Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury

被引:6
|
作者
Alp, Bilal Firat [1 ]
Malkoc, Ercan [2 ]
Demirer, Zafer [1 ]
Guragac, Ali [1 ]
Turker, Turker [3 ]
Altayli, Ertan [4 ,5 ]
Ozcan, Ayhan [6 ]
Uysal, Bulent [7 ]
Topal, Turgut [7 ]
Akgul, Emin Ozgur [8 ]
Yildirim, Ibrahim [1 ]
Guven, Ahmet [9 ]
机构
[1] Gulhane Mil Med Fac, Dept Urol, TR-06017 Ankara, Turkey
[2] Mil Hosp, Div Urol, Tekirdag, Turkey
[3] Gulhane Mil Med Fac, Dept Epidemiol, TR-06017 Ankara, Turkey
[4] Gulhane Mil Med Fac, Dept Res, TR-06017 Ankara, Turkey
[5] Gulhane Mil Med Fac, Dev Ctr, TR-06017 Ankara, Turkey
[6] Gulhane Mil Med Fac, Dept Pathol, TR-06017 Ankara, Turkey
[7] Gulhane Mil Med Fac, Dept Physiol, TR-06017 Ankara, Turkey
[8] Gulhane Mil Med Fac, Dept Biochem, TR-06017 Ankara, Turkey
[9] Gulhane Mil Med Fac, Dept Pediat Surg, TR-06017 Ankara, Turkey
关键词
1400W; iNOS inhibitor; oxidative stress; renal injury; shock wave therapy; ISCHEMIA/REPERFUSION INJURY; ISCHEMIA-REPERFUSION; IN-VITRO; LITHOTRIPSY; PEROXYNITRITE; SUPEROXIDE; MELATONIN; 1400W; ASSAY; RATS;
D O I
10.3109/0886022X.2014.884396
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Objectives: Shock wave lithotripsy treatment (SWT) is not completely free from side effects; one of the accused mechanisms for renal injury during SWT is oxygen-and nitrogen-derived free radical productions. Therefore, we aimed to evaluate the effect of inhibition of nitric oxide (NO) production by N-[3(aminomethyl) benzyl) acetamidine] (1400W), highly selective inducible nitric oxide synthase (iNOS) inhibitor, at SWT-induced kidney damage. Materials and methods: Twenty-four rats those underwent right nephrectomy procedure were divided equally into three groups as control, SWT, and SWT + 1400W. 1400W was administered at a dose of 10 mg/kg at 2 h prior to SWT procedure and at the beginning of SWT procedure via intraperitoneal route and continued daily for consecutive 3 days. At the end of the fourth day, animals were killed via decapitation and trunk blood and the left kidneys were taken for biochemical and histopathologic evaluation. Results: SWT caused renal tubular damage and increased lipid peroxidation and antioxidant enzyme activities and SWT also significantly increased nitro-oxidative products. Inhibition of iNOS via administration of 1400W ameliorated renal injury and decreased tissue lipid peroxidation (malondialdehyde), superoxide dismutase, glutathione peroxidase and nitrite/nitrate levels (NOx). In addition, it was seen that histolopathological changes were attenuated in the SWT + 1400W group when compared to SWT group. Conclusion: SWT-induced renal injury might be due to excessive production of oxygen free radicals and NO production. Inhibition of iNOS attenuates renal injury following SWT treatment. It can be concluded that iNOS inhibitors or peroxynitrite scavengers might be used to protect the kidneys against SWT-induced morphological and functional injuries.
引用
收藏
页码:774 / 780
页数:7
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