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首页> 外文期刊>Biochemical Pharmacology >Tissue kallikrein is required for the cardioprotective effect of Cyclosporin A in myocardial ischemia in the mouse
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Tissue kallikrein is required for the cardioprotective effect of Cyclosporin A in myocardial ischemia in the mouse

机译:组织激肽释放酶是环孢菌素A对小鼠心肌缺血的心脏保护作用所必需的

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摘要

Clinical and experimental studies suggest that pharmacological postconditioning with Cyclosporin A (CsA) reduces infarct size in cardiac ischemia and reperfusion. CsA interacts with Cyclophilin D (CypD) preventing opening of the mitochondrial permeability transition pore (mPTP). Tissue kallikrein (TK) and its products kinins are involved in cardioprotection in ischemia. CypD knockout mice are resistant to the cardioprotective effects of both CsA and kinins suggesting common mechanisms of action. Using TK gene knockout mice, we investigated whether the kallikrein-kinin system is involved in the cardioprotective effect of CsA.
机译:临床和实验研究表明,用环孢菌素A(CsA)进行药理学后处理可减少心肌缺血和再灌注时的梗塞面积。 CsA与亲环蛋白D(CypD)相互作用,阻止线粒体通透性转换孔(mPTP)的打开。组织激肽释放酶(TK)及其激肽在缺血中参与心脏保护。 CypD基因敲除小鼠对CsA和激肽的心脏保护作用均具有抗性,提示其共同的作用机制。使用TK基因敲除小鼠,我们调查了激肽释放酶激肽系统是否参与CsA的心脏保护作用。

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