氧化苦参碱磷脂复合物对CCl4致大鼠慢性肝损伤的影响

目的:观察氧化苦参碱磷脂复合物对四氯化碳(CCl4)致慢性肝损伤大鼠肝功能的影响,并探讨其作用及机制。方法:将66只SD大鼠随机分为正常对照组、模型组、氧化苦参碱组(54 mg/kg)及氧化苦参碱磷脂复合物低、中、高剂量组(27,54,108 mg/kg),每组11只。除正常对照组外,其余各组大鼠采用10%CCl4橄榄油灌胃,每周2次,共8周,制备大鼠慢性肝损伤模型。期间记录摄食量和体质量。8周后,采血测定血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总蛋白(TP)、白蛋白(ALB)、球蛋白(GLB)的含量,计算肝脏指数,HE染色观察肝组织的病理变化。结果:与模型组比较,氧化苦参碱磷脂复合物低、中剂量组大鼠血清ALT、AST水平减低(P<0.05),TP升高(P<0.05),ALB含量显著升高(P<0.01);肝脏指数降低(P<0.05)。HE染色分析肝组织病理学变化结果表明,氧化苦参碱磷脂复合物低、中剂量能够有效改善肝组织损伤程度。结论:氧化苦参碱磷脂复合物对CCl4诱导的大鼠慢性肝损伤具有显著保护作用,其作用机制可能与增强抗氧化活性有关。

Effect of Oxymatrine Phospholipid Complex on Rats with Chronic Liver Injury Induced by CCl_4

Objective:To investigate the effect of oxymatrine phospholipid complex on rats with chronic liver injury induced by carbon tetrachloride(CCl_4) and to explore its role and mechanism. Methods:A total of 66 SD rats were randomly divided into the normal control group,model group,oxymatrine group(54 mg/kg)and oxymatrine phospholipid complex low,medium and high dose groups(27,54,108 mg/kg). All the rats except the normal control group were intragastrically administrated with 10% CCl_4 twice a week for 8 weeks to establish chronic injury model. Food intake and body weight were recorded during the period. After 8 weeks,the serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),total protein(TP),albumin(ALB) and globulin(GLB) were measured,the liver index was calculated,and the pathological changes of liver tissue were observed by HE staining. Results:Low and medium doses of oxymatrine phospholipid complex significantly inhibited the serum levels of ALT and AST in rats with chronic liver injury(P< 0.05),increased the levels of TP(P< 0.05),and significantly increased the content of ALB(P< 0.01),and decreased the liver index(P< 0.05). HE staining was used to observe the histopathological changes of liver,the results showed that low and medium doses of oxymatrine phospholipid complex can effectively reduce the degree of liver injury. Conclusion:Oxymatrine phospholipid complex has significant protective effect on rats with chronic liver injury induced by CCl_4,and its mechanism may be related to the enhancement of antioxidant activity.