摘要
目的探讨复方甘草酸苷对大鼠亚急性酒精性肝损伤的保护作用及其相关机制。方法将72只健康SD大鼠随机分为6组:空白组、模型组、复方甘草酸苷低剂量组、中剂量组、高剂量组和阳性对照药葵花护肝片组。采用白酒灌胃的方法建立大鼠亚急性酒精性肝损伤模型,在造模的同时灌胃复方甘草酸苷及葵花护肝片水溶液。连续灌胃1周,然后检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)及肝组织中超氧化物岐化酶(SOD)、丙二醛(MDA)水平;并对肝脏作组织病理学检查。结果与空白组比较,模型组大鼠血清ALT、AST活性和肝组织MDA含量显著增加(P<0.01);肝组织SOD活性显著降低(P<0.01)。与模型组比较,复方甘草酸苷高剂量组大鼠血清ALT活性水平显著降低(P<0.01);低、中、高剂量组血清AST活性和肝组织MDA含量降低(P<0.05);中、高剂量组大鼠肝组织SOD活性升高(P<0.05)。结果提示,复方甘草酸苷各剂量组能改善肝脏组织病理损伤。结论复方甘草酸苷对酒精所致大鼠亚急性肝损伤具有保护作用。
Objective To investigate the protective effects and the mechanisms of Stronger Neo-Minophagen C(SNMC) on subacute alcohol induced liver injury in rats.Methods 72 healthy SD rats were randomly divided into 6 groups: control group,model group,low,middle,high dosage of SNMC groups and protective liver tablets group of sunflower.The subacute liver injury rat models were treated by feeding alcohol,meanwhile the rats were fed SNMC and sunflower tablets solution by gavage.One week later,the followings were assayed:the activities of serum alanine transarninase(ALT),aspartate transarninase(AST);the contents of liver superoxide dismutase(SOD) and malondialdehyde(MDA);The liver tissues were tested by pathological method.Results Compared with control group,serum ALT,AST activities and MDA content in liver tissues increased significantly in model group(P0.01);SOD content in liver tissues decreased(P0.01).Compared with model group,serum ALT activity decreased significantly in high dosage of SNMC group(P0.01);Serum AST activity and MDA content in liver tissues decreased in every SNMC group(P0.05);SOD content in liver tissues increased in middle and high dosage of SNMC groups(P0.05).The results suggest that the histological liver injury was improved in different dosage of SNMC groups.Conclusion Under the experimental conditions,SNMC has the protective effects against the subacute alcoholic injury of liver function in rats.
出处
《公共卫生与预防医学》
2011年第3期8-11,共4页
Journal of Public Health and Preventive Medicine
基金
咸宁学院校级课题编号SK0814
关键词
复方甘草酸苷
酒精性肝损伤
保护
Stronger Neo-Minophagen C(SNMC)
Subacute alcohol induced liver injury
Protection