Induction of a 72-kDa Heat Shock Protein and Cytoprotection Against Thioacetamide-Induced Liver Injury in Rats

Heat shock proteins are ubiquitous intracellularproteins induced by various physiological stress-relatedevents. A 72-kDa heat shock protein (HSP72) has beenreported to be an endogenous cytoprotectant in variety of cells in vitro . In order tostudy the cytoprotective function of HSP72 in the liver,the effect of preinduction of HSP72 in rat liver bysystemic hyperthermia on thioacetamide-induced hepatic injury was investigated in this study.Expression of HSP72 in the liver was investigated byimmunoblot and densitometric analysis. Rats wereinjected with thioacetamide (100 mg/kg, subcutaneously)with or without preinduction of HSP72 byhyperthermia. Serum AST and ALT concentrations weremeasured before and after thioacetamide injection inboth group. Histologic alteration of the liver wasevaluated also. Systemic hyperthermia (42.5°C, 20min) significantly induced HSP72 in the liver.Thioacetamide-induced hepatic injury was clearlyprevented by preinduction of HSP72 by hyperthermia.Prevention of hepatocyte damage was more clear in the areaaround central veins where HSP72 induction was apparent.Our findings might suggest that HSP72 has an importantfunction in the liver with respect to cytoprotection. These results might be important forunderstanding the mechanism of adaptivecytoprotection in the liver mediated by thefunction of heat shock proteins as molecularchaperons as reported in vitro.