲座摘要/Abstract:

Alcoholic liver disease (ALD) is a type of chronic liver disease caused by chronic ethanol overconsumption. The pathogenesis of ALD is complex and there is no effective clinical treatment thus far. SIRT3 is an NAD+-dependent deacetylase primarily located inside mitochondria, and reports on the effect of chronic alcohol exposure on liver SIRT3 expression are scarce. This study aims to investigate the effect of chronic alcohol consumption on hepatic SIRT3 expression and its role in alcoholic-induced liver injury. Using the Lieber-DeCarli mouse model of ALD, we analyzed the regulation of SIRT3 and the effect of liver-specific knocking-down of SIRT3 on alcohol-induced liver injury. HepG2 and AML12 hepatocytes were employed to detect the biological function of SIRT3 on alcohol-induced hepatic cytotoxicity and its potential mechanism. Chronic alcohol exposure led to hepatic SIRT3 upregulation and liver-specific SIRT3 knockdown alleviated alcoholic feeding-induced liver injury and lipid accumulation, which is associated with improved autophagy induction. In addition, autophagy induction contributed to the cytoprotective effect of SIRT3 knockdown on ethanol-induced hepatocyte cell death. In summary, our data suggest that hepatic SIRT3 upregulation in response to chronic alcohol exposure and liver-specific SIRT3 knockdown, induced autophagy activation further alleviating alcoholic-induced liver injury, which represents a novel mechanism in this process.

联系人/Contact：

生命科学学院

于文越 yuwenyue@westlake.edu.cn