Kanani Fatemeh, Fazelnia Faezeh, Mojarradfard Mohaddeseh, Nematbakhsh Mehdi, Moslemi Fatemeh, Eshraghi-Jazi Fatemeh, Talebi Ardeshir
Water & Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Water & Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran ; Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran ; Isfahan MN Institute of Basic & Applied Sciences Research, Isfahan, Iran.
J Renal Inj Prev. 2016 Feb 28;5(1):29-33. doi: 10.15171/jrip.2016.06. eCollection 2016.
Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI).
This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI.
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.
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).
SMT not only prevent the kidney during IRI, but also promotes kidney function disturbance and severity of renal injury.
通过诱导型一氧化氮合酶（iNOS）过度产生一氧化氮（NO）与肾缺血再灌注损伤（IRI）有关。
本研究旨在探讨S-甲基异硫脲（SMT）作为iNOS选择性抑制剂在肾IRI中的作用。
雄性Wistar大鼠通过双侧肾血管闭塞进行45分钟的双侧肾缺血，随后再灌注24小时。在肾IRI之前，大鼠接受溶剂（生理盐水，第2组）或SMT（50mg/kg，第3组），并与假手术动物（第1组）进行比较。在再灌注期结束时，处死大鼠进行肾组织病理学检查。
第2组和第3组的血清肌酐（Cr）、血尿素氮（BUN）、亚硝酸盐水平和肾脏重量显著增加（P<0.05）。第2组和第3组的肾组织损伤评分也高于假手术组（P<0.05）。
SMT不仅在IRI期间不能保护肾脏，反而会促进肾功能紊乱和肾损伤的严重程度。
