Correlation between heat shock protein 32 and chronic heat-induced liver injury in developing mice

Heat stress is one of a wide variety of factors causing liver injury, a small heat shock protein (HSP), HSP32, is induced by heat stress in the liver. But the biological function of HSP32 in this injury is unclear. To investigate the underlying role of HSP32, RT-PCR, immunocytochemical staining and ELISA were applied to confirm the expression of HSP32. And the underlying mechanism in the pathogenesis of hepatic dysfunction following hyperthermic challenge and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions in developing mice were investigated in this study. Caspase-3mRNA expression and caspase-3 activity of heated liver were also analysed. The results showed that liver injury caused by chronic heat stress(39°C, 1.5h/day for 6 weeks) was reversible, caspase-3mRNA expression and caspase-3 activity of heat treated mice were increased after the first three weeks of heat exposure (P<0.05) and high expression levels of HSP32 were observed throughout the duration of experiment (P<0.01). A strong correlation exists between heat-induced liver injury and the induction of HSP32, which suggested that the reversibility of liver injury is involved in the induction of HSP32 in the hepatic cells under continuing heat stress.