Hoshovs'ka Iu V, Shymans'ka T V, Sahach V F
Fiziol Zh (1994). 2011;57(6):38-45.
The functional significance of uncoupling proteins UCP2 and UCP3 in the cell and the organism remains unknown. There have been reports about their involvement in cellular protection mechanisms underlying the phenomenon of ischemic preconditioning. The purpose of this study was to elucidate the role of uncoupling proteins UCP2 and UCP3 in the formation of cardioprotective effect of ischemic preconditioning. In experiments on isolated rat hearts we show here an increase in the level of UCP2 and UCP3 gene expression in the heart tissue under the influence of ischemic preconditioning with three episodes of 5 min stopping the flow perfusion. Similar effects were induced by a prolonged ischemia-reperfusion of myocardium. The blockade of the UCP2 activity by genipin (Wako Inc., USA, 10(-5) mol/L, isolated heart perfusion for 15 minutes) abolished the protective effect of adaptation to ischemia. It was concluded that uncoupling proteins take part in the cardioprotective effect ofischemic preconditioning.
解偶联蛋白UCP2和UCP3在细胞和机体中的功能意义尚不清楚。已有报道称它们参与了缺血预处理现象背后的细胞保护机制。本研究的目的是阐明解偶联蛋白UCP2和UCP3在缺血预处理心脏保护作用形成中的作用。在离体大鼠心脏实验中，我们发现，经过3次5分钟停止血流灌注的缺血预处理后，心脏组织中UCP2和UCP3基因表达水平升高。心肌长时间缺血再灌注也会产生类似效果。京尼平（美国和光株式会社，10(-5)mol/L，离体心脏灌注15分钟）对UCP2活性的阻断消除了缺血适应的保护作用。得出的结论是，解偶联蛋白参与了缺血预处理的心脏保护作用。
