Objective To investigate the effect of acupuncture at points Taiyang and Fengchi on the expression of heat shock protein 70 (HSP70) and neural cell apoptosis during local cerebral ischemia and reperfusion in rabbits and explore its protective action on nerve cells and the mechanism.Methods Rabbits were randomized into sham operation, model and acupuncture groups. Each group was randomly allocated to three time points: one, three and seven days. A rabbit model of local cerebral ischemia and reperfusion was made by middle cerebral artery occlusion (MCAO)using an intraluminal thread. Reperfusion was performed at two hours after cerebral ischemia. In the acupuncture groups, points Taiyang and Fengchi were electro-acupunctured at six hours after cerebral ischemia. Treatment was given once daily. The rabbits were sacrificed to take materials at one, three and seven days after reperfusion. Pathological changes in brain tissue were observed by HE staining. Cerebral HSP70 expression was determined by immunohistochemical method. Neural cell apoptosis was examined by TdT-mediated dUTP nick end labeling (TUNEL).Results Pathological staining showed that cerebral infarction area decreased significantly, the number of nerve cells increased and inflammatory infiltration reduced at every time point in the acupuncture group of rabbits compared with the model group. The results of histochemical examination showed that HSP70 expression decreased in the sham operation group and increased in the model group. It increased significantly at every corresponding time point in the acupuncture group compared with the model group (P<0.01). The number of apoptotic cells increased gradually with reperfusion prolongation and reached the peak at three hours in the model group. The number of apoptotic cells decreased significantly at every time point in the acupuncture group and there was a statistically significant difference by comparison with the model group (P<0.01).Conclusions Electroacupuncture at points Taiyang and Fengchi can increase cerebral HSP70 expression and decrease neural cell apoptosis to produce a nerve-protecting effect in rabbits with cerebral ischemia-reperfusion injury.