Effects of L-tetrahydropalmatine on Neuronal Apoptosis and the Expression of Caspase-3 Protein after Focal Cerebral Ischemia Reperfusion Injure in Rats

Objective To explore the effects of l-tetrahydropalmatine(L-THP)on neuronal apoptosis and the expression of Caspase-3 in cerebral cortex after transient focal cerebral ischemia reperfusion injure in rats.Methods The experimental rats were randomly divided into 4 groups:sham group,model group,L-THP high dose group(40 mg kg-1 d-1) and L-THP low dose group(20 mg kg-1 d-1).Transient focal cerebral ischemia reperfusion model of rats' middle cerebral artery occlusion(MCAO) was induced by inserting a nylon filament through left internal carotid artery.After 1 h MCAO the nylon filament was withdrawn to allow reperfusion.At 6,24,48 h of reperfusion,neurological deficit was scored,neurons apoptosis in ischemic cerebral cortex was characterized by terminal deoxynucleotide transferase mediated uridine 5'-triphosphate-biotin nick end-labeling(TUNEL) staining.The expression of Caspase-3 was determined by immunohistochemistry method.Results TUNEL positive neurons and the expression of Caspase-3 appeared at 6 h after reperfusion and increased gradually,it reached at peak value at 24 h and reduced gradually at 48 h.The time phase of Caspase-3 protein expression was consistent with that of neuronal apoptosis.Compared with model group at each time point of the reperfusion,in L-THP high dose group and L-THP low dose group,TUNEL positive neurons were markedly decreased(P0.05),the expression of Caspase-3 were significantly lower(P0.01) and neurological deficit scores were significantly reduced(P0.05).Conclusion L-THP protects neurons from ischemis-reperfusion mediated damage by inhibiting the expression of Caspase-3 protein and decreasing neuronal apoptosis.