首页> 外文期刊>Biochemical and Biophysical Research Communications >Effect of atorvastatin on expression of IL-10 and TNF-alpha mRNA in myocardial ischemia-reperfusion injury in rats.
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Effect of atorvastatin on expression of IL-10 and TNF-alpha mRNA in myocardial ischemia-reperfusion injury in rats.

机译:阿托伐他汀对大鼠心肌缺血再灌注损伤中IL-10和TNF-αmRNA表达的影响。

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Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. Because statins protect the myocardium against ischemia-reperfusion injury via a mechanism unrelated to cholesterol lowering, we hypothesized that the protective effect of statins was related to the expression of TNF-alpha (TNF-alpha) and interleukin-10 (IL-10) mRNA. Seventy-two rats were randomly divided into three groups as follows: sham, I/R and I/R+atorvastatin. Atorvastatin (20 mg kg(-1)day(-1)) treatment was administered daily via oral gavage to rats for 2, 7 or 14 days. Ischemia was induced via a 30-min coronary occlusion. Reperfusion was allowed until 2, 7 or 14 days while atorvastatin treatment continued. We measured infarct size, hemodynamics and the plasma levels and the mRNA expression of TNF-alpha and IL-10 in the three groups. We demonstrated that the up-regulation of expression of both TNF-alpha mRNA and IL-10 mRNA was associated the increased plasma levels of TNF-alpha and IL-10 in the ischemic and reperfused myocardium compared with that in the sham group (P<0.01). Atorvastatin treatment prevented ischemia-reperfusion-induced up-regulation of both TNF-alpha and IL-10 mRNA, and improved left ventricular function (P<0.01). Our findings suggested that atorvastatin may attenuate MI/R and better recovery of left ventricle function following ischemia and reperfusion and IL-10 was not directly likely involved in this protective mechanism.
机译:心肌缺血和再灌注(MI / R)与强烈的炎症反应相关,这可能导致心肌细胞损伤。因为他汀类药物通过与胆固醇降低无关的机制保护心肌免受缺血再灌注损伤,所以我们假设他汀类药物的保护作用与TNF-α(TNF-alpha)和白介素10(IL-10)mRNA的表达有关。 72只大鼠随机分为三组:假手术,I / R和I / R +阿托伐他汀。阿托伐他汀(20 mg kg(-1)day(-1))每天通过管饲法给予大鼠2、7或14天。缺血是通过30分钟的冠状动脉闭塞引起的。在继续进行阿托伐他汀治疗之前,允许再灌注直至2、7或14天。我们测量了三组的梗死面积,血流动力学,血浆水平以及TNF-α和IL-10的mRNA表达。我们证明与假手术组相比,缺血和再灌注心肌中TNF-α和IL-10 mRNA表达的上调与TNF-α和IL-10血浆水平升高相关(P < 0.01)。阿托伐他汀治疗可防止缺血再灌注诱导的TNF-α和IL-10 mRNA上调,并改善左心室功能(P <0.01)。我们的发现表明,阿托伐他汀可能会减轻MI / R,并在缺血和再灌注后更好地恢复左心室功能,而IL-10不可能直接参与这种保护机制。

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