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Gastroenterology Research and Practice
Volume 2017 (2017), Article ID 9724217, 15 pages
https://doi.org/10.1155/2017/9724217
Research Article

Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-κB Pathway

1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China
2Department of Clinical Laboratory, Kunshan First People’s Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu 215300, China
3Department of Gastroenterology, Shanghai Tenth People’s Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, China
4Department of Gastroenterology, Jinshan Hospital of Fudan University, Jinshan, Shanghai 201508, China

Correspondence should be addressed to Xiaoming Fan; moc.anis@75nafgnimoaix and Chuanyong Guo; moc.liamtoh@gnoynauhcoug

Received 16 March 2017; Revised 20 May 2017; Accepted 12 June 2017; Published 16 October 2017

Academic Editor: Eiji Sakai

Copyright © 2017 Liwei Wu et al. 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.

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-κB 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-κB 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-κB pathway.