Functional Recovery of Ischemic Penumbra in Hippocampus Indirectly Stimulated by Ischemic Cerebral Injury through Activation of Endogenous GAP-43 and Bcl-2

Objective:To explore the effect of activated endogenous growth associated protein-43 (GAP-43) and Bcl-2 promoting plasticity regeneration of apoptotic neurons and mediating a compensated repair of ischemic penumbral region in hippocampus after cerebral ischemia reperfusion injury in rats. Methods:The healthy adult male Wister rats (n=100) were randomly divided into normal control group, sham-operation group and reperfusion 2、6、12、24 and 48 h, 3、7 and 14 days after ischemia 1 h groups (n=10 in each group). The models of cerebral ischemia reperfusion were induced by intraluminal middle cerebral artery occlusion (MCAO) with a nylon monofilament suture. The expression of GAP-43 and Bcl-2 proteins was detected by immunohistochemistry method, and apoptosis of neurons was tested by TUNEL. Infarction size was observed by TTC staining. Results:The apoptotic neurons were increased in ischemia/reperfusion 2 h, reached the peak at 48 h, and reduced to the lowest level at 14 day. GAP-43 in neurons showed a basic expression background in ischemia/reperfusion 2 h, peaked at 3-7 day, and reduced to the lowest at 14 day. The expression of Bcl-2 was increased in ischemia/perfusion 2 h, reached the peak at 7 day, and reduced to the lowest at 14 day. Infarction size began to form in ischemia/reperfusion 2 h, reached the peak at 48 h, then gradually reduced, and returned to the normal level at 14 day. Conclusion:The expression of endogenous GAP-43 and Bcl-2 could stimulate neurons axon regeneration and synaptic linkage formation after ischemia injury. Neuron apoptosis might participate in the activation channel of endogenous correlated apoptosis genes.