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

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).