Yamaoka Y, Shimohama S, Kimura J, Fukunaga R, Taniguchi T
Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Neurosci Lett. 1993 May 14;154(1-2):20-2. doi: 10.1016/0304-3940(93)90161-d.
The effects of hypoxia on protein kinase C (PKC) isozymes (alpha, beta I, beta II, and gamma) were examined in the hippocampus from rats subjected to hypoxic conditions (5% O2 in 95% N2) for 30 min in a chamber. Western blot analysis revealed that the total amounts of PKC-alpha (-26.0% of control) and -gamma (-32.7% of control) were decreased significantly at the end of hypoxia, which was followed by the reduction of that of PKC-beta II (-23.7% of control at 7 days after hypoxia). Whereas, the PKC activities, which were measured by the incorporation of [gamma-32P] into a specific PKC substrate peptide, in both the cytosolic and the particulate fractions did not change. The reductions of PKC-gamma and -alpha at the end of hypoxia may be related to the following neuronal degeneration.
在缺氧舱中对大鼠进行30分钟缺氧处理（95%氮气中含5%氧气），检测缺氧对海马体中蛋白激酶C（PKC）同工酶（α、βI、βII和γ）的影响。蛋白质印迹分析显示，缺氧结束时PKC-α（对照组的-26.0%）和PKC-γ（对照组的-32.7%）的总量显著降低，随后PKC-βII的总量在缺氧7天后降低（对照组的-23.7%）。然而，通过将[γ-32P]掺入特定PKC底物肽来测量的细胞质和颗粒部分的PKC活性并未改变。缺氧结束时PKC-γ和PKC-α的减少可能与随后的神经元变性有关。
