【摘要】 目的研究大黄素与黄芪多糖对大鼠实验性肝癌的抑制作用并探讨其机制。方法采用二乙基亚硝胺(dieth-ylnitrosamine,DEN)诱发大鼠肝癌模型。50只清洁级雄性SD大鼠随机分为5组:正常对照组、肝癌模型组(DEN诱癌)、大黄素组(诱癌同时给大黄素)、黄芪多糖组(诱癌同时给黄芪多糖)、大黄素和黄芪多糖联合给药组(诱癌同时联合用大黄素和黄芪多糖干预),每组10只。联合灌胃14周。实验第18周处死所有大鼠,检测血清ALT、ALP、γ-GT和AFU,并行肝脏病理检查,用SABC法检测谷胱甘肽-S-转移酶(GST-P)、转化生长因子β1(TGF-β1)的表达情况。结果造模各组大鼠的ALT、ALP、-γGT、AFU均明显升高(P<0.05),两种药物干预可以减轻肝脏损害(P<0.05)。病理检查证实各实验组大鼠均诱发出肝癌。两种药物均能减少GST-P和TGF-β1的表达(P<0.05),但联合应用未显示明显的协同作用。结论大黄素、黄芪多糖干预治疗可以减轻肝损害,降低肝癌标志物GST-P的表达。抑癌作用可能与这两种药物抑制了肝癌组织TGF-β1的表达有关。更多还原

【Abstract】 Objective To study the inhibiting effect of emodin and astragalus polysaccharides on experimental hepatocarcinoma in rats and to explore its possible mechanism.Methods Hepatocarcinogenesis model rat was induced by diethylnitrosamine（DEN）.Fifty SD male rats were randomly divided into 5 groups: normal control group,hepatocarcinogenesis model group（induced by DEN）,emodin group,astragalus polysaccharides group,combined emodin with astragalus polysaccharides group.Rats were administered with emodin and astragalus polysaccharides when they were induced by DEN.All rats were killed in the 18^th week,Then serum ALT,ALP,γ-GT,α-L-fucoxidase（AFU） was detected.All rats’ livers were observed by routine histological.GST-P and TGF-β₁ were tested with SABC.Results The results of liver function in the 18^th week displayed that ALT,ALP,γ-GT and AFU of all groups were increased than that of negative control（P<0.05）.The two drugs could relieve hepatic injures.88% of rats were induced to hepatocellular carcinoma confirmed by HE staining.The expressions of GST-P and TGF-β₁ in normal control were higher than that in groups which used emodin and astragalus polysaccharides（（P<0.05））.Conclusion Emodin and astragalus polysaccharides can relieve hepatic injure and inhibit the expression of GST-P and TGF-β₁.The inhibiting effect on TGF-β₁ may be one of the mechanisms to control hepatocarcinoma.更多还原