Background: Electroacupuncture (EA) can promote nerve and vascular regeneration,
confer neuroprotection, inhibit apoptosis and inflammatory reactions, reduce oxidative stress
injury, regulate neurochemicals and inhibit the formation of brain oedema in cerebral ischemic.
However, the precise site of EA stimulation in the treatment of cerebral ischemic is unclear.
Objective: In the present study, we investigated the effect of EA at the acupoints of different
meridians in motor function recovery and the involvement of Vascular Endothelial Growth Factor
(VEGF), phosphorylated Protein Kinase B (P-Akt), phosphorylated endothelial nitric oxide
synthase (p-eNOS) and Platelet Endothelial Cell Adhesion Molecule-1(CD31) were examined in
the peri-infarction cortex of rats.
Methods: The Middle cerebral artery occlusion (MCAO) model or sham surgery was performed in
a total of Ninety male Sprague-Dawley rats. Rats were randomly divided into five groups: a sham
group, a middle cerebral artery occlusion (MCAO) group, a Yang meridian group, a Yin meridian
group and a combined Yang and Yin meridian group. EA stimulus was given during the middle
cerebral artery occlusion. The neurobehavioural function was measured using Modified Neurological
Severity Scores (mNSS), the rotarod test and the ladder rung walking test, and the protein
expression of VEGF, P-Akt, p-eNOS in the peri-infarction cortex was detected by Western blot.
Immunofluorescence was used to measure the vascular density of the peri-infarction cortex.
Results: EA at different meridian acupoints has no effect on the infarction volume, while EA at
Yin meridian acupoints significantly promoted neurobehavioural functional recovery, increased
the vascular density and enhanced protein kinase B/Endothelial nitric oxide synthase (Akt/eNOS)
phosphorylation and VEGF expression.
Conclusion: In the early stage of stroke, EA at Yin meridian acupoints can improve neurobehavioural
functional recovery and the mechanism of this effect may be related to the enhanced expression
of VEGF, P-Akt and p-eNOS in the peri-infarction cortex of rats.