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The renal protective effect of telmisartan on 5/6 nephrectomy rats with renal failure

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Author:
No author available
Journal Title:
China Medicine
Issue:
4
DOI:
10.3760/cma.j.issn.1673-4777.2012.04.001
Key Word:
5/6肾切除;替米沙坦;过氧化物酶增殖体活化受体γ;神经型一氧化氮合酶;5/6 nephrectomy;Telmisartan;Peroxisome proliferators actived receptor γ;Neuronal nitric oxide synthase

Abstract: Objective To investigate the renal protective effect and possible mechanism of Angiotensin Ⅱ AT1 Receptor antagonist telmisartan on 5/6 nephrectomy rats with renal failure.Methods Sprague Dawley SD male rats were randomly divided into sham-operation group,model group and telmisartan group.The 12th week rats were killed with decapitation method and serum urea nitrogen,creatinine and 24 h urinary protein were detected.Residual kidney tissue was taken for pathological examination to determine glomerular sclerosis and tubulointerstitial injury.Reverse transcription polymerase chain reaction (RT-PCR) and Western Blot were used to detect the expression of peroxisome proliferator-activated receptor-gamma PPARγ and neuronal nitric oxide synthase nNOS.Results 24 h urine protein,serum urea nitrogen and creatinine of rats in model and telmisartan group were significantly higher than those in sham group (P < 0.01 ) ; these indicators in telmisartan group was significantly lower than those in model group ( P < 0.05).The renal glomerular sclerosis and tubulointerstitial damage,glomerular sclerosis index and tubulointerstitial damage index of model group rats were significantly higher than those in sham-operated group (P < 0.01 ) ; these index in telmisartan group were significantly lower than those in model group (P < 0.05 ).Compared with the shame group,the protein and mRNA expression of PPARγ and nNOS were significantly decreased in model group and telmisartan group(P < 0.05),while the expression of PPARγ and nNOS in telmisartan group was significantly increased than that in model group (P < 0.05).Conclusions The 5/6 nephrectomy rats granted with telmisartan can significantly reduce glomerulosclerosis and the degree of renal interstitial fibrosis.The mechanism may be related to increased gene expression of PPARγ and nNOS.

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