Louis J C, Magal E, Brixi A, Steinberg R, Yavin E, Vincendon G
Centre de Neurochimie du CNRS, Strasbourg, France.
Brain Res. 1991 Feb 8;541(1):171-4. doi: 10.1016/0006-8993(91)91094-h.
Acute forebrain ischemia reduced protein kinase C (PKC) activity in the adult rat cortex, striatum and hippocampus by 60-70% after 20 min ischemia episodes, followed by 48 h of recirculation. Ischemia of 1 min, followed by recirculation, produced a less pronounced but significant decrease in PKC activity. The ischemia-induced decrease of PKC affected both the soluble and the membrane-bound kinase. Alterations of PKC predate neuronal death following ischemia.
急性前脑缺血使成年大鼠皮质、纹状体和海马体中的蛋白激酶C(PKC)活性在经历20分钟缺血发作及随后48小时再灌注后降低60 - 70%。1分钟缺血后再灌注,PKC活性有较不明显但显著的降低。缺血诱导的PKC降低影响了可溶性激酶和膜结合激酶。PKC的改变在缺血后神经元死亡之前就已出现。