Abstract
Introduction: Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI). Objectives: This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI. Materials and Methods: Male Wistar rats were subjected to 45 minutes of bilateral renal ischemia by occlusion of renal vessels of both kidney followed by 24 hours of reperfusion. Prior to renal IRI, the rats received either vehicle (saline, group 2) or SMT (50 mg/kg, group 3), and were compared with the sham-operated animals (group 1). At the end of reperfusion period, the rats were sacrificed for kidney tissue pathology investigation. Results: Serum creatinine (Cr), blood urea nitrogen (BUN), nitrite levels, and kidney weight significantly increased in groups 2 and 3 (P < 0.05). Kidney tissue damage scores in groups 2 and 3 were also higher than that in the sham-operated group (P < 0.05). Conclusion: SMT not only prevent the kidney during IRI, but also promotes kidney function disturbance and severity of renal injury.
Highlights
Excessive production of nitric oxide (NO) via inducible nitric oxide synthase is associated in renal ischemia reperfusion injury (IRI)
NO is synthesized from L-arginine, and this free radical is produced from three isoforms of NO synthase (NOS)
The serum levels of blood urea nitrogen (BUN) and Cr in IR + SMT group was significantly higher than those in the control group (P < 0.05). This data did not show any protective role of SMT against kidney IRI (Figure 1)
Summary
Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI). Objectives: This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI. Conclusion: SMT prevent the kidney during IRI, and promotes kidney function disturbance and severity of renal injury. Kidney ischemia is the most common disturbance in clinic, accompanied with renal failure [1]. Still there is no practical sufficient solution for amelioration of acute renal failure (ARF) as a consequence of ischemia reperfusion injury (IRI) [2,3]. It is reported that under IRI condition, the renal cell can induce iNOS [18].
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