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Premium BENAZEPRIL, AN ANGIOTENSIN‐CONVERTING ENZYME INHIBITOR, ALLEVIATES RENAL INJURY IN SPONTANEOUSLY HYPERTENSIVE RATS BY INHIBITING ADVANCED GLYCATION END‐PRODUCT‐MEDIATED PATHWAYS
Author(s)
Liu XuePing,
Pang YueJiu,
Zhu WeiWei,
Zhao TingTing,
Zheng Min,
Wang YiBing,
Sun ZhiJian,
Sun SiaoJing
Publication year2009
Publication title
clinical and experimental pharmacology and physiology
Resource typeJournals
PublisherBlackwell Publishing Asia
SUMMARY1 Advanced glycation end‐products (AGE) and their receptors (RAGE) have been implicated in renal damage in diabetes. The aim of the present study was to investigate the effects of benazepril, an angiotensin‐converting enzyme inhibitor (ACEI), on the formation of AGE, the expression RAGE and other associated components in the oxidative stress pathway in spontaneously hypertensive rats (SHR). 2 Groups of SHR were treated with or without 10 mg/kg per day benazepril for 12 weeks. Systolic blood pressure (SBP) and angiotensin (Ang) II levels were evaluated in SHR and control Wistar‐Kyoto (WKY) rats. Renal function was investigated by determining levels of proteinuria and glomerulosclerosis. Furthermore, reactive oxygen species (ROS) in the rat renal cortex were analysed using an H 2 O 2 ‐based hydroxyl radical‐detection assay and the renal content of AGE, RAGE, NADPH oxidase p47phox, nuclear factor (NF)‐κB p65, phosphorylated (p‐) NF‐κB p65, vascular cell adhesion molecule (VCAM)‐1 and transforming growth factor (TGF)‐β1 was determined by immunohistochemistry, quantitative real‐time polymerase chain reaction and western blot analysis. 3 Treatment with benazepril inhibited the formation of AngII, reduced SBP and alleviated renal lesions in SHR compared with both untreated SHR and control WKY rats. Benazepril treatment significantly suppressed the accumulation of AGE and expression of RAGE in the kidney of SHR. In addition, benazepril treatment reduced the upregulation of NADPH oxidase p47phox, ROS generation and NF‐κB p65, p‐NF‐κB p65, VCAM‐1 and TGF‐β1 expression in the kidney of SHR compared with both untreated SHR and control WKY rats. 4 The results of the present study provide new insights into the regulation by the renin–angiotensin system of AGE–RAGE, oxidative stress and nephropathy, increasing our understanding of the role of the RAS in nephropathy.
Subject(s)ace inhibitor , advanced glycation end product , angiotensin converting enzyme , angiotensin ii , benazepril , biology , blood pressure , chemistry , endocrinology , glomerulosclerosis , glycation , kidney , medicine , nadph oxidase , neuroscience , oxidative stress , proteinuria , rage (emotion) , receptor , spontaneously hypertensive rat
Language(s)English
SCImago Journal Rank0.752
H-Index103
eISSN1440-1681
pISSN0305-1870
DOI10.1111/j.1440-1681.2008.05078.x

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