The Research of Intracellular Energy-Related Metabolic Regulatory Enzymes on Delayed Neuronal Cell Death

p-AMPKα2和p-AMPKβ1在大鼠断头后60分钟内呈升高趋势。这表明AMPK在神经元缺血时被激活。AICAR是AMPK的一种激活剂，可以减少局灶性缺血大鼠的梗死体积。然而，AICAR加重了沙鼠前脑缺血的神经元损伤，并且在给药化合物C （AMPK抑制剂之一）时观察到同样的加重。

The tendency of increasing in p-AMPKα2 and p-AMPKβ1 was observed in the brain samples 60 minutes after decapitation of rats. This result suggested that AMPK was activated by neuronal ischemia. Infarction volumes in focal ischemia with rat model were decreased by AICAR, which is one of the activators of AMPK. However, AICAR exacerbated neuronal damage in gerbil forebrain ischemia, and the same exacerbation was observed in the administration of Compound C, one of the AMPK inhibitors.