当前位置： SCI文献检索 > MOLECULAR AND CELLULAR BIOCHEMISTRY期刊下所有文献 > Lisinopril attenuates renal oxidative injury in L-NAME-induced hypertensive rats.

Lisinopril attenuates renal oxidative injury in L-NAME-induced hypertensive rats.

Abstract：

:Hypertension and related oxidative stress are involved in the pathogenesis of any renal diseases. Angiotensin-converting enzyme inhibitors have multi-directional renoprotective effects. In this study, we aimed to investigate whether lisinopril treatment has any biochemical alterations on renal tissue in L-NAME (Nε-nitro-L-arginine methyl ester) induced hypertension model. Twenty-eight Sprague-Dawley rats were included in this study and divided into four equal groups (n = 7): control group, L-NAME treated group (75 mg/kg/day), L-NAME plus lisinopril treated group and only lisinopril treated group (10 mg/kg/day). L-NAME and lisinopril were continued for 6 weeks. Systolic blood pressures were measured by using tail cuff method. In biochemical analysis, malondialdehyde (MDA, an index of lipid peroxidation) levels, the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in renal tissues were used as markers of oxidative stress-induced renal impairment. Microalbumin and N-acetyl-β-D-glucosaminidase (NAG) in urine were determined as markers of renal tubular damage related to hypertension. Chronic L-NAME administration resulted in a significant depletion of serum nitric oxide (NO). When compared with control group, serum creatinine, microalbumin, urine NAG, renal tissue MDA level, and CAT activities were significantly high, while renal tissue SOD and GSH-Px activities low in L-NAME group. In the L-NAME plus lisinopril treated group, serum creatinine, microalbumin and urine NAG, renal MDA level and CAT activity decreased, whereas SOD, GSH-Px activities in renal tissue and serum NO levels were increased. Thus, lisinopril treatment reversed these effects. There were not any significant difference between L-NAME plus lisinopril treated group and control group concerning serum creatinine, renal tissue MDA level and SOD, GSH-Px, CAT activities. These results suggest that lisinopril could diminish biochemical alterations in L: -NAME induced hypertensive renal damage that occurs by oxidative stress.

journal_name

Mol Cell Biochem

journal_title

Molecular and cellular biochemistry

authors

Oktem F,Kirbas A,Armagan A,Kuybulu AE,Yilmaz HR,Ozguner F,Uz E

doi

10.1007/s11010-011-0760-2

subject

Has Abstract

pub_date

2011-06-01 00:00:00

pages

247-53

issue

1-2

eissn

0300-8177

issn

1573-4919

journal_volume

352

pub_type

杂志文章

在线工具

Lisinopril attenuates renal oxidative injury in L-NAME-induced hypertensive rats.