Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-κB Pathway. (16th October 2017)

• Record Type: Journal Article
• Authors: Wu, Liwei; Zhang, Qinghui; Dai, Weiqi; Li, Sainan; Feng, Jiao; Li, Jingjing; Liu, Tong; Xu, Shizan; Wang, Wenwen; Lu, Xiya; Yu, Qiang; Chen, Kan; Xia, Yujing; Lu, Jie; Zhou, Yingqun; Fan, Xiaoming; Guo, Chuanyong
• Other Names: Sakai Eiji Academic Editor.
• Is Part Of: Gastroenterology research and practice. Volume 2017(2017)
• Publication Date: 2017-10-16
• Subjects: Gastroenterology -- Periodicals; Digestive organs -- Diseases -- Periodicals; 616.33005
• DOI: 10.1155/2017/9724217
• Languages: English
• ISSNs: 1687-6121

Abstract

Abstract : Background . Hepatic ischemia reperfusion (IR) injury is a common phenomenon in transplantation or trauma. The aim of the present study was to determine the protective effect of quercetin (QE) on hepatic IR injury via the ERK/NF- κ B pathway. Methods . Mice were randomized into the sham, IR, QE100 + IR, and QE200 + IR groups. Quercetin was administered intragastrically daily at two doses (100 mg/kg and 200 mg/kg) for 5 days prior to IR injury. The expression levels of liver enzymes, inflammatory cytokines, and other marker proteins were determined at 2, 8, and 24 hours after IR. And they were compared among these groups. Results . Compared with the IR group, the treatment of QE reduced the release of cytokines, leading to inhibition of apoptosis and autophagy via downregulation of the ERK/NF- κ B pathway in this model of hepatic IR injury. Conclusion . Apoptosis and autophagy caused by hepatic IR injury were inhibited by QE following a reduction in the release of inflammatory cytokines, and the relationship between the two may be associated with inactivation of the ERK/NF- κ B pathway.