Objective: To study the synthesis of heat shock protein 70 (HSP70) by zinc (ZnSO4) and its protective effect during cold preservation in rat liver by establishment of a simple cold preservation model.
Methods: Wistar rats were divided into 5 groups (n=6): control group untreated before operation; Zn-1, Zn-2, and Zn-3 groups treated before operation with zinc sulfate (Zn2+ 5 mg/kg, 10 mg/kg, 15 mg/kg respectively); H group treated with heat shock (42.5 ℃×15 min). The livers of the rats were preserved in UW solution for 6, 12, 24 hours. The results of heat shock protein (HSP) synthesis were analyzed with Western blot. The aspartate aminotransferase (AST) and lactic dehydrogenase (LDH) values of perfusion and histological findings were evaluated.
Results: A great amount of HSPs was synthesized after pretreatment with zinc and heat shock. The AST and LDH values of the Zn-l, Zn-2 and H groups were significantly lower than those of the C group (P<0.05). But the value of the Zn-3 group was much higher. Histologically, mild injury was observed in the Zn-1, Zn-2 and H groups, but severe injury in the Zn-3 group.
Conclusions: Zn2+, as a potent and feasible inducer of HSP expression, is able to protect the liver for cold preservation. Proper induction dosage of Zn2+ ranges from 5 mg/kg to 10 mg/kg, and Zn2+ 15 mg/kg could not be a stress conditioning factor for its adverse effect on rat liver.