Kim H, Kim D J, Chung H S, Shim S J, Yoo U H, Rah B J, Kim H D
Department of Histology, College of Medicine, Chung-Ang University, Seoul, Korea.
J Korean Med Sci. 1998 Oct;13(5):473-82. doi: 10.3346/jkms.1998.13.5.473.
We tested recent evidence that ischemic preconditioning (PC) involves in translocation of protein kinase C (PKC) from the cytosol to myocyte membrane. Isolated Langendorff-perfused rabbit hearts (n=96) were subjected to 60 or 45 min of ischemia (I) and 120 min of reperfusion (R) with or without PC (4 cycles of 5 min I and 5 min R; or single dose of 5 min I and 10 min R), respectively. Left ventricular function and infarct size (IS) were measured; myocardial cytosolic and membrane PKC activity were determined by 32P-gamma-ATP incorporation into PKC-specific peptide. PC enhanced improvement of functional recovery and reduced IS (26.9+/-1.4% versus 15.3+/-1.9%, p<0.01, in 60 min of I; 18.3+/-2.6% versus 8.6+/-2.5%, p<0.05, in 45 min of I); cytosolic PKC activity decreased 74% of total activity (p<0.05) both in 60 and 45 min of I; membrane PKC activity increased (1.7-fold of baseline, p<0.01, in 60 min of I; 1.8-fold, p<0.01, in 45 min of I; 1.5-fold, p<0.05, in 60 of min I and 120 min of R). From these results, it is concluded that translocation of PKC from the cytosol to myocyte membranes is an important mechanism responsible for PC effect.
我们检测了近期有关缺血预处理（PC）涉及蛋白激酶C（PKC）从胞质溶胶转位至心肌细胞膜的证据。将离体Langendorff灌注兔心脏（n = 96）分别进行60分钟或45分钟的缺血（I）以及120分钟的再灌注（R），有无PC处理（5分钟缺血和5分钟再灌注的4个循环；或单次5分钟缺血和10分钟再灌注）。测量左心室功能和梗死面积（IS）；通过将³²P-γ-ATP掺入PKC特异性肽来测定心肌胞质溶胶和膜PKC活性。PC增强了功能恢复并减小了梗死面积（60分钟缺血时为26.9±1.4%对15.3±1.9%，p<0.01；45分钟缺血时为18.3±2.6%对8.6±2.5%，p<0.05）；在60分钟和45分钟缺血时，胞质溶胶PKC活性均降至总活性的74%（p<0.05）；膜PKC活性增加（60分钟缺血时为基线的1.7倍，p<0.01；45分钟缺血时为1.8倍，p<0.01；60分钟缺血和120分钟再灌注时为1.5倍，p<0.05）。从这些结果得出结论，PKC从胞质溶胶转位至心肌细胞膜是PC效应的重要机制。
