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首页> 外文期刊>European review for medical and pharmacological sciences. >Renoprotective activity of telmisartan versus pioglitazone on ischemia/reperfusion induced renal damage in diabetic rats
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Renoprotective activity of telmisartan versus pioglitazone on ischemia/reperfusion induced renal damage in diabetic rats

机译:替米沙坦与吡格列酮对糖尿病大鼠肾缺血/再灌注的肾保护作用

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Objectives: Diabetes mellitus (DM) causes organ dysfunction and increases the sensitivity of organs to damages.To test this hypothesis, we used renal ischemia/reperfusion (I/R) experiment to evaluate the renoprotective activity of telmisartan versus pioglitazone on I/R induced renal damage in diabetic rats. Materials and Methods: Renal I/R was performed in both normal and diabetic rats. The protocol comprised ischemia for 45 minutes followed by the reperfusion for 24 hours and a treatment period of two weeks before induction of ischemia. Results: Renal I/R in both control and diabetic rats induced marked renal dysfunction associated with a significant increase in the arterial pressure, tumor necrosis factor alpha (TNF-a) levels, and the malondialdehyde formation (MDA). The activities of the anti-oxidant enzymes such as reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were found to be decreased significantly compared to control rats. Diabetic animals that underwent renal I/R exhibited a significant increase in all the studied parameters with a reduction in the anti-oxidant enzymes as compared to non-diabetic rats. Histo- pathological studies confirm these results. Treatment with pioglitazone or telmisartan demonstrated a significant improvement in the reperfusion- induced renal injury in comparison with diabetic I/R group, without difference between the two treated groups. Therefore, the treatment with pioglitazone or telmisartan have the same corrective effect. Conclusions: Type 2 diabetes had exaggerated renal I/R injury in STZ-NAD induced diabetes. Telmisartan treatment is equieffective as pioglitazone in attenuating acute I/R-induced renal injury in diabetic rats by a modification in the oxidative stress and the inflammation.
机译:目的:糖尿病(DM)引起器官功能障碍,并增加器官对损伤的敏感性。为了验证这一假设,我们使用肾脏缺血/再灌注(I / R)实验评估替米沙坦与吡格列酮对经I / R诱导的肾保护活性。糖尿病大鼠的肾脏损害。材料和方法:在正常和糖尿病大鼠中进行肾脏I / R。该方案包括缺血45分钟,然后再灌注24小时和诱导缺血前两周的治疗期。结果:对照组和糖尿病大鼠的肾脏I / R均引起明显的肾功能不全,与动脉压,肿瘤坏死因子α(TNF-a)水平和丙二醛形成(MDA)的显着增加有关。与对照大鼠相比,发现还原型谷胱甘肽(GSH),超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等抗氧化酶的活性明显降低。与非糖尿病大鼠相比,接受肾I / R的糖尿病动物在所有研究参数中均表现出显着增加,同时抗氧化酶降低。组织病理学研究证实了这些结果。与糖尿病I / R组相比,吡格列酮或替米沙坦治疗显示再灌注诱导的肾损伤显着改善,而两个治疗组之间无差异。因此,吡格列酮或替米沙坦治疗具有相同的矫正效果。结论:2型糖尿病在STZ-NAD诱发的糖尿病中夸大了肾脏I / R损伤。替米沙坦治疗与吡格列酮等效,可通过改变氧化应激和炎症减轻糖尿病大鼠急性I / R引起的肾损伤。

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