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Review
. 2014 Jul 27;6(7):122-8.
doi: 10.4240/wjgs.v6.i7.122.

Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide

Lian-Yue Guan  1 , Pei-Yao Fu  1 , Pei-Dong Li  1 , Zhuo-Nan Li  1 , Hong-Yu Liu  1 , Min-Gang Xin  1 , Wei Li  1
Affiliations
Review

Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide

Lian-Yue Guan et al. World J Gastrointest Surg. .

Abstract

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.

Keywords: Chemokine; Cytokine; Ischemia-reperfusion injury; Kupffer cells; Liver; Mitochondria; Nitric oxide.

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Figures

Figure 1
Figure 1
Cytokine network on the regulation of liver ischemia-reperfusion injury. IRI: Ischemia-reperfusion injury; IL: Interleukin; IFN-γ: Interferon-gamma; HGF: Hepatocyte growth factor; MIP: Macrophage inflammatory protein; ICAM-1: Intercellular adhesion molecule 1; NF: Nuclear factor; MAPK: Mitogen-activated protein kinase.
Figure 2
Figure 2
The protective effects of nitric oxide on liver ischemia-reperfusion injury. ATP: Adenosine triphosphate; IL: Interleukin.
Figure 3
Figure 3
Mechanisms of hepatic ischemia reperfusion injury. ATP: Adenosine triphosphate; IL: Interleukin; ROS: Reactive oxygen species; IRI: Ischemia-reperfusion injury; IFN-γ: Interferon-gamma; ICAM: Intercellular adhesion molecule; VCAM: Vascular cell adhesion molecule; TNF: Tumor necrosis factor.
See this image and copyright information in PMC

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