机构地区:[1]河北联合大学公共卫生学院,河北唐山063000
出 处:《中国职业医学》2015年第2期194-198,共5页China Occupational Medicine
摘 要: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 study the intervention effects of 18α-glycyrrhizic acid and 18β-glycyrrhizic acid on liver injury of mice exposed to cadmium. Methods Seventy-two healthy specific pathogen free male Kunming mice were randomly divided into 6 groups, namely the control group, model group (pure cadmium group), 18α-glycyrrhizic acid low dose group, 18α-glycyrrhizic acid high dose group, 18β-glycyrrhizic acid low dose group and 18β-glycyrrhizic acid high dose group ; all groups except the control group were intraperitoneally injected with cadmium chloride of 0. 40 mg/mL mass concentration at the dose of 2. 5 mg/kg body weight for 20 days. In the meantime, the low and high dose groups were given 18ct-glycyrrhizic acid and 18β-glycyrrhizic acid at the dose of 30 mg/kg and 60 mg/kg body weight respectively for 6 weeks. The flow cytometry was used to detect the apoptosis of liver cells. Activities of liver aspartate transaminase ( AST), alanine transaminase (ALT) enzyme were measured and the ultrastructure of liver cells was observed by transmission electron microscope (TEM). Results The apoptosis rates of liver ceils in mice of all dose groups were lower than that of the model group (P 〈 0. 05 ). The apoptosis rate of liver cells in 18α-glycyrrhizic acid low dose group was lower than that of 18β-glycyrrhizic acid low dose group ( P 〈 0.05 ). Compared with those in the control group, Liver AST and ALT activities in model group and all dose groups were higher (P 〈0. 05) ; except the activity of ALT in 18β-glycyrrhizic acid low dose group, liver AST and ALT activities of the dosed groups were all lower than those of model group ( P 〈 0. 05 ). Liver AST and ALT activities in 18α-glycyrrhizic acid low dose group were higher than those of the 18β-glycyrrhizic acid low dose group (P 〈 0. 05 ) ; liver AST activity in 18α-glycyrrhizic acid high dose group were higher than those of the 18β- glycyrrhizic acid high dose group ( P 〈 0.05 ). Pathology histology slices showe
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