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目的研究18α-甘草酸和18β-甘草酸对镉染毒小鼠肝损伤的干预作用。方法无特定病原体级雄性昆明种小鼠72只,随机分为对照组、模型组、18α-甘草酸低剂量组、18α-甘草酸高剂量组、18β-甘草酸低剂量组和18β-甘草酸高剂量组;除对照组外,其余各组均按2.50 mg/kg体质量腹腔注射质量浓度为0.40 g/L氯化镉溶液,连续染毒20 d。各剂量组染毒的同时分别按30.00和60.00 mg/kg体质量剂量给予18α-甘草酸、18β-甘草酸干预,连续6周。流式细胞仪检测各组小鼠肝细胞凋亡情况,测定肝脏天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活力,透射电镜观察肝细胞超微结构的改变。结果各剂量组小鼠肝细胞凋亡率均低于模型组(P<0.05),18α-甘草酸低剂量组肝细胞凋亡率低于18β-甘草酸低剂量组(P<0.05)。模型组和各剂量组小鼠肝脏AST、ALT活力均高于对照组(P<0.05);除18β-甘草酸低剂量组肝脏ALT活力外,其余各剂量组小鼠肝脏AST和ALT活力均低于模型组(P<0.05)。18α-甘草酸低剂量组小鼠肝脏AST和ALT活力均低于18β-甘草酸低剂量组(P<0.05),18α-甘草酸高剂量组小鼠肝脏AST活力低于18β-甘草酸高剂量组(P<0.05)。肝脏病理组织学切片显示:模型组小鼠的肝脏细胞有大面积坏死和凋亡,而各剂量组小鼠肝脏细胞凋亡减少,细胞结构完整。透射电镜观察显示:模型组肝脏细胞超微结构破坏较严重,各剂量组细胞超微结构虽较对照组有破坏,但较模型组明显好转。结论 18α-甘草酸比18β-甘草酸对镉染毒所致小鼠肝脏损害有更好的保护作用。
Objective To investigate the effects of 18α-glycyrrhizin and 18β-glycyrrhizinate on liver injury induced by cadmium in mice. Methods Seventy-two male Kunming mice without specific pathogen were randomly divided into control group, model group, 18α-glycyrrhizin low dose group, 18α-glycyrrhizinate high dose group, 18β-glycyrrhizinate low dose group and 18β- High dose group. Except for the control group, all the other groups were given intraperitoneal injection of cadmium chloride solution (0.40 g / L) at 2.50 mg / kg body weight for 20 days. Each dose group were given 18α-glycyrrhizic acid and 18β-glycyrrhizinate for 30 weeks at doses of 30.00 and 60.00 mg / kg, respectively, for 6 weeks. The apoptosis of hepatocytes in each group was detected by flow cytometry. The activity of hepatic AST and ALT was measured. The ultrastructure of hepatocytes was observed by transmission electron microscope . Results The apoptotic rates of hepatocytes in all dose groups were lower than those in model group (P <0.05). The apoptosis rate of hepatocytes in 18α-glycyrrhizin low dose group was lower than that of 18β-glycyrrhizinate low dose group (P <0.05). The activities of AST and ALT in the liver of model group and each dose group were higher than those of the control group (P <0.05). The activities of AST and ALT in the liver of mice in each dose group were lower than those in the low dose 18β-glycyrrhizinate group In model group (P <0.05). The liver AST and ALT activities of 18α-glycyrrhizin low-dose group were lower than those of 18β-glycyrrhizinate low-dose group (P <0.05). The liver AST activity of 18α-glycyrrhizinate high-dose group was lower than that of 18β- Group (P <0.05). Histopathological sections of liver showed large area of necrosis and apoptosis of liver cells in model group, while the apoptosis of liver cells of mice in each dose group decreased and cell structure was intact. Transmission electron microscopy showed that the ultrastructural damage of liver cells in the model group was more serious. The ultrastructures of the cells in each dose group were more damaged than those in the control group, but were significantly improved compared with the model group. Conclusion 18α-glycyrrhizin has better protective effect on liver damage induced by cadmium than 18β-glycyrrhizinate.