The experiment research of neuroprotection of hypoperfusion postconditioning on XXXX .

@entity2806 @entity35 @entity13335 @entity551 @entity13336
In this study, we tested the hypothesis that the alternating of hypoperfusion and full reperfusion (hypoperfusion postconditioning) could improve neuroprotection on @entity2806 in @entity35 and explored the role of TAp63 and    Np63 in this process. Eighty male @entity35 were randomly divided into 4 groups: the sham group, the cerebral ischemic/reperfusion group (I/R), the hypoperfusion group 1 ( @entity13335 ), and the hypoperfusion group 2 ( @entity13336 ). @entity2806 was established by clamping the bilateral common carotid artery with @entity551 for 20 minutes. For the @entity35 in the @entity13335 group, the blood pressure was maintained to 80 to 90 mm Hg in clamping bilateral common carotid artery minutes and then unclamped. For the @entity35 in the @entity13336 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 I/R, @entity13335 , and @entity13336 groups decreased significantly after @entity2806 , and scores in the @entity13336 group were significantly higher than those in the I/R group (P < 0.05). Neuronal densities in the @entity13335 and @entity13336 groups were significantly higher than that in the I/R group (P < 0.05). Neuronal apoptosis in the @entity13335 and @entity13336 groups was significantly lower than that in the I/R group (P < 0.05). TAp63 and S100b concentration decreased, and    Np63 increased significantly in the @entity13335 and @entity13336 groups as compared with the I/R group (P < 0.05). No significant difference in these parameters between the @entity13335 and @entity13336 groups (P > 0.05). Alternating of hypoperfusion and normal perfusion postconditioning had neuroprotection function on @entity2806 in the @entity35 . 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.
