Scavenging reactive oxygen species using tempol in the acute phase of renal ischemia/reperfusion and its effects on kidney oxygenation and nitric oxide levels.
Scavenging reactive oxygen species using tempol in the acute phase of renal ischemia/reperfusion and its effects on kidney oxygenation and nitric oxide levels.
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DOI：
10.1186/s40635-015-0057-y
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发表时间：
2015-12
影响因子：
3.5
通讯作者：
Ince C
中科院分区：
文献类型：
--
作者：
Aksu U;Ergin B;Bezemer R;Kandil A;Milstein DM;Demirci-Tansel C;Ince C
肾缺血/再灌注（I/R）损伤是肾移植中常见的损伤，影响移植肾的存活率。我们的目的是验证我们的假设，即用tempol清除活性氧（ROS）可以保护肾I/R急性期的肾氧合和一氧化氮（NO）水平。将大鼠随机分为：（1）无I/R，无tempol;（2）无I/R，但有tempol;（3）无tempol的I/R;和（4）有tempol的I/R。通过夹闭肾动脉30分钟诱导I/R。在I/R前15 min给予Tempol（200 μmol/kg/h/i.v）。无tempol的I/R导致肾氧输送和微血管氧合显著减少。然而，Tempol保护I/R后的肾氧合。在R90时，与其他组相比，未接受tempol的I/R组的肌酐清除率较低。无tempol治疗的I/R损伤导致组织丙二醛水平显著增加，组织NO水平显著降低。在I/R之前给予Tempol可以防止氧化应激和改变组织NO水平。这强调了氧、NO和ROS之间的不平衡形成了I/R诱导的阿基发病机制的重要组成部分，因此在设计移植中肾I/R损伤的预防/治疗策略时应考虑到这一点。
Renal ischemia/reperfusion (I/R) injury is commonly seen in kidney transplantation and affects the allograft survival rates. We aimed to test our hypothesis that scavenging reactive oxygen species (ROS) with tempol would protect renal oxygenation and nitric oxide (NO) levels in the acute phase of renal I/R. Rats were randomly divided: (1) no I/R, no tempol; (2) no I/R, but with tempol; (3) I/R without tempol; and (4) I/R with tempol. I/R was induced by 30-min clamping of the renal artery. Tempol (200 μmol/kg/h/i.v) was administered 15 min prior to I/R. I/R without tempol led to a significant decrease in renal oxygen delivery and microvascular oxygenation. Tempol, however, protected renal oxygenation after I/R. At R90, the creatinine clearance rate was lower in the I/R-subjected group that did not receive tempol compared to that in the other groups. I/R injury without tempol treatment led to a significant increase in tissue malondialdehyde levels and a significant decrease in tissue NO levels. Tempol administration before I/R could prevent oxidative stress and altered tissue NO levels. This underscores that unbalance between oxygen, NO, and ROS forms an important component of the pathogenesis of I/R-induced AKI and should therefore be taken into account when designing a prevention/treatment strategy for renal I/R injury in transplantation.