期刊
WORLD JOURNAL OF GASTROINTESTINAL SURGERY
卷 6, 期 7, 页码 122-128出版社
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.4240/wjgs.v6.i7.122
关键词
Liver; Ischemia-reperfusion injury; Cytokine; Chemokine; Kupffer cells; Mitochondria; Nitric oxide
资金
- National Natural Science Foundation of China [81170416, 81273264]
- Doctoral Fund of Ministry of Education of China [20100061110069]
- Jilin Province Science and Technology Bureau International Cooperation Fund [2011742]
- Techpool Research Fund [01201046]
- Jilin Province Nature Science Foundation [201015178]
Hepatic ischemia-reperfusion injury (IRI) is a pathophysiological event post liver surgery or transplantation and significantly influences the prognosis of liver function. The mechanisms of IRI remain unclear, and effective methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabolism, mitochondria, oxidative stress, intracellular calcium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide (NO) in protecting against liver IRI has recently been reported. NO has been found to attenuate liver IRI through various mechanisms including reducing hepatocellular apoptosis, decreasing oxidative stress and leukocyte adhesion, increasing microcirculatory flow, and enhancing mitochondrial function. The purpose of this review is to provide insights into the mechanisms of liver IRI, indicating the potential protective factors/pathways that may help to improve therapeutic regimens for controlling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据