Effects of acupoint catgut embedding therapy on nerve cell apoptosis in hippocampus CA1 area of rats with vascular dementia

Objective To observe the effect of Acupoint Catgut Embedding therapy( ACET) on nerve cell apoptosis and expression of Bcl-2 and Bax protein in hippocampus CA1 area of rats with vascular dementia and to explore their roles in the neuroprotection mechanism of cerebral ischemic injury. Methods VD models were established with the modified Pulsinelli four vessel occlusion( 4-VO) method. The VD model rats were randomly divided into four groups by the stochastic indicator method: VD model group( group M),ACET group( group A) and nimodipine group( group N),and sham-operated group( group S). Two treatment groups were treated with ACET and nimodipine treatment. Learning and memory abilities of rats in 4 groups were detected with Morris Water Maze test after all rats ended treatment. The brain tissue containing hippocampus was collected,and the nerve cell apoptosis of CA1 area of hippocampus of rats was detected with TUNEL,and the expression of Bcl-2 and Bax protein in hippocampus CA1 area were detected with hybridization in situ. Changes of nerve cell apoptosis and content of Bcl-2 and Bax in hippocampus CA1 area were observed and compared.Results A large amount of apoptotic cells showed. The content of Bcl-2 mRNA reduced,the content of Bax mRNA increased in hippocampal CA1 region of rats in group M,and the differences were statistically significant by comparing with group S( P 0. 01). The obvious learning and memory disorder appeared in group M,and the difference was significant by comparing with group S( P 0. 01). Compared with group M,the ability of learning and memorizing of rats in group A significantly increased( P 0. 01) and the apoptosis cells were significantly reduced( P 0. 01). Bcl-2 mRNA expression in the CA1 area of hippocampus of group A had a significant increasing but Bax mRNA expression decreased. ConclusionACET may improve the ability of learning and memorizing ability of VD rats,and its mechanism may be related to upregulation of Bcl-2 mRNA,down-regulation of Bax mRNA in hippocampus CA1 area and inhibition of the nerve cell apoptosis of rats with vascular dementia.