Expression And Mechanism Of HSP32 Gene In Heat Stress Mouse Liver

In this paper, the effects of various type heat stresses on liver histology, oxidative stress parameters, liver function, and the HSP32 and caspase-3 gene expression in mice were detected. By intraperitoneal injection of hemin and tin-protoporphyrin to induce and inhibit the expression of HSP32, we investigate the functional role of HSP32 in protecting liver tissue against heat stress in mice and the mechanism by which it achieves this protective effect.1 Correlation between heat shock protein 32 and chronic heat-induced liver injury in developing miceHeat 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-3 mRNA expression and caspase-3 activity of heated liver were also analysed. The results showed that liver injury caused by chronic heat stress(39℃,1.5 h/day for 6 weeks) was reversible, caspase-3 mRNA 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). In conclusion, 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.2 Expression and mechanism of HSP32 gene in heat stress mouse liverHeat shock protein 32 (HSP32) is a stress response protein that can be induced by heat stress in the liver and its induction can act as an important cellular defense mechanism against heat-induced liver injury. To investigate the functional role of HSP32 in protecting liver tissue against heat stress in mice and the mechanism by which it achieves this protective effect, HSP32 expression and carbon monoxide(CO)contents in a model of mice subjected to acute, transient heat exposure were examined. Furthermore, functional and histological parameters of liver damage and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions and caspase-3 expression were also investigated in this study. We found that heat treatment of mice produced severe hepatic injury, whereas upregulation of HSP32 with hemin pretreatment prevented mice from liver damage. In contrast, addition of Sn-protoporphyrin (SnPP) to inhibit HSP32 expression completely reversed its hepatoprotective effect. In conclusion, upregulation of HSP32 by hemin could alleviate acute heat-induced hepatocellular damage in mice, and its byproduct CO seems to play a more important role in hepatoprotective mechanism.