Effect Of Electro-acupuncture On Expression Of SrGAP1 And Cdc42 In Rat Cortex After Cerebral Infarction

Background:Stroke is one of the three major diseases which endangers the human life and health,and it is the primary cause of death and disability in worldwide population. Stroke is the traditional acupuncture treatment in China,which has been widely proved to have definite clinical efficacy,but we need more research on its mechanism. Stroke recovery is related to neural plasticity, and effects of axon guidance factor on neural plasticity is one of the hotspot.On the basis of it, to observe the expression of Slit-Robo GTPase-activating protein(srGAP1) and celldivisioncycle42(Cdc42) in the cortex of rats after middle cerebral occlusion(MCAO),and determine the effect of electro-acupuncture(EA) intervention in the recovery of nerve function, so as to explore the mechanism of electro-acupuncture in neural plasticity after cerebral infarction.Objective:1. To observe the effect of electroacupuncture on neural function after modified neurological severity scores(mNSS);2. To observe the effect of the expression of srGAP1 and Cdc42 after electroacupuncture; 3.To explore the mechanism of electroacupuncture on cerebral infarction. Methods:48 male Sprague Dawley(SD) rats were absolutely divided into four groups:control group(n= 12), model group(n= 12), non acupoints EA group(non acupoints group)(n=12) and EA group(n=12). Using the improved Longa method to sift the MCAO, and further assigned into 4 time point(1d,3d,7d and 14d)for postoperative rats,which were evaluated neurologic injury at every time point by modified neurologic severity scores(mNSS). Immunofluorescence assay was used to detect the fluorescence intensity and distribution of srGAP1 and Cdc42 in the cortical ischemic region. Western blotting was employed to detect the expression of srGAP1 and Cdc42 in the affected cortex.Results:The mNSS displayed that the control group had not neurologic deficit. EA group had obviously differences with model group and non acupoints group at 7d,14d(P<0.01).But there was no differences between Model group and non acupoints group. Immunofluorescence results showed that srGAP1 and Cdc42 expressed mainly in the cytoplasm.The fluorescence intensity of srGAP1 in EA group was significantly lower than that in the model group and non acupoint group (p<0.01), model group and non acupoint group were higher than the control group(p<0.01). The fluorescence intensity of Cdc42 EA group was higher than that in the model group and non acupoint group (p<0.01), model group and non acupoint group were lower than the control group(p<0.01). Western blotting indicated that srGAP1 in the model group was obviously higher than control group (P<0.01),and the EA group was significantly lower than model group and non acupoint group(p<0.01).There was no significant difference between non acupoint group and model group(P> 0.05).The protein expression of Cdc42 in the model group was a little higher than control group (P>0.05),and EA group was obviously higher than model group, non acupoint group and control group(p<0.01). There was no significant difference between non acupoint group and model group(P> 0.05).Conclusion:Cerebral infarction made srGAP1 increase and Cdc42 decrease,but after EA intervention,srGAP1 was down-regulated and Cdc42 was up-regulated. It may be related to srGAP1 inactivated Cdc42.This may be one of mechanisms of EA promotes the recovery of neurological function after cerebral infaction.