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Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide 被引量:44

Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide
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摘要 Hepatic ischemia-reperfusion injury(IRI) is a patho-physiological event post liver surgery or transplantation and significantly influences the prognosis of liver func-tion. The mechanisms of IRI remain unclear, and effec-tive methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabo-lism, mitochondria, oxidative stress, intracellular cal-cium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide(NO)in protecting against liver IRI has recently been report-ed. 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 enhanc-ing 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 control-ling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI. Hepatic ischemia-reperfusion injury(IRI) is a patho-physiological event post liver surgery or transplantation and significantly influences the prognosis of liver func-tion. The mechanisms of IRI remain unclear, and effec-tive methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabo-lism, mitochondria, oxidative stress, intracellular cal-cium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide(NO)in protecting against liver IRI has recently been report-ed. 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 enhanc-ing 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 control-ling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI.
出处 《World Journal of Gastrointestinal Surgery》 SCIE CAS 2014年第7期122-128,共7页 世界胃肠外科杂志(英文版)(电子版)
基金 Supported by National Natural Science Foundation of China,No.81170416 and No.81273264 Doctoral Fund of Ministry of Education of China,No.20100061110069 Jilin Province Science and Technology Bureau International Cooperation Fund,No.2011742 Techpool Research Fund,No.01201046 Jilin Province Nature Science Foundation,No.201015178
关键词 Liver ISCHEMIA-REPERFUSION injury Cyto-kine CHEMOKINE KUPFFER cells MITOCHONDRIA NITRIC oxide Liver Ischemia-reperfusion injury Cytokine Chemokine Kupffer cells Mitochondria Nitric oxide
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