电针预处理抑制癫痫持续状态诱发的海马区神经元凋亡机制研究

Mechanism of electro-acupuncture pretreatment-suppressed hippocampal neuron apoptosis induced by status epilepticus

目的:探讨电针(electro-acupuncture,EA)预处理抑制癫痫持续状态(status epilepticus,SE)诱发的海马区神经元凋亡的机制。方法:20只S-D大鼠被随机分为对照组、癫痫组、电针组、电针对照组;电针组和电针对照组给予电针预处理3周后,按经典方法建立锂-匹罗卡品大鼠癫痫模型,用免疫荧光法观察海马区Bid、Bim、Bax、Caspase-3的表达。结果:电针百会及大椎穴预处理抑制了海马CA1/CA3区SE诱发的Bcl-2蛋白家族促凋亡因子Bax、Bim和Bid的表达增高(P<0.05),同时海马区Caspase-3阳性神经元减少(P<0.05);电针阿是穴预刺激对SE诱发的Bcl-2蛋白家族凋亡调节因子的表达无统计学意义(P>0.05)。结论:电针预处理可能通过抑制SE后海马区促凋亡因子Bax、Bim和Bid的表达,进而减少神经元的凋亡。

Objective： To investigate the mechanism of electro-acupuncture （EA） pretreatment- suppressed hippocampal neuron apoptosis induced by status epilepticus（SE）.Methods： Twenty SD rats were randomly divided into four groups：control group,EA group,pilo group and placebo group.The rats in EA group and placebo group were pretreated with electro-acupuncture for 3 weeks. Li-pilocarpine status epileptic model was established according to the previous reported schedule. Immunofluorescence was applied to observe the expression of Bid,Bim,Bax and Caspase- 3 in neurons of hippocampus.Results： EA pretreatment suppressed the SE induced over-expression of pro-apoptotic protein Bax,Bim,and Bid （P 〈0.05）, and decreased the number of Capase- 3 positive neurons in hippocampus （P 〈 0.05）. EA stimulation at two non-acupoints （located in close vicinity to the baihui and dazhui acupoints） didn＇t alter the expression of Bcl-2 family proteins （P〉0.05）.Conclusion：EA pretreatment, especially at the dazhui and baihui acupoints,has protective effects on neuron during epilepsy.The mechanism can be attributed to downregulated expression of Bcl-2 family protein Bax,Bim and Bid.