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作 者:王志举[1] 乔鹏[1] 刘素芳[1] 赵文超[1] 董子明[2] 季宇彬[3]
机构地区:[1]郑州大学基础医学院生理学教研室,郑州450052 [2]郑州大学基础医学院病理生理学教研室,郑州450052 [3]哈尔滨商业大学药学院,哈尔滨150076
出 处:《中国实用神经疾病杂志》2006年第5期25-26,共2页Chinese Journal of Practical Nervous Diseases
摘 要:目的观察海嘧啶对荷瘤小鼠肝脏脂质过氧化反应的影响。方法S180(骨肉瘤)及EAC(艾氏腹水癌)荷瘤小鼠随机分为三组:正常组、阴性对照组和海嘧啶治疗组。海嘧啶治疗组:小鼠接瘤后24h后腹腔注射药物,50mg/kg,连续给药7d。阴性对照组给相同体积的生理盐水。分别测定肝组织的LPO、GSH-PX和SOD的含量。结果荷瘤小鼠肝中LPO含量升高,而GSH-PX和SOD均含量降低;海嘧啶治疗组荷瘤小鼠肝中GSH-PX和SOD的活性升高,LPO的含量降低。结论海嘧啶的抗肿瘤机制可能与它能提高抗氧化酶的活性,清除过多自由基有一定关系。Objective To observe the effect of the sea pyrimidine on lipid peroxidation of liver in tumor bearing mice. Methods Mice were divided into 3 groups., normal group, treat ment group and control group. Mice of treat group were transplanted with tumor cells of S180 and EAC, and treated with Sea pyrimidine for 7 days (50mg/kg, ip). Mice of control group were transplanted with tumor cells of S180 and EAC, and treated with 0.9% NaCl for 7 days. And LPO, GSH-PX and SOD were examined respectively. Results Sea primidine can reduce the levels of LPO of liver tumor bearing mice and increase the levels of SOD and GSH-PX. Conclusion The antitumor pharmacologic mechanism of the sea pyrimidine is related to it's increasing the levels of SOD and GSH-PX, and to it's inhibition the action of lipid peroxidation.
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