Abstract
The aim of the present study was to evaluate the effect of electroacupuncture (EA) on cognitive function following cerebral ischemia‑reperfusion (I/R) injury, and to clarify the mechanism through which Rho GTPase is associated with EA analgesia modulation of dendritic spine plasticity. Rats were randomly divided into three groups: The sham surgery group, the middle cerebral artery occlusion (MCAO) model of ischemia group, and the MCAO with EA (MCAO+EA) treatment group. The MCAO+EA group received treatment with EA at points of Baihui (DU20) and Shenting (DU24) following surgery. It was demonstrated that treatment with EA significantly (P<0.05) protected the cognitive function of rats from impairment caused by cerebral I/R injury. Furthermore, EA treatment increased the density of dendritic spines in the hippocampus of cerebral I/R‑injured rats. Simultaneously, EA increased the expression of cell division cycle 42, Ras‑related C3 botulinum toxin substrate 1 and F‑actin proteins. By contrast, EA treatment inhibited the expression of Ras homologous member A. Collectively, these findings suggest that Rho GTPases and dendritic spine plasticity are critical in mediating the effects of EA treatment at the points of Shenting and Baihui, and that EA protects against impairment of cognitive function following ischemic stroke.