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机构地区:[1]蚌埠医学院生理学教研室,安徽蚌埠233003
出 处:《中国药理学与毒理学杂志》2000年第6期454-457,共4页Chinese Journal of Pharmacology and Toxicology
基 金:安徽省教委科研基金资助项目(96JL0088)
摘 要:以跨膈压 ,膈肌诱发电位及膈肌中丙二醛(MDA)和超氧化物歧化酶 (SOD)为指标 ,同时电镜观察膈肌组织超微结构改变 ,研究绞股蓝总甙 (GP)对多柔比星 (Dox)膈肌毒性的保护作用 .结果表明1 0 mg·kg-1Dox使跨膈压 ,膈肌诱发电位幅度降低 ,膈肌中 MDA增加 ,SOD活性降低 ,电镜下肌小节断裂溶解 ,线粒体肿胀 ,嵴减少 . 1 0 0 mg· kg-1GP可抑制上述变化 .结果提示 ,GP对After administering doxorubicin 10 mg·kg -1 , the function of diaphragm was assessed by measurement of the transdiaphragmatic pressure(Pdi) and diaphragm evoked potential(DEP) in rabbits. Supero xide dismutase(SOD) and malondialdehyde(MDA) were tested. The ultrastructure of diaphragm cells was investigated by electron microscopy. The findings were as follows: ①The Pdi and amplitude of DEP were lowered by doxorubicin. ②The levels of MDA was increased and activity of SOD was decreased in diaphragm. ③The disorder of myofibrils; swelling of mitochondria with broken cristae could be observed. The above changes were inhibited by gypenoside. The results suggest that the gypenoside scavenge toxic oxygen radicals induced by doxorubicin and protect the diaphragm myocytes.
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