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雷公藤多苷对糖尿病大鼠肾脏的保护作用及机制 被引量:10

Protective effect and mechanism of tripterygium wilfordii polyglycoside on the kidney in experimental diabetic rats
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摘要 目的观察雷公藤多苷(TWP)对糖尿病大鼠肾脏的保护作用及可能机制。方法用链尿佐菌素腹腔注射法构建糖尿病大鼠模型,动物随机分为正常组、模型组、TWP组(1.8 g.kg-1.d-1灌胃)。于第8周末观察各组大鼠血糖、血肌酐、血尿素氮和24 h尿蛋白量的变化;测定肾组织匀浆超氧化物歧化酶(SOD)活性、肾组织及尿中丙二醛(MDA)含量、血清转化生长因子(TGF-β1)水平;观察肾脏病理形态学的改变。结果 TWP可降低糖尿病大鼠血糖、血肌酐、血尿素氮和24 h尿蛋白水平,能使肾组织和尿MDA含量及血清TGF-β1水平下降,使肾组织SOD活性升高,改善肾脏组织病理学变化。结论雷公藤多苷能明显改善肾脏功能,其机制可能与抑制氧化应激、增强机体抗氧化能力和抑制TGF-β1表达有关。 Objective To investigate the protective effect and its mechanism of tripterygium wilfordii polyglycoside(TWP) on the kidney of experimental diabetic rats.Methods The diabetes mellitus Sprague Dawley rats were induced by streptozotocin.The diabetic rats were randomly divided into three groups:control group,diabetic model group and TWP group(1.8 g·kg-1·d-1 orally administered once a day for 8 week).Blood sugar,serum creatinine,blood urea nitrogen at the end of the 8th week were measured and 24 h urine protein was measured.The superoxide dismutase(SOD) activity in the renal tissue,the level of malondia1dehyde(MDA) in the renal tissue and urine,the level of serum transformed growth factor-β1(TGF-β1) in urine,and the pathology changing of the rat kidney were observed.Results TWP can reduce the level of blood sugar,serum creatinine,blood urea nitrogen and 24 h urine protein,TWP also can reduce the level of MDA in the kindey and the level of serum TGF-β1.TWP increased the activity of SOD in the kindey and improved the renal histopathological changing.Conclusion TWP has a protective effect on the kidney of experimental diabetic rats.The mechanism may be related to the oxidative stress,enhancing the body's antioxidant capacity and decreasing the expression of TGF-β1.
出处 《中国临床药理学杂志》 CAS CSCD 北大核心 2012年第6期450-452,共3页 The Chinese Journal of Clinical Pharmacology
基金 河南省教育厅自然科学研究计划基金资助项目(2011C310003)
关键词 雷公藤多苷 糖尿病肾病 超氧化物岐化酶 丙二醛 转化生长因子-Β1 tripterygium wiifordii polyglycoside diabetic nephropathy superoxide dismutase malondia1dehyde transformed growthfactor-β1
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