The Experiment Research of Neuroprotection of Hypoperfusion Postconditioning on Cerebral Ischemia

In this study, we tested the hypothesis that the alternating of hypoperfusion and full reperfusion (hypoperfusion postconditioning) could improve neuroprotection on cerebral ischemia in rats and explored the role of TAp63 and Np63 in this process. Eighty male Sprague Dawley rats were randomly divided into 4 groups: the sham group, the cerebral ischemicreperfusion group (IR), the hypoperfusion group 1 (HR1), and the hypoperfusion group 2 (HR2). Cerebral ischemia was established by clamping the bilateral common carotid artery with hypotension for 20 minutes. For the rats in the HR1 group, the blood pressure was maintained to 80 to 90 mm Hg in clamping bilateral common carotid artery minutes and then unclamped. For the rats in the HR2 group, the clamping was performed at one side of the common carotid artery and one half of the other side of common carotid artery. Neurologic behavior scores in the IR, HR1, and HR2 groups decreased significantly after cerebral ischemia, and scores in the HR2 group were significantly higher than those in the IR group (P< 0.05). Neuronal densities in the HR1 and HR2 groups were significantly higher than that in the IR group (P< 0.05). Neuronal apoptosis in the HR1 and HR2 groups was significantly lower than that inthe IR group (P< 0.05). TAp63 and S100 concentration decreased, and Np63 increased significantly in the HR1 and HR2 groups as compared with the IR group (P< 0.05). No significant difference in these parameters between the HR1 and HR2 groups (P> 0.05). Alternating of hypoperfusion and normal perfusion postconditioning had neuroprotection function on cerebral ischemia in the rats. This could relate with decreasing expression of TAp63 and increasing expression of Np63 in hippocampal region of the first area in the hippocampal circuit to inhibit neuronal apoptosis.