Objective To observe the effect of electroacupuncture(EA)stimulation on the expression of c-Jun terminal kinase(JNK)signaling pathway-related proteins in the hippocampus of vascular dementia(VD)rats

so as to explore its mechanisms underlying improvement of VD.Methods Male Sprague-Dawley rats were randomly divided into sham operation

model and EA groups(n=10 rats per group).The VD model was prepared by repeated occlusion of the bilateral common carotid arteries for10 min and reperfusion for 10 min(3 times in total).The rats in the EA group received EA(2 Hz

2 mA)at "Dazhui"(GV14)

"Baihui"(GV20)

and bilateral"Housanli"(ST36)

"Geshu"(BL17)for 10 min

once daily for 14 days.The learning-memory ability was detected by Morris water maze tests

the distribution of hippocampal neurons detected by Nissl staining

and the apoptosis of hippocampal neurons detected by using TdT-mediated dUTP nick-end labeling(TUNEL)method.The expressions of JNK

phosphorylated JNK(p-JNK)

cysteine-containing aspartate-specific proteases-8(Caspase-8)and Caspase-3 proteins were detected by Western blot.Results After modeling and compared with the sham operation group

the escape latency was significantly prolonged(P<0.01)and the number of safe-platform quadrant crossing obviously decreased(P<0.01)

suggesting a reduction of learning-memory ability.The number of hippocampal neurons was considerably reduced(P<0.01)

and that of hippocampal apoptotic neurons remarkably increased in the model group(P<0.01).Whereas

the expression levels of hippocampal apoptosis-related proteins as JNK

p-JNK

Caspase-8 and Caspase-3

as well as the apoptotic index were significantly up-regulated(P<0.01).Following EA intervention

the learning-memory ability was apparently improved(P<0.01)

and the number of hippocampal neurons was considerably increased(P<0.01)

the hippocampal apoptotic cell number

apoptosis index and the expression levels of JNK

p-JNK

Caspase-8 and Caspase-3 were significantly down-regulated(P<0.01).Conclusion EA intervention can improve the learning-memory ability of VD rats

which may be associated with its effects in reducing hippocampal apoptosis by suppressing JNK signaling pathway.