Electroacupuncture Promoted Neurological Functional Recovery via Retinoic Acid Signaling Pathway in Rats with Cerebral Ischemia reperfusion Injury

doi:10.3969/j.issn.16721349.2014.07.041

Abstract：Objective To investigate the effects of electroacupuncture (EA)on the expression of retinoic acid(RA)mRNA and protein in the brain tissues after cerebral ischemia reperfusion inj ury.Methods One hundred and forty four Sprague Dawley (SD) rats were randomly divided into 3 groups:Sham group,model group (ischemic rats without EA stimulation)and EA group (ischemic rats with EA stimulation on ST36 and LI11).Transient middle cerebral artery occlusion (tMCAO)was produced for 120 min using the external carotid artery insertion method.Behavioral deficits were detected with high resolution digital analysis of 24 hour home cage video recordings.The expression of RA mRNA and protein were measured with RT PCR and western blotting,respectively.Results Neurological function was found to have improved in a time dependent manner in the EA and model groups (P<0.05).Time spent walking,rearing and grooming was increased,while time spent feeding was reduced in the EA group at 7 and 14 days after tMCAO(P<0.05)compared with the model group.No significant differences in neurological function were observed between the EA and model groups at 1 and 28 days after tMCAO (P>0.05).In the model group,Raldh1 and Raldh2 mRNA was greatly increased at 7 days, peaked at 14 days,and then gradually decreased.Additionally,in the model group,higher Raldh1 and Raldh2 mRNA levels were found at 7 and 14 days (P<0.05)compared with the sham group.In the EA group,the Raldh1 and Raldh2 mRNA levels were higher than those in the model group at 7 and 14 days (P<0.05).No significant differences were detected in the Raldh1 and Raldh2 mRNA expression levels between the EA and model groups at 1 and 28 days after tMCAO (P>0.05),and the pattern of protein expression of Raldh1 and Raldh2 was similar to their respective mRNA levels.Conclusion EA could promote neurological functional recovery and sugges-ted that this neuroprotective effect was attributed,at least in part,to the expression of RA mRNA and protein.