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目的探讨金属硫蛋白对镍致小鼠肝损伤的保护作用及其机制。方法利用硫酸镍染毒复制小鼠肝损伤的模型,然后腹腔注射不同剂量的金属硫蛋白7 d,检测肝脏器系数、肝功能及肝组织脂质过氧化等指标,并行肝组织病理学观察。结果肝损伤模型组与金属硫蛋白(MT)保护组小鼠肝脏器系数差异有统计学意义(P<0.05),随着MT剂量的增加,肝脏器系数逐渐降低(P<0.05);MT保护组肝细胞炎性浸润、水肿及坏死明显减轻,肝窦结构有恢复;MT保护组小鼠血清AST、ALT、GGT及总胆汁酸均低于损伤模型组(P<0.05),肝组织MDA、GSH低于损伤模型组(P<0.05),而SOD、GSH-Px活性则高于损伤模型组(P<0.05),并均有较强的剂量依赖关系。结论金属硫蛋白对镍致小鼠肝损伤有保护作用,保护机制可能与减轻氧化损伤有关。
Objective To investigate the protective effect of metallothionein on liver injury induced by nickel and its mechanism. Methods The model of hepatic injury induced by nickel sulfate was replicated in mice. Then different doses of metallothionein were injected intraperitoneally for 7 d. The indices of hepatic function, liver function and lipid peroxidation of liver tissue were detected, and histopathological observation was performed. Results The liver coefficient of liver injury model group was significantly lower than that of the MT group (P <0.05). With the increase of MT dose, the liver coefficient decreased gradually (P <0.05). MT protection The serum levels of AST, ALT, GGT and total bile acid were lower in the MT-treated group than in the injury model group (P <0.05), and the levels of MDA, GSH was lower than the injury model group (P <0.05), while SOD, GSH-Px activity was higher than the injury model group (P <0.05), and have a strong dose-dependent relationship. Conclusion Metallothionein has a protective effect on liver injury induced by nickel, and the protective mechanism may be related to the reduction of oxidative damage.