Yoshida K, Kawamura S, Mizukami Y, Kitakaze M
Department of Legal Medicine, Yamaguchi University School of Medicine, Ube.
J Biochem. 1997 Sep;122(3):506-11. doi: 10.1093/oxfordjournals.jbchem.a021781.
Ischemic preconditioning is a phenomenon in which one or several cycle(s) of brief ischemia-reperfusion protects the myocardium against the cell injury caused by subsequent prolonged ischemia. Protein kinase C (PKC) inhibitors blunt the cardioprotection arising from ischemic preconditioning. To investigate which PKC isoform is involved in ischemic preconditioning, we identified the PKC isoform that translocates to the membrane fraction by means of immunoblotting with specific antibodies. PKC-alpha, delta, epsilon isoforms all increased in the membrane fraction after three cycles of 3 min ischemia and 5 min reperfusion (ischemic preconditioning) in the perfused rat heart. The ischemic preconditioning significantly improved the recovery of left ventricular developed pressure (LVDP) during reperfusion following 20 min of ischemia. A PKC specific inhibitor, chelerythrine (1.0 microM) blocked the effect of ischemic preconditioning on LVDP recovery and the translocation of PKC-alpha, delta, epsilon isoforms. These data suggest that one or more of these three isoforms of PKC is involved in ischemic preconditioning by phosphorylating membrane proteins.
缺血预处理是一种现象，即一个或几个短暂的缺血-再灌注周期可保护心肌免受随后长时间缺血所引起的细胞损伤。蛋白激酶C（PKC）抑制剂可消除缺血预处理产生的心脏保护作用。为了研究哪种PKC亚型参与缺血预处理，我们通过用特异性抗体进行免疫印迹来鉴定易位至膜部分的PKC亚型。在灌注的大鼠心脏中，经过3分钟缺血和5分钟再灌注的三个周期（缺血预处理）后，PKC-α、δ、ε亚型在膜部分均增加。缺血预处理显著改善了20分钟缺血后再灌注期间左心室舒张末压（LVDP）的恢复。一种PKC特异性抑制剂白屈菜红碱（1.0微摩尔）阻断了缺血预处理对LVDP恢复的作用以及PKC-α、δ、ε亚型的易位。这些数据表明，这三种PKC亚型中的一种或多种通过使膜蛋白磷酸化而参与缺血预处理。
