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. 2012:2012:738785.
doi: 10.1155/2012/738785. Epub 2012 Nov 11.

Antioxidant Stress and Anti-Inflammation of PPARα on Warm Hepatic Ischemia-Reperfusion Injury

Zhixin Gao  1 , Yuan-Hai Li
Affiliations

Antioxidant Stress and Anti-Inflammation of PPARα on Warm Hepatic Ischemia-Reperfusion Injury

Zhixin Gao et al. PPAR Res. 2012.

Abstract

Hepatic ischemia-reperfusion (IR) injury is a serious clinical problem. Minimizing the adverse effect of ischemia-reperfusion injury after liver surgery or trauma is an urgent need. It has been proved that besides the effect of regulating the lipid and lipoprotein metabolism, PPARα also undertakes the task of organ protection. In this paper, related literature has been summarized and we come to the conclusion that administration of PPARα agonists can strengthen the antioxidant and anti-inflammation defense system by the upregulation of the expression of antioxidant enzymes and inhibition of NF-κB activity. This may provide a potential clinical treatment for hepatic ischemia-reperfusion injury.

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Figures

Figure 1
Figure 1
Protection mechanism of PPARα in the liver during IR injury. Ischemic stress results in the generation of reactive oxygen species (ROS) in Kupffer cells. ROS activates NF-κB and induces mitochondrial dysfunction in neighboring hepatocytes. Activation of NF-κB consequences in the production of proinflammatory cytokines, chemokines and adhesion molecules which can recruit neutrophils and propagate the inflammatory response. This vicious circle is breaked by PPARα which is a ligand-activated transcription factor that upon heterodimerization with the retinoic X receptor (RXR), recognizes PPAR response elements (PPRE), located in the promoter of target genes. Abbreviations: Neutrophil (N), Kupffer cell (KC).
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