Objective The present study aimed at observing the effect of moxibustion pretreatment on the expression of cerebral microRNAs and Aquaporin protein-4(AQP 4)in rats with cerebral ischemia and reperfusion(CI/R)

so as to reveal its mechanism underlying improvement of cerebral infarction.Methods A total of 130 Wistar rats were randomly divided into blank control(n=10)

CI/R model(n=30)

electroacupuncture(EA

n=30)

moxibustion(n=30)

Aspirin groups(n=30).Before modeling

EA(2Hz/5Hz

1-2mA)or moxibustion was applied to"Baihui"(GV 20)

"Fengfu"(GV 16)and"Dazhui"(GV 14)for 20 min

once daily for 7days.The rats of the Asprin group were treated by intragastric administration of Aspirin(10mg/kg

1mg/mL)

once daily for 7days before modeling.The CI/R model was established by occlusion of the bilateral carotid arteries.The expression levels of cerebral miRNAs and AQP 4were detected by real-time PCR and Western blot

respectively.ResultsCompared with the blank control group

the expression levels of cerebral miRNA 290 and miRNA 494 were significantly reduced

while that of AQP 4was obviously up-regulated in the model group(P<0.01).After pretreatment with EA and moxibustion

the relative expression levels of miRNA 290 and miRNA 494 were significantly higher in the EA

moxibustion and Aspirin pretreatment groups than in the model group(P<0.01)

while cortical AQP 4expression levels were significantly lower in the EA

moxibustion and Aspirin pretreatment groups than in the model group(P<0.01

P<0.05).The effects of both EA and moxibustion groups were significantly superior to those of Aspirin pretreatment group in up-regulating expression of miRNA 290 and miRNA 494 and down-regulating expression of AQP 4(P<0.01

P<0.05).In addition

the EA pretreatment was markedly superior to moxibustion pretreatment in the aforementioned effects(P<0.05).Conclusion EA pretreatment of GV 14

GV 16 and GV 20 can effectively up-regulate cerebral cortical miRNA 290 and miRNA 494 and down-regulate AQP 4in CI/R rats

which may contribute to its effect in preventing the cerebral tissue from ischemia/reperfusion injury.