文献类型：期刊文献

英文题名：Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway

作者：Niu, Qibing[1];Sun, Wanli[1];Chen, Quan[1];Long, Yang[1];Cao, Wanjun[1];Wen, Shiqi[1];Li, Anqiang[1];Dong, Fang[1];Shi, Hao[1]

第一作者：Niu, Qibing

通信作者：Chen, Q[1]

机构：[1]Gansu Univ Chinese Med, Peoples Hosp Gansu Prov, Dept Vasc Surg, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Peoples Hosp Gansu Prov, Dept Vasc Surg, Lanzhou, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2020

卷号：26

外文期刊名：MEDICAL SCIENCE MONITOR

收录：;Scopus(收录号：2-s2.0-85088351193);WOS:【SCI-EXPANDED(收录号:WOS:000550065500001)】；

语种：英文

外文关键词：Glycogen Synthase Kinase 3; Ischemic Attack, Transient; Ischemic Postconditioning; Ischemic Preconditioning; Proto-Oncogene Proteins c-fyn; Reperfusion Injury

摘要：Background: Ischemia/reperfusion (I/R) injury not only exists in ischemic tissues and organs, but also can cause damage to distant tissues and organs. As the largest metabolic organ of the human body, the liver is very vulnerable to injury after limb I/R. However, the mechanism of liver injury caused by limb I/R injury has not been fully elucidated. This study investigated the effect and mechanism of ischemic postconditioning (IPO) on the liver after hindlimb I/R in rats. Material/Methods: A rat model of hindlimb I/R was established and treated by IPO. Liver function, changes of oxidative stress index and inflammation, Bcl-2 and Bax proteins, and apoptosis were assessed. The structural changes were observed by electron microscopy. GSK-3 beta/Fyn/Nrf2 levels were detected by quantitative PCR and Western blot. Results: IPO significantly reduced serum AST, ALP, LDH, and ALT levels induced by I/R. Compared with the I/R group, the levels of SOD, GSH-Px, and CAT in the IPO group were significantly increased, while the levels of MDA, MPO, and ROS were significantly decreased. The IPO group had significantly higher Bcl-2 level and significantly lower Bax level compared to the I/R group. Consistently, IPO decreased the apoptosis rate induced by I/R. Furthermore, IPO lowered the levels of TNF-alpha, IL-1 beta, IL-10, and INF-gamma and alleviated the ultrastructural changes of hepatocytes. Finally, Nrf2, Fyn, and GSK-3 beta mRNA and protein levels in the IPO group were significantly higher than in the I/R group. Conclusions: IPO protects against liver injury caused by I/R injury of the hindlimb, possibly via the GSK-3b/Fyn/Nrf2 pathway.