从维甲酸信号途径探讨电针促进脑梗死大鼠神经功能恢复的研究

目的：检测维甲酸（retinoic acid,RA）蛋白及 RA mRNA在局灶性脑缺血再灌注大鼠脑组织中表达量的变化,探讨电针促进脑梗死大鼠神经功能恢复的机制。方法将144只成年雄性SD大鼠随机分为假手术组、模型组、针刺组各48只。建立大脑中动脉梗死模型（MCAO）,针刺组于术后24 h开始电针曲池、足三里穴。术后1 d、7 d、14 d、28 d使用 Homecage Scan监测系统观察大鼠舔毛、进食、行走、后肢站立4个行为的变化,Western blot及RT PCR法检测大鼠脑组织Raldh1、2各亚型蛋白及mRNA的表达。结果针刺组在术后7 d、14 d各项行为学评分与模型组比较有统计学意义（P〈0.05）,1 d、28 d两组各项评分比较无统计学意义。模型组及针刺组 Raldh1mRNA、Raldh2 mRNA的表达在术后第7天升高,第14天达到高峰,之后表达减少,至第28天趋于正常；针刺组7 d、14 d的 Raldh1mRNA、Raldh2 mRNA的表达同模型组比较有统计学意义（P〈0.05）；Raldh1、Raldh2蛋白的表达模式与 Raldh1 mRNA、Raldh2 mRNA的表达模式类似。结论电针能改善脑梗死大鼠的神经功能,其机制可能与调控 RA的表达有关。

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

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