豆茶决明对小鼠CCl_4和乙醇急性肝损伤的保护作用

Protective Effect of Cassia nomame Against Acute Liver Injury Induced by CCl_4 and Ethanol in Mice

目的:探讨豆茶决明对小鼠四氯化碳(CCl4)和乙醇急性肝损伤的保护作用。方法:将60只小鼠随机分为6组,即正常组、模型组、豆茶决明给药高、中、低剂量组(0.9,0.6,0.3 g·kg-1)、联苯双酯组(0.15 g·kg-1),每组10只,除正常组外,其余各组分别用CCl4,乙醇对小鼠造成急性肝损伤模型,造模成功后,每天ig给药1次,连续给药3 d,观察肝损伤小鼠血清中丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)的变化,测定肝脏指数及肝组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)水平,并对肝组织进行常规HE染色,进行组织病理学检查。结果:与正常组比较,模型组急性肝损伤小鼠肝脏指数,ALT,AST,MDA水平明显升高(P<0.01),SOD,GSH水平明显降低(P<0.01);与模型组比较,豆茶决明给药高、中、低剂量组及联苯双酯组明显降低急性肝损伤小鼠肝脏指数,ALT,AST,MDA水平(P<0.05),明显升高SOD,GSH水平(P<0.05)。病理观察显示,模型组小鼠肝细胞排列层次紊乱,细胞核溶解、固缩,细胞结构变形现象明显,各给药组上述病理变化均有明显减轻,肝细胞肿胀度下降。结论:豆茶决明对CCl4和乙醇所致的小鼠急性肝损伤有一定的保护作用。

Objective： To investigate the protective effects of Cassia nomame against acute liver injury induced by carbon tetrachloride（CCl4） and ethanol in mice. Method： Sixty mice were randomly divided into six groups： the control group,the model group,the high-,medium-,low-dose C. nomame groups（0. 9,0. 6,0. 3g·kg- 1）,and the bifendate group（0. 15 g·kg- 1）. The mouse models of acute liver injury were established by CCl4 and ethanol. After intragastrical administration of the corresponding medicines once daily for 3 days,the effects on serum alanine aminotransferase（ALT） and aspartate aminotransferase（AST）,the liver index,the contents of malonaldehyde（MDA）,the activities of superoxide dismutase（SOD）,the levels of glutathione（GSH） in liver tissues were measured. The protective effects on liver tissues were evaluated by using microscopic examination of hematoxylin-eosin（HE） staining. Result： Compared with the normal group,the levels of ALT,AST,MDA and the liver index increased,levels of SOD and GSH decreased in the model group（P〈0. 01）.Compared with model group,the levels of ALT,AST,MDA and the liver index decreased,levels of SOD and GSH increased in the C. nomame groups（P〈0. 05）. Moreover,the alleviated pathological changes in liver tissues were observed in the C. nomame groups. Conclusion： C. nomame showed a protective effect against acute liver injury induced by CCl4 and ethanol in mice.