问荆硅化物对四氯化碳急性肝损伤的保护作用及机制  

Protective actions and mechanisms of silicon compound of equisetum in carbon tetrachloride induced acute liver injury of mice

作　　者：骆勤[1] 鞠洋[1] 党月兰[2] 宋平顺[3] 

机构地区：[1]兰州大学第二医院药剂科,甘肃兰州730030 [2]兰州大学药学院,甘肃兰州730000 [3]甘肃省药品检验所,甘肃兰州730000

出　　处：《兰州大学学报（医学版）》2008年第3期60-62,65,共4页Journal of Lanzhou University（Medical Sciences）

摘　　要：目的研究问荆硅化物(SCE)对CCl_4急性肝损伤的保护作用及机制。方法采用小鼠CCl_4急性肝损伤模型进行实验,检测小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、NO及肝糖原、肝蛋白、肝甘油三酯、肝丙二醛、肝细胞色素P_(450)含量及肝超氧化物歧化酶(SOD)活性。结果SCE(灌胃1.0～2.0 g/kg)能明显降低CCl_4肝损伤小鼠血清ALT、AST活性、NO含量及肝甘油三酯、肝丙二醛含量。提高肝糖原、肝蛋白、肝细胞色素P_(450)含量及肝SOD活性。结论SCE对CCl_4引起的小鼠急性肝损伤具有明显保护作用,其机制可能与其清除自由基、抑制脂质过氧化及降低NO浓度有关。Objective To study the protective actions and mechanisms of silicon compound of equisetum（SCE） in CC14 induced acute liver injury of mice. Methods The model of CClainduced acute liver injury of mice was used. Serum alanine aminotransferase（ALT）, aspartate aminotransferase（AST）, NO and liver triglycerides, protein, glycogen, malondiadehgde, hepatocyte cytochrome P450（P450）, superoxide dismutase（SOD） were detected to evaluate the protective actions of SCE on CC14-induced acute liver injury. Results SCE（ig, 1.0-2.0 g/kg） inhibited the rise of serum ALT, AST, NO levels and hepatic triglycerides, malondiadehgde contents, and increased the contents of hepatic protein, glycogen, P450 and SOD activities in CC14-intoxicated mice. Gonclusion SCE possesses protective actions on CC14-induced acute liver injury in mice, and its mechanisms are related to the clearance of free radicals, inhibition of lipid peroxidation and the reduction of serum NO.

关 键 词：问荆硅化物 四氯化碳肝损伤 保肝作用 脂质过氧化 

分 类 号：R965[医药卫生—药理学]