电针预处理对新生大鼠缺氧缺血性脑损伤保护作用的可能机制

Possible Mechanism of Electroacupuncture Preconditioning for Hypoxia/Ischemic Brain Injury Protection Effect in Neonatal Rats

目的 :观察新生大鼠缺氧缺血后大脑早期即刻基因c fos和c jun蛋白含量的变化 ,电针预处理及合用ATP敏感钾通道 (KATP)阻滞剂对其影响 ,以探讨电针预处理对缺氧缺血性脑损伤保护作用的可能机制。方法 :采用免疫印迹方法 ,结合计算机图像处理 ,测定其积分光度值 (ID)。结果 :新生大鼠脑缺氧缺血后海马和皮层部位可同时诱导出c fos和c jun蛋白 ,2～ 4h达到峰值 ;海马的表达较皮层高 ;电针预处理可以降低KATP阻滞剂所致的海马区域的持续高表达。结论 :针刺预处理抗脑缺氧缺血作用可能与激活KATP、抑制早期即刻基因诱发缺氧缺血后神经细胞凋亡有关。

Objective: To explore the possible mechanism of electroacupuncture preconditioning (EAPC) and combined with ATP-sensitive potassium channel (K ATP) blocker preconditioning for hypoxia/ischemic brain injury protection by observing the changes of the immediate genes (c-fos and c-jun protein content) in brain at the early stage after cerebral hypoxia/ischemic injury, and the effect of EAPC on these changes. Methods: Integrated density (ID) of c-fos and c-jun expression was measured by Western blot and computerized image processing. Results: Hypoxia/ischemia could induce c-fos and c-jun protein in both cerebral cortex and hippocampus simultaneously, with the peak appearing 2-4 hrs later, and the expression in hyppocampus was higher than that in cortex. EAPC could lower K ATP blocker induced permanent high expression in hyppocampus. Conclusion: The effect of EAPC preconditioning in antagonizing cerebral hypoxia/ischemic injury may be related with its action in activating K ATP, inhibiting the neuron apoptosis induced by the immediate genes at early stage of injury.