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茅台酒与乙醇影响二乙基亚硝胺引发小鼠肝细胞癌的比较
引用本文:易旭,龙黎,程明亮.茅台酒与乙醇影响二乙基亚硝胺引发小鼠肝细胞癌的比较[J].贵阳医学院学报,2013(6):567-572.
作者姓名:易旭  龙黎  程明亮
作者单位:贵阳医学院附院感染科。贵州贵阳550004
摘    要:目的:观察茅台酒与乙醇在协同二乙基亚硝胺(DEN)引发小鼠肝细胞癌(HCC)的差异。方法:74只雄性C57BL/6J小鼠随机分为正常对照组、茅台酒组、乙醇组、DEN组、茅台酒干预组及乙醇干预组,实验35周末检测各组小鼠血清谷氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)与肝组织匀浆中丙二醛(MDA)水平,观察肝组织病理学变化和HCC相关磷脂酰肌醇蛋白聚糖3(GPC3)表达。结果:肝功能检测发现,茅台酒干预组与正常对照组比较,ALT和MDA差异无统计学意义(P〉0.05),而AST高于正常对照组,差异有统计学意义(P〈0.05);乙醇干预组ALT、AST与ADM高于正常对照组、茅台酒组、乙醇组、DEN组、茅台酒干预组,均P〈0.05;病理组织学检查发现乙醇干预组小鼠肝纤维化程度和GPC3表达明显高于其他各组,P〈0.05。茅台干预组肝脏细胞学检查未见癌前病变及HCC,仅在汇管区有少量PGC3表达。结论:乙醇可以协同DEN诱发小鼠HCC,茅台酒没有这种协同作用。

关 键 词:茅台酒  乙醇  二乙基亚硝胺    肝细胞  谷氨酸氨基转移酶  天冬氨酸氨基转移酶  丙二醛    疾病  酒精性

The Comparison of Different Effects of Maotai Liquor and Ethanol on the Oncogenesis of Hepatocellular Carcinoma Induced by Diethylnitrosamine
YI Xu,LONG Li,CHENG Mingliang.The Comparison of Different Effects of Maotai Liquor and Ethanol on the Oncogenesis of Hepatocellular Carcinoma Induced by Diethylnitrosamine[J].Journal of Guiyang Medical College,2013(6):567-572.
Authors:YI Xu  LONG Li  CHENG Mingliang
Institution:(Department of lnfectious Diseases, the Affiliated Hospital of Guiyang Medical College, Guiyang 550004, Guizhou, China)
Abstract:Objective: To observe the different effects of Maotai liquor and the equal amount of ethanol on the oncogenesis of hepatocellular carcinoma (HCC) induced by diethyl nitrosamine (DEN). Meth- ods: Male C57BL/6J mice 5 -8 weeks were divided into 6 groups, control, Maotai liquor, ethanol, Maotai liquor treating ( Maotai liquor + DEN), ethanol treating ( ethanol + DEN) group. The serum and liver tissue samples were collected to evaluate the function and structure alteration of liver with bio-chem- istrical and pathological methods after the mice were decapitated in the end of 35 weeks. Results: The level of alanine aminotransferase (ALT), aspartate transaminase (AST), and malondialdehyde (MDA) in ethanol treating group was higher than those of control and Maotai liquor treating groups (P 〈 0.05 ), while between the later two groups, significantly difference was not found ( P 〉 0.05 ). The results of pathological observation suggested that the histological alteration of liver tissue were found clearly in eth- anol treating group. Contrasted with other groups, the expression of glypican-3 increased obviously in ethanol treating group. Precancerous change and HCC could not be found in Maotai liquor treating by group cytological observation, in which less expression of PGC3 was found in portal area of liver. Con- clusions: Ethanol, but not Maotai liquor, can facilitate DEN on the function of oncogenesis of HCC.
Keywords:maotai liquor  ethanol  diethylnitrosamine  carcinoma  hepatocellular  alanine trans-aminase  aspartate transaminase  malondialdehyde  liver diseases  alcohohic
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