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机构地区:[1]上海医科大学华山医院肾脏病科
出 处:《上海医科大学学报》1999年第2期87-90,共4页Journal of Fudan University(Medical Science)
摘 要:目的探讨血管转换酶抑制剂贝那普利对糖尿病大鼠体内非酶促糖化反应的作用及机制。方法以链脲佐菌素诱发的单侧肾切除糖尿病大鼠为模型,检测4周糖尿病大鼠血胰岛素水平、肾功能指标、血清及肾组织糖化产物水平在贝那普利用药后的改变。结果用药的糖尿病大鼠,肾功能指标、血清糖化蛋白水平以及动脉胶原含量明显下降,肾小球ECM积聚被抑制、非酶糖化反应程度也明显改善。血浆游离胰岛素水平升高,高血糖程度有轻度改善。结论贝那普利抑制糖尿病大鼠体内蛋白非酶糖化程度,其作用途径与其部分改善胰岛功能、降低血糖或其他不依赖于血糖浓度降低的作用有关。Purpose To investigate whether benazepril can affect the process of nonenzymatic glycosylation in vivo and to study its mechanism. Methods Three groups of uninephrectominzed rats, control,streptozotocin induced diabetic rats with or without benazepril treatment were followed up for 4 weeks. Results In untreated diabetic rats, significant increases of blood glucose (BG),BUN and Scr were observed,but the level of serum insulin was markedly reduced [DM vs Con:(9.02±2.34) vs (32.14±10.02) mU/L, P <0.001].Benazepril as one kind of ACEI,when administrated to diabetic rats,ameliorated all those alterations mentioned above. The results also showed that the concentration of Amadori products in plasma examined by nitroble tetrazolium (NBT) method in untreated diabetic rats was significantly increased [DM vs Con: (5.30±0.12)vs (0.79± 0.14 )mmol/L P <0.001].Similarly,the intensity of NBT staining in the glomerular mesangial areas and capillary walls was marked in diabetic rats.This group of rats were also associated with marked glomerular extracellular matrix accumulation and mesangial expansion (PAS staining).Benazepril administration made the changes restore nearly to normal status. Conclusions Benazepril may inhibit nonenzymatic glycation of proteins,especially the early glycosylation products formation in renal tissue,which could contribute to retarding effectively the development of renal injury in diabetes.The effect was performed partly by the amelioration of glucose metabolism in vivo in STZinduced diabetes.
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