降脂酮对CCl4诱导的大鼠慢性肝损伤的保护作用

目的：观察降脂酮对四氯化碳（CCl₄）诱导的慢性肝损伤的保护作用及其作用机制。方法：建立CCl₄慢性肝损伤动物模型，大鼠72只随机分为6组（每组12只），分别设为空白对照组以及CCl₄慢性肝损伤模型组（简称模型组）、阳性药对照组及降脂酮低、中和高剂量组（50、100和200 mg•kg^-1•d^-1）。测定大鼠血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）。肝组织中过氧化氢酶（CAT）活性及各胱甘肽（GSH）含量。结果：与模型组比较，降脂酮低、中和高剂量组血清ALT、AST活性均明显降低（P<0.05或P<0.01），肝组织CAT活性及GSH含量显著升高（P<0.05或P<0.01）；与阳性药对照组比较，降脂酮高剂量组ALT活性明显降低（P<0.01），低、中剂量组ALT活性与阳性对照组比较差异均无显著性（P>0.05）；3个剂量组中，降脂酮高剂量组ALT活性低于低、中剂量组（P<0.05），低、中剂量之间比较差异无显著性（P>0.05），中、高剂量组AST活性较低剂量组均明显降低（P<0.05）。结论：降脂酮对CCl₄所致大鼠慢性肝损伤具有保护作用，其机制可能与抗氧化的作用有关。

Effects of Jiangzhitong on carbon tetrachloride-induced chronic liver injury in rats

Objective To observe the protective effects of Jiangzhitong on carbon tetrachloride-induced chronic hepatic injury in rats and find its possible mechanisms.Methods Seventy two rats were randomly divided into 6 groups: control,model,positive control and jiangzhitong groups with different doses (50,100,200 mg·kg-1·d-1). The effects of Jiangzhitong on hepatic injury were observed by measuring enzyme level (AST and ALT) in serum,reduced glutathione hormone(GSH) content and catalase(CAT) activity of hepatic tissue section.Results Compared with model group,the serum ALT and AST concentrations in Jiangzhitong groups with different doses were decreased significantly (P<0.05 or P<0.01),the GSH contents of hepatic tissue in Jiangzhitong groups with different doses were increased (P<0.05 or P<0.01).CAT activities were increased (P<0.05),Compared with positive control,the ALT concentration in high dose group was reduced obviously (P<0.01). There was no difference of ALT actvity between low,middle dose groups and control group(P>0.05).The ALT activity in high dose group was lower than those in low and middle dose groups,there was no difference of ALT activity between low and middle dose groups(P>0.05),the activities in middle and high doses groups were significantly lower than that in low dose group(P<0.05).Conclusion Jiangzhitong has the hepatoprotective effect on carbon tetrachloride-induced chronic hepatic injury in rats, its mechanism is likely related to potent antioxidative.