The Role of Caspase-3 Protein and Bcl-2 and Bax Genes Expression in Nerve Injury Following Cerebral Ischemia

Objective:To explore the mechanism of Caspases-3 protein and Bax and Bcl-2 genes regulating apoptosis of neurons in experimental rats with ischemia/reperfusion injury and clinical significance.Methods:Sixty-four healthy adult male wistar rats were randomly assigned into a control group(n=32)and an experimental group(n=32).A model of middle cerebral artery occlusion was established by a filament method from left external-internal carotid artery.The ischemic time lasted 1 h.And each group was subdivided into eight sub-groups according to the reperfusion time(3 h,6 h,12 h,24 h,48 h,3 days,7 days and 14 days).The cognitive and motor behaviors in all animals were determined by Bederson's standard,balancing beam and forelimb placing test.TUNEL method was used to assay neuronal apoptosis,and immunohistochemistry was used to detect the expression of Caspases-3,Bax and Bcl-2,respectively.Results:The scores of Bederson and Feeney were reduced significantly in experimental group during 6 h-7 days,but forepaw position test positive(%)score was increased gradually.Bederson and Feeney score was 0 at 14th day,and forepaw position test positive(%)score was highest.In experimental group,the number of Caspase-3 and Bax positive neurons in cerebral cortex and hippocampus reached the peak at 48 h,then began to decrease,and at 14th day,close to that at the 3rd h,but significantly greater than in control group(P0.01).In experimental group,the expression of Bcl-2 in the positive neurons showed a reduced tendency during 6 h-7 days of reperfusion in two regions,and at 14th day,that was close to that at the 3rd h,but significantly higher than in control group(P0.01).Conclusion:The expression of Caspases-3 protein and Bax gene and Bcl-2 gene after cerebral ischemia regulates apoptosis of neurons and promotes nerve damage.