AIM:To observe the protective effect of heat shock protein72 (HSP 72) induced by pretreatment of doxorubicin (DXR)on long-term cold preservation injury of rat livers.METHODS:Sprague-Dawley rats were administeredintravenously DXR at a dose of 1mg/kg body mass in DXRgroup and saline in control group.After 48h,the rat liverwas perfused with cold Linger’s and University of Wisconsin(UW) solutions and then was preserved in UW solution at4℃ for 24,36 and 48 h.AST,ALT,LDH and hyaluronic acidin preservative solution were determined.Routine HE,immunohistochemical staining for HSP 72 and electronmicroscopic examination of hepatic tissues were performed.RESULTS:After 24,36 and 48 h,the levels of AST,ALTand hyaluronic acid in preservative solution were significantlyhigher in control group than in DXR group (P<0.05),whileLDH level was not significantly different between the 2 groups(P>0.05).Hepatic tissues in DXR group were morphologicallynormal and significantly injured in control group.HSP 72was expressed in hepatocytes and sinusoidal endothelialcells in DXR group but not in control group.CONCLUSION:Pretreatment of DXR may extend the time ofrat liver cold preservation and keep liver alive.The expressionof HSP 72 in liver can prevent hepatocytes and sinusoidalendothelial cells from long-term cold preservation injury. AIM: To observe the protective effect of heat shock protein72 (HSP 72) induced by pretreatment of doxorubicin (DXR) on long-term cold preservation injury of rat livers. METHODS: Sprague-Dawley rats were administered in a dose of 1 mg / kg body mass in DXRgroup and saline in control group. After 48 h, the rat liver was perfused with cold Linger’s and University of Wisconsin (UW) solutions and then was preserved in UW solution at 4 ° C for 24, 36 and 48 h.AST, ALT, LDH and hyaluronic acid preservative solution were determined. Routine HE, immunohistochemical staining for HSP 72 and electron microscopic examination of hepatic tissues were performed .RESULTS: After 24, 36 and 48 h, the levels of AST, ALT and hyaluronic acid in preservative solution were significantlyhigher in control while the level of LDH was significantly different between the two groups (P> 0.05) .Hepatic tissues in DXR group were morphologically normal and significantly injured in control group. HSP 72wa s expressed in hepatocytes and sinusoidal endothelial cells in DXR group but not in control group. CONCLUSION: Pretreatment of DXR may extend the time of liver cold preservation and keep liver alive. The expression of HSP 72 in liver can prevent hepatocytes and sinusoidalendothelial cells from long-term cold preservation injury.