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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Effect of trimetazidine on renal ischemia/reperfusion injury in rats.
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Effect of trimetazidine on renal ischemia/reperfusion injury in rats.

机译：曲美他嗪对大鼠肾脏缺血/再灌注损伤的影响。

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摘要

There is increasing evidence to suggest that toxic oxygen radicals play a role in the pathogenesis of ischemia/reperfusion (I/R) injury in the kidney. This study was designed to investigate the effects of trimetazidine, in I/R induced renal failure in rats. The protective effect of trimetazidine (Tmz) against the damage inflicted by reactive oxygen species (ROS) during renal I/R was investigated in Sprague-Dawley rats using histopathological and biochemical parameters. In one set of experiments animals were unilaterally nephrectomized, and subjected to 45min of left renal pedicle occlusion and in another set both the renal pedicles were occluded for 45min followed by 24h of reperfusion. Trimetazidine (3mgkg(-1), i.p.) was administered 30min prior to ischemia and repeated 12h after the first dose. At the end of the reperfusion period, rats were sacrificed. Thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) levels, glutathione reductase (GR) catalase (CAT), and superoxide dismutase (SOD) activities were determined in renal tissue. Serum creatinine and blood urea nitrogen (BUN) concentrations were measured for the evaluation of renal function. Ischemic control animals demonstrated severe deterioration of renal function, renal morphology and a significant renal oxidative stress. Pretreatment of animals with trimetazidine markedly attenuated renal dysfunction, morphological alterations, reduced elevated TBARS levels and restored the depleted renal antioxidant enzymes. The findings imply that ROS play a causal role in I/R induced renal injury and trimetazidine exert renoprotective effects probably by the radical scavenging and antioxidant activities.
机译：越来越多的证据表明，毒性氧自由基在肾脏缺血/再灌注（I / R）损伤的发病机理中起作用。这项研究旨在研究曲美他嗪在I / R诱导的大鼠肾衰竭中的作用。在Sprague-Dawley大鼠中，使用组织病理学和生化参数研究了曲美他嗪（Tmz）对活性氧（ROS）造成的肾脏I / R损伤的保护作用。在一组实验中，对动物进行单侧肾切除术，并使其左肾蒂蒂闭塞45分钟，而在另一组实验中，将两个肾蒂均闭塞45min，然后再灌注24h。在缺血前30min给予Trimetazidine（3mgkg（-1），i.p.），并在第一次给药后12h重复。在再灌注期结束时，处死大鼠。确定了肾组织中的硫代巴比妥酸反应性物质（TBARS），降低的谷胱甘肽（GSH）水平，谷胱甘肽还原酶（GR）过氧化氢酶（CAT）和超氧化物歧化酶（SOD）活性。测量血清肌酐和血尿素氮（BUN）浓度以评估肾功能。缺血对照动物表现出肾功能，肾形态和严重的肾脏氧化应激的严重恶化。用曲美他嗪预处理动物可显着减轻肾功能障碍，形态改变，降低TBARS水平升高并恢复耗尽的肾脏抗氧化酶。该发现暗示ROS在I / R诱导的肾损伤中起因果作用，曲美他嗪可能通过自由基清除和抗氧化活性发挥肾保护作用。

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