Objective To observe the effect of electroacupuncture(EA) on blood-brain barrier(BBB) permeability and proinflammatory cytokines interleukin-1β(IL-1β) and interleukin-18(IL-18) in the hippocampus of vascular dementia(VD) rats

so as to explore the mechanism of EA on treatment of VD. Methods SD male rats were randomly divided into sham operation

model

and EA groups

with 15 rats in each group. The VD rat model was established by permanently occlusion of the bilateral middle cerebral artery. Rats of the EA group received EA at “Baihui”(GV20)

“Dazhui”(GV14)

and bilateral “Shenshu”(BL23) for 30 min

6 days a week for a total of 4 weeks. Morris water maze test was used to assess the cognitive function of rats. Evans blue staining was used to detect the BBB permeability

transmission electron microscopy and ELISA were used to detect the ultrastructure of BBB and the contents of hippocampal IL-1β and IL-18

respectively. Results Following modeling

compared with the sham operation group

the mean escape latency of model group was significantly prolonged(P<0.01)

the times of crossing the platform were significantly decreased(P<0.01)

the content of Evans blue

and the contents of IL-1β and IL-18 in hippocampus were increased(P<0.01). After the intervention

comparison between the model and EA groups showed that the average escape latency of rats in EA group was significantly shortened(P<0.01)

the times of crossing the platform were increased(P<0.05)

the content of Evans blue

and the contents of IL-1β and IL-18 in hippocampus were significantly decreased(P<0.01). The ultrastructure of BBB was moderately damaged in the model group

which was evidenced by blurred endothelial cell membrane structure

obviously dropsical astrocyte foot process

and decreased tight junctions. The ultrastructure of BBB was slightly damaged and astrocyte foot had no obvious edema in the EA group. Conclusion EA can significantly improve the learning and memory ability of VD rats and improve the BBB permeability

which may be related to its effect in inhibiting the expression of IL-1β and IL-18 in the hippocampus.