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作 者:李才[1] 邓义斌[1] 王丽娟[1] 张秀云[1] 邹雅斌[1] 侯芳玉[1]
机构地区:[1]白求恩医科大学应用基础医学研究所,白求恩医科大学基础医学院微生物教研室
出 处:《中国病理生理杂志》1995年第6期638-641,共4页Chinese Journal of Pathophysiology
摘 要:观察了链脲佐菌素诱导的糖尿病大鼠于发病后4、6、12和16周肾脏自由基防御机能的变化。结果表明,在各观察时点,糖尿病大鼠肾脏超氧化物岐化酶(SOD)、过氧化氢酶(CAT)活性明显低于对照组,肾脏脂质过氧化物(LPO)水平显著升高,SOD/LPO和CAT/LPO明显降低,且随着病程延长,这些改变更趋明显。糖尿病发病后6、12和16周时糖尿病大鼠肾脏谷胱甘肽过氧化物酶(GSH─PX)活性明显高于对照动物,而4周时则否。这些结果提示,糖尿病大鼠肾脏自由基防御机能明显减低,这种变化可能在糖尿病肾病的发生发展中起重要作用。Alterations of kidney defensive function against free radical were exa─mined in streptozotocin─induced diabetic rats. The results showed that, during the experi─mental peroid, activities of CuZn─superoxide dismutase(CuZnSOD)and catalase(CAT )in kidney of diabetic rats were significantly lower than that of the control, the lipidperoxides(LPO)levels of diabetic kidney were markedly higher than that of the control. Diabetic rats were associated with decreased renal SOD/LPO and CAF/LPO significantly. These changes became more pronounced with prolongation of diabetic course. The renalglutathione peroxidase(GSH─PX) activity was markedly increased in the 6-, 12-, and 16- week─diabetic rats, but not in the 4─week─diabetic rats compared with the control. Thesefindings suggested that the renal defensive function against free radical in diabetic ratswas decreased obviously and this change might play an important role in the develop─ment of diabetic nephropathy.
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