红芪和黄芪水煎剂对四氯化碳致肝损伤小鼠的保护作用

Protective effects of the aqueous extracts from Hedysari Radix and Astragali Radix against acute hepatic injury induced by carbon tetrachloride in mice

目的 研究红芪和黄芪水煎剂（HR/AR）对四氯化碳（CCl4）致急性肝损伤小鼠肝脏氧化应激的防治作用及其机制。方法将昆明种小鼠90只随机均分为模型组、秋水仙碱组（0.6 mg·kg^（-1））、对照组、红芪不同产地水煎剂组（HAF13）、黄芪不同产地水煎剂组（AAF13）。除对照组外,其余各组小鼠均于颈背部sc 20%CCl4花生油溶液,5 d一次,造模,HAF/AAF组小鼠每日ig给药1次,连续给药6周。末次给药后,测定各组小鼠血清中丙氨酸转氨酶（ALT）、天冬氨酸氨基转移酶（AST）的活性及总蛋白（TP）、白蛋白（ALB）和白球比（A/G）的水平;测定肝组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSHPx）的活力和丙二醛（MDA）的水平。结果 与模型组比较,HAF/AAF均能降低小鼠血清中升高的ALT、AST活性,提高ALB含量及肝脏组织中SOD、GSH-Px的活力、降低脂质过氧化产物MDA的水平。结论 HR/AR对CCl4诱导的肝损伤均有一定的保护作用,其机制可能与降低小鼠肝脏氧化应激有关。

OBJECTIVE To investigate the preventive and therapeutic effects of aqueous fractions from Hedysari Radix and Astragali Radix（HR/AR） on hepatic oxidative stress in mice with liver injury induced by carbon tetrachloride （CCl4 ）. METHODS 90 Kunming mice were randomly divided into nine groups ： model control group, colchicine treated group （0.6 mg· kg^- 1 ）, normal control group ; HR 1 - 3 and AAR 1 - 3 treated groups. All mice except those in the normal control group received a subcutaneous injection of 20% CCl4 （ Once each 5 days） in the neck and baek. While the mice in the other groups received an intragastric administration of HR/ AR or colchicine every day. After 42 d, the levels of serum alanine aminotransferase （ ALT）, aspartate aminotransferase （ AST）, total protein（ TP）, album protain （ALB） and the ratio of A/G were assayed. Superoxide dismutase （SOD）, glutathioneperoxidase （GSH - Px） and the contents of malondialdehyde（MDA） in liver were measured. RESULTS HR/AR could inhibit the increasing of ALT, AST in serum of mice and increase the level of ALB and the SOD, GSH - Px activities in liver tissue. HR/AR could also decrease the MDA content in liver. There was a significant difference compared with the model group. CONCLUSION HR/AR can reduce hepatic oxidative stress in mice with acute liver injury induced by CCl4, there by showing the protective effect on mice with acute liver injury induced by CCl4.