Effects of captopril and losartan on lipid peroxidation, protein oxidation and nitric oxide release in diabetic rat kidney

IF 3.2 Prostaglandins, leukotrienes, and essential fatty acids Pub Date : 2003-10-01 Epub Date: 2003-08-01 DOI:10.1016/S0952-3278(03)00088-7

Dilek Yavuz , Belgin Küçükkaya , Goncagül Haklar , Önder Ersöz , Emel Akoğlu , Sema Akalın

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Abstract

Increased oxidative stress has an important role in the pathogenesis of diabetic nephropathy. The aim of this study was to evaluate the effects of renin–anigiotensin system blockage, either by angiotensin-converting enzyme inhibition or angiotensin receptor blockage, on oxidative stress and nitric oxide release in diabetic rat kidneys.

After induction of diabetes, six rats were given captopril, six rats were given losartan, and six rats served as diabetic controls. Six healthy rats were also included. At the end of an 8-week period nitric oxide release, lipid peroxidation and protein oxidation were measured in kidney cortices, and urinary albumin excretion (UAE) was determined in 24-h urine samples.

Losartan- and captopril-treated diabetic rats had lower levels of UAE than diabetic controls. Diabetic rats had higher levels of lipid peroxidation and protein oxidation compared to healthy rats. NO release was significantly lower in diabetic groups than healthy controls. UAE levels showed a positive correlation with lipid peroxidation and a negative correlation with NO release.

Inhibition of lipid peroxidation could be one of the protective mechanisms of renin–angiotensin axis inhibition in diabetic kidney tissues.

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卡托普利和氯沙坦对糖尿病大鼠肾脏脂质过氧化、蛋白质氧化和一氧化氮释放的影响

氧化应激增加在糖尿病肾病的发病机制中起重要作用。本研究旨在评价血管紧张素转换酶抑制或血管紧张素受体阻断肾素-抗紧张素系统对糖尿病大鼠肾脏氧化应激和一氧化氮释放的影响。诱导糖尿病后，6只大鼠给予卡托普利，6只大鼠给予氯沙坦，6只大鼠作为糖尿病对照组。还包括6只健康大鼠。8周结束时，测量肾皮质一氧化氮释放、脂质过氧化和蛋白质氧化，并测定24小时尿白蛋白排泄（UAE）。氯沙坦和卡托普利治疗的糖尿病大鼠的UAE水平低于糖尿病对照组。与健康大鼠相比，糖尿病大鼠的脂质过氧化和蛋白质氧化水平更高。糖尿病组一氧化氮释放明显低于健康对照组。UAE水平与脂质过氧化正相关，与NO释放负相关。脂质过氧化抑制可能是糖尿病肾组织肾素-血管紧张素轴抑制的保护机制之一。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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