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首页> 外文期刊>Biological & pharmaceutical bulletin >Protective Effects of Cyclo(L-Leu-L-Tyr) against Postischemic Myocardial Dysfunction in Guinea-Pig Hearts
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Protective Effects of Cyclo(L-Leu-L-Tyr) against Postischemic Myocardial Dysfunction in Guinea-Pig Hearts

机译：Cyclo（L-Leu-L-Tyr）对豚鼠心脏缺血后心肌功能障碍的保护作用

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The protective effects of cyclic dipeptides in alcoholic beverages were investigated in the perfused guinea-pig hearts subjected to ischemia and reperfusion. Subsequently, in order to determine the importance of cyclic dipeptide structure, the effects of cyclo(L-Leu-L-Tyr) (cLY) were compared with those of the newly synthesized non-cyclic dipeptides, L-Leu-L-Tyr (LY) and L-Tyr-L-Leu (YL). After reperfusion, pressure recovery (%) in the left ventricle reached a peak of over 90% in the presence of cLY (10~(-6) M and 10~(-5) M) (control: 22.9%). The recovery by LY and YL was significantly lower than that by cLY, and ATP levels simultaneously monitored using P-31-NMR were already lower during the ischemic end period than those observed with cLY treatment. In perfused mitochondrial preparations, cLY significantly inhibited mitochondrial Ca~(2+) ([Ca~(2+)]_m) elevation in a similar way to that of the mitochondrial permeability transition pore (MPTP) inhibitor cyclosporin A. In vitro electron paramagnetic resonance (EPR) revealed that the active oxygen radicals quenching activity of cLY was greater than those of non-cyclic dipeptides. cLY inhibited caspase-3-induced apoptosis. The cyclic dipeptide structure inhibits opening of the MPTP by preventing [Ca~(2+)]_m overload-induced apoptosis related to mitochondrial active oxygen radical accumulation in ischemia-reperfusion hearts.
机译：在经历缺血和再灌注的豚鼠心脏灌注中，研究了环二肽在酒精饮料中的保护作用。随后，为了确定环状二肽结构的重要性，将环（L-Leu-L-Tyr）（cLY）的作用与新合成的非环状二肽L-Leu-L-Tyr（ LY）和L-Tyr-L-Leu（YL）。再灌注后，在存在cLY（10〜（-6）M和10〜（-5）M）的情况下，左心室的压力恢复（％）达到90％以上的峰值（对照组：22.9％）。 LY和YL的回收率显着低于cLY，并且在缺血结束期间使用P-31-NMR同时监测的ATP水平已经低于cLY处理所观察到的水平。在灌注的线粒体制剂中，cLY以与线粒体通透性转换孔（MPTP）抑制剂环孢菌素A类似的方式显着抑制线粒体Ca〜（2+）（[Ca〜（2 +）] _ m）升高。共振（EPR）表明，cLY的活性氧自由基猝灭活性大于非环状二肽。 cLY抑制caspase-3诱导的细胞凋亡。环状二肽结构通过防止[Ca〜（2 +）] _ m超负荷诱导的缺血再灌注心脏线粒体活性氧自由基积累相关的凋亡，从而抑制MPTP的开放。

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