Cardell M, Bingren H, Wieloch T, Zivin J, Saitoh T
Laboratory for Experimental Brain Research, Lund University, Sweden.
Neurosci Lett. 1990 Nov 13;119(2):228-32. doi: 10.1016/0304-3940(90)90840-6.
The subcellular distribution of PKC(alpha) and PKC(gamma) was studied in homogenates of cerebral cortex from rats subjected to 10 and 15 min of ischemia and 15 min of ischemia followed by 1 h, 6 h, 24 h, 48 h, and 7 days of reperfusion. During ischemia no significant changes in the levels of PKC (alpha) were seen. During the first hour of reperfusion, a transient 2.5-fold (P less than 0.05) increase in PKC (alpha) levels was observed in the particulate fraction. In contrast, a three-fold increase of PKC(gamma) in the particulate fraction concomitant with a 40% decrease in the cytosol was noted during ischemia. In the postischemic phase the levels in the cytosol decreased to 35% of control values at 2 days following ischemia, with a concomitant decrease in the particulate fraction to control levels. The redistribution of PKC to the cell membranes during and following ischemia could be due to ischemia induced receptor activation, increased levels of diacylglycerols, arachidonate and intracellular calcium, and may be of importance for the development of ischemic neuronal damage.
研究了经历10分钟和15分钟缺血以及15分钟缺血后再灌注1小时、6小时、24小时、48小时和7天的大鼠大脑皮质匀浆中蛋白激酶C（α）[PKC(α)]和蛋白激酶C（γ）[PKC(γ)]的亚细胞分布。在缺血期间，未观察到PKC(α)水平有显著变化。在再灌注的第一个小时，在微粒部分观察到PKC(α)水平短暂增加2.5倍（P<0.05）。相比之下，在缺血期间，微粒部分的PKC(γ)增加了三倍，同时胞质溶胶减少了40%。在缺血后阶段，缺血后2天胞质溶胶中的水平降至对照值的35%，微粒部分也随之降至对照水平。缺血期间及缺血后PKC向细胞膜的重新分布可能是由于缺血诱导的受体激活、二酰基甘油、花生四烯酸和细胞内钙水平升高所致，这可能对缺血性神经元损伤的发展具有重要意义。
