Cardell M, Boris-Möller F, Wieloch T
Department of Neurobiology, University Hospital, Lund, Sweden.
J Neurochem. 1991 Nov;57(5):1814-7. doi: 10.1111/j.1471-4159.1991.tb06387.x.
The effect of hypothermia on the ischemia-induced changes in the subcellular distribution of protein kinase C (PKC) (gamma), -(beta II), and -(alpha) and the activity of PKC was studied in striatal homogenates of rats subjected to 20 min of cerebral ischemia. The effect of postischemic cooling was also studied. During normothermic ischemia, PKC(gamma) and -(beta II) increased 3.9- and 2.9-fold, respectively, in the particulate fraction, signifying a translocation of PKC to cell membranes. The levels of PKC(alpha) did not change significantly. PKC activity decreased during ischemia by 52% and 47% (p less than 0.05) in the particulate and cytosolic fractions, respectively, and remained inhibited for the 1 h recovery period. In hypothermic animals, there was no evidence of translocation, and the inhibition of PKC activity was completely abolished. Hypothermia induced in the recovery phase, however, did not affect PKC distribution or activity. The protective effect of intraischemic hypothermia may in part be due to the prevention of the ischemia-induced translocation and subsequent downregulation of PKC, possibly through a temperature-dependent modification of the cell membranes.
研究了低温对脑缺血20分钟的大鼠纹状体匀浆中蛋白激酶C（PKC）（γ）、-（βII）和-（α）亚细胞分布的缺血诱导变化以及PKC活性的影响。还研究了缺血后降温的作用。在常温缺血期间，颗粒部分的PKC（γ）和-（βII）分别增加了3.9倍和2.9倍，这表明PKC易位至细胞膜。PKC（α）的水平没有显著变化。缺血期间，颗粒部分和胞质部分的PKC活性分别降低了52%和47%（p<0.05），并且在1小时的恢复期内仍受到抑制。在低温动物中，没有易位的证据，并且PKC活性的抑制被完全消除。然而，在恢复阶段诱导的低温并不影响PKC的分布或活性。缺血期间低温的保护作用可能部分归因于预防了缺血诱导的PKC易位及随后的下调，这可能是通过细胞膜的温度依赖性修饰实现的。
