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机构地区:[1]遵义医学院药理学教研室 [2]上海医科大学基础医学院药理学教研室
出 处:《遵义医学院学报》1997年第4期1-5,共5页Journal of Zunyi Medical University
摘 要:本研究观察GSH与化疗药合用对DEN大鼠肝癌模型的作用。DEN灌胃8mg/kg/d诱发大鼠肝癌模型。GSH预防性给药合用Adr治疗无一大鼠出现肿瘤,ChH+Adr治疗给药大鼠肝癌发生率为12.5%(p<0.01),Cisp和Taxol不论单用或与CSh治疗性合用大鼠肝癌发生率与DEN对照组无明显差异(P>0.05),但3种化疗药与CSH合用模型鼠的死亡率降低。DEN诱发肝癌形成和化疗药的毒性反应均与自由基生成有关,GSH预防DEN致癌作用及降低化疗药毒性则基于它的抗氧化作用。Effects of combining glutathione (GSH) with chemotherapeutic drugs in rat DEN-hepatoma model were studied. Rat hepatoma was induced by drinistered diethylnitrosamine(DEN) 8mg/kg/di. g. Hepatoma was not observed in group that GSH was given protectivelyand treated with adriamycin (Adr). The incidence of hepatoma in group treated with GSH andAdr was l2.5%, which was ber than 76.5% in DEN control group (P < 0.0l ). In the groups treated with cisplatin (Cisp) or taxol, and Cisp + GSH or taxol + GSH, the incidence ofhepatorna were related to the DEN control gnup (P > 0. 05 ). Treatment of comhining GSHwith chemotherapeutic drugs decreased significantly the mortality rates of rat model as comparedwith only chemotherapeutic drug (Adr, Cisp or taxol) treatment. The careinogenisis of DEN inrats may be related to the produce of lipid peroxide (LPO), and Cisp and taxol could aggravatethe produce of LPO in DEN pretreated rats whereas GSH reduced this action.
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