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

Liwei Wu,Qiang Yu,Qinghui Zhang,Jie Lu,Sainan Li,Shizan Xu,Wenwen Wang,Xiaoming Fan,Yujing Xia,Kan Chen,Chuanyong Guo,Yingqun Zhou,Jingjing Li,Jiao Feng,Tong Liu,Xiya Lu,Weiqi Dai

doi:10.1155/2017/9724217

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.

Highlights

Ischemia reperfusion (IR) injury, the interruption of blood supply to an organ and its subsequent restoration, leads to irreversible damage
The results showed that the serum level of liver enzymes and the expression of marker proteins in the 5 groups were not obviously different (Figures 1(a) and 1(b))
Our findings showed that quercetin reduced hepatic ischemia reperfusion (IR) injury in Balb/c mice

Summary

Introduction

Ischemia reperfusion (IR) injury, the interruption of blood supply to an organ (ischemia) and its subsequent restoration (reperfusion), leads to irreversible damage. The expression levels of liver enzymes, inflammatory cytokines, and other marker proteins were determined at 2, 8, and 24 hours after IR. 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. 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

Objectives

Methods

Results

Conclusion