Objective To observe the protective effect of electroacupuncture(EA)intervention on the expression of brain-derived neurotrophic factor(BDNF)and tropomyosin receptor kinase B(TrkB)proteins and genes in the hippocampus areas in myocardial ischemia(MI)rats

so as to reveal its underlying mechanisms in protecting hippocampal cells under MI.Methods Eighty healthy male SD rats were randomized into sham-operation(sham)

MI model

Shenmen(HT 7)

HT 7-Zhizheng(SI 7)and HT 7-Xinshu(BL 15)groups(n=15in each group).The MI model was established by occlusion of the anterior descending branch of the left coronary artery.EA(2Hz

2mA)was applied to bilateral HT 7

HT 7-SI 7

and HT 7-BL 15

respectively for15 min

once per day for a week.The number of BDNF and its receptor TrkB positive cells in the left hippocampus and that of mRNAs in the right hippocampus tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR

respectively.Results In comparison with the sham group

the numbers of both BDNF and TrkB positive cells in the left hippocampus and the expression levels of BDNF mRNA and TrkB mRNA in the right hippocampus were increased slightly(P>0.05).After EA intervention

the numbers of hippocampal BDNF and TrkB positive cells and the expression levels of BDNF mRNA and TrkB mRNA were evidently up-regulated(P<0.05

P<0.01)

and the effects of HT 7-SI 7and HT 7-BL 15 were obviously superior to those of simple HT 7in up-regulating BDNF and TrkB expression(P<0.01

P<0.05).No significant differences were found between the HT 7-SI 7and HT 7-BL 15 groups in increasing the number of hippocampal BDNF and TrkB positive cells and in up-regulating expression of both BDNF mRNA and TrkB mRNA(P>0.05).Conclusion EA intervention is effective in increasing the expression of hippocampal BDNF and TrkB in MI rats

which may contribute to its effect in protecting hippocampal cells from injury under MI condition.The effect of EA stimulation of HT 7-SI 7and HT 7-BL 15 was obviously superior to that of simple HT 7in up-regulating BDNF and TrkB expression.