Objective To observe the effect of manual acupuncture(MA)+ electroacupuncture(EA)on changes of neurological function and expression of monocarboxylate transporter 2(MCT2)in cerebral ischemia(CI)rats

so as to explore its mechanism underlying improvement of ischemic cerebrovascular disease.Methods Eighty male Wistar rats were equally randomized into four groups:normal control(normal)

sham operation(sham)

model and acupuncture.The CI model was induced by middle cerebral artery occlusion(MCAO)with a thread embolus.Manual acupuncture stimulation(mild twisting reinforcingreducing method)was applied to"Baihui"(GV20)and"Fengfu"(GV16)for 10 min.EA(1 mA

2 Hz/15 Hz)was respectively applied to bilateral"Quchi"(LI11)and"Zusanli"(ST36)for 20 min

once per day for 7 days.The neurological deficit severity was evaluated according to Zea Longa's methods.The activity of lactate dehydrogenase(LDH)

fructose-6-phosphate kinase(PFK)and pyruvate kinase(PK)in the peri-ischemic cortex tissue was detected by enzymatic chemistry

and the expression of MCT2 detected by immunofluorescence histochemistry

Western blot and quantitative real-time PCR

separately.Results After CI and in comparison with the normal and sham groups

the Zea Longa's score

the fluorescence intensity and the expression level of MCT2 protein were significantly increased(P<0.01)

and the activity of LDH

PFK and PK in the peri-ischemic cortex was significantly decreased in the model group(P<0.01).There was no significant change in the relative expression of MCT2 mRNA(P>0.05).Following the intervention and in comparison with the model group

the Zea Longa's score was considerably decreased in the acupuncture group(P<0.01)

the activity of LDH

PFK and PK

and the expression levels of MCT2 protein and mRNA were considerably or further up-regulated in the acupuncture group(P<0.01

P<0.05).Conclusion Acupuncture intervention can improve neurological function in CI rats

which is possibly related with its effects in up-regulating the expression of MCT2 and promoting the utilization of lactate in peri-ischemic cortex.