Acupuncture up-regulates MCT2 expression of peri-ischemic cortex in middle cerebral artery occlusion rats / 针刺研究

ABSTRACT

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 reinforcing-reducing 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 (P0.05). 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.