OBJECTIVE: A simple liver cold preservation model was established to study the synthesis of heat shock protein 70 (HSP70) induced by zinc (ZnSO(4), i.p.) and its protection during liver cold preservation in rat. METHO...OBJECTIVE: A simple liver cold preservation model was established to study the synthesis of heat shock protein 70 (HSP70) induced by zinc (ZnSO(4), i.p.) and its protection during liver cold preservation in rat. METHODS: Male Wistar rats were divided into 5 groups (n = 6). In control group rat received no pretreatment; in Zn-1 group, Zn-2 group, and Zn-3 group rats were pretreated with zinc sulfate at a dose of 5 mg/kg, 10 mg/kg, 15 mg/kg respectively; and in H group rat received heat shock preconditioning (42.5 degrees C x 15 min). Livers were preserved in UW solution for 6, 12 and 24 h, respectively. HSP70 was analyzed by Western blot. Aspartate transaminase (AST) and lactate dehydrogenase (LDH) values of the perfusion solution and the histology of the liver were evaluated. RESULTS: HSP70 expression was markedly elevated after pretreatment with zinc and heat shock. AST and LDH values in the Zn-1, Zn-2 and H groups were significantly lower than those in the control group, respectively (P 0.05), whereas the AST and LDH values in the Zn-3 group were much higher than those in the control group. Histology results showed that liver injury in the Zn-1, Zn-2 and H groups were minimal, while it was severe in the Zn-3 group. CONCLUSIONS: Zn(2+) is a potent and feasible inducer of HSP expression and is able to protect liver from cold preservation injury. The proper inducing dosage of Zn(2+) ranged from 5 mg/kg to 10 mg/kg. The dosage of 15 mg/kg for Zn(2+) as a HSP inducer is not indicated for its severe toxicity to the liver.展开更多
文摘OBJECTIVE: A simple liver cold preservation model was established to study the synthesis of heat shock protein 70 (HSP70) induced by zinc (ZnSO(4), i.p.) and its protection during liver cold preservation in rat. METHODS: Male Wistar rats were divided into 5 groups (n = 6). In control group rat received no pretreatment; in Zn-1 group, Zn-2 group, and Zn-3 group rats were pretreated with zinc sulfate at a dose of 5 mg/kg, 10 mg/kg, 15 mg/kg respectively; and in H group rat received heat shock preconditioning (42.5 degrees C x 15 min). Livers were preserved in UW solution for 6, 12 and 24 h, respectively. HSP70 was analyzed by Western blot. Aspartate transaminase (AST) and lactate dehydrogenase (LDH) values of the perfusion solution and the histology of the liver were evaluated. RESULTS: HSP70 expression was markedly elevated after pretreatment with zinc and heat shock. AST and LDH values in the Zn-1, Zn-2 and H groups were significantly lower than those in the control group, respectively (P 0.05), whereas the AST and LDH values in the Zn-3 group were much higher than those in the control group. Histology results showed that liver injury in the Zn-1, Zn-2 and H groups were minimal, while it was severe in the Zn-3 group. CONCLUSIONS: Zn(2+) is a potent and feasible inducer of HSP expression and is able to protect liver from cold preservation injury. The proper inducing dosage of Zn(2+) ranged from 5 mg/kg to 10 mg/kg. The dosage of 15 mg/kg for Zn(2+) as a HSP inducer is not indicated for its severe toxicity to the liver.
