水飞蓟宾对小鼠急性肝损伤的保护作用

目的:研究水飞蓟宾对四氯化碳(carbon tetrachlitied,CCl_4)与D-氨基半乳糖(D-galactosamine,D-Gal)所致的急性肝损伤的保护作用。方法:分别取健康昆明种小鼠84只,随机分为6组,即正常组、急性肝损伤模型组、水飞蓟宾低、中、高剂量组、阳性药组,除正常组外,分别ip 0.2%CCl_4和800 mg·kg~(-1)D-Gal,造模后1,6 h这2个时间点,尾静脉注射不同剂量的水飞蓟宾(120,240,480 mg·kg~(-1)),CCl_4所致的急性肝损伤给予阳性药硫普罗宁(40 mg·kg~(-1)),D-Gal所致的肝损伤给予甘草酸二铵组(30 mg·kg~(-1));造模24 h后,检测血清中天门冬氨酸氨基转移酶(AST),谷氨酸氨基转移酶(ALT)水平及肝组织匀浆中超氧化歧化酶(SOD),丙二醛(MDA),还原型谷胱甘肽(GSH)水平,苏木素-伊红(HE)染色观察肝组织切片的病理变化。结果:与正常组比较,CCl_4和D-Gal所致的急性肝损伤模型中AST,ALT,MDA的水平明显升高(P0.01),SOD,GSH的水平明显降低(P0.01);与CCl_4,D-Gal所致的急性肝损伤模型组比较,水飞蓟宾低、中、高3个剂量组明显降低AST,ALT和MDA的水平及升高SOD,GSH的水平(P0.01)。肝脏的病理切片结果显示,模型组肝细胞明显的坏死、变性等病变,水飞蓟宾给药后肝小叶结构尚完整,肝细胞未见明显病灶。结论:水飞蓟宾对CCl_4和D-Gal所致的小鼠急性肝损伤具有良好的保护作用。

Protective Effects of Silibinin on Acute Liver Injury in Mice

Objective: To investigate the protective effects of Silibinin on acute liver injury induced by carbon tetrachlitied (CCl₄) and D-galactosamine (D-Gal). Method: Totally 84 healthy Kunming mice were randomly divided into normal group, acute liver injury model group, silibinin low dose group, middle dose group and high dose group, and positive drug group. All the other groups except normal group received intraperitoneal injection of carbon tetrachlitied (0.2%) and galactosamine (800 mg·kg^-1). 1 hour and 6 hours after modeling, silibinimin of different doses (120, 240, 480 mg·kg^-1) was applied by the tail vein injection. Positive drug Tiopronin (40 mg·kg^-1) was given for the acute liver injury induced by CCl₄, and diammonium glycyrrhizinate (30 mg·kg^-1) was given for the liver injury induced by D-Gal. 24 hours after modeling, the levels of aspartate transaminase (AST), alanine transaminase (ALT) in serum, and superoxide dismutase (SOD), malonal dehyde (MDA), reduced glutathione (GSH) levels in liver homogenate were detected. Pathological changes of liver slices were investigated by htoxylin-eosin(HE) staining. Result: As compared with the normal group, the levels of AST, ALT and MDA were significantly increased in CCl₄ and D-Gal models (P < 0.01);SOD and GSH levels were decreased significantly (P < 0.01). As compared with CCl₄ and D-Gal model groups, the levels of AST, ALT and MDA were significantly reduced in the silibinin treatment groups, while the levels of SOD and GSH were increased (P < 0.01). Pathological results showed that the hepatic cells of the model group had obvious necrosis and lesions;the structure of hepatic lobule was still completed and no obvious lesion were found in hepatic cells after silibinin treatment. Conclusion: Silibinin could well protect the acute hepatic injury induced by carbon tetrachlitied and galactosamine.