Liver transplantation therapy is well accepted for severe liver diseases. The incidence of primary dysfunction and initial graft non-function is dependent on the cold preservation period and is associated with organ harvest, preservation and reperfusion, i.e., ischemia-reperfusion injury (IRI).The basic mechanism of IRI is still poorly understood. In liver transplantation, it is generally accepted that the lesion and/or activation of non-parenchymal cells is the main cause of IRI. The parenchymal cells (hepatocytes) appear morphologically well preserved even after long periods of cold preservation and its injury is considered a consequence of the death or alteration of non-parenchymal cells (Lemasters & Thurman, 1997).We found that the rat liver ischemia-reperfusion injury is characterized by an initial event of sinusoidal endothelial cells necrosis followed by a late phase of hepatocytes apoptosis (Huet et al., 2004).Recently we found the cytoprotective role of chondroitin sulfate in bile duct ligation model (Guedes et al, 2013). So the objective of this project is to verify the role of chondroitin sulfate as cytoprotective substance in rat liver undergoing experimental model of cold ischemia and warm reperfusion ex vivo.
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