Objective To observe the effect of electroacupuncture(EA)intervention on the neurological function and the expression change of Slit-Robo GTPase-activating protein-1(srGAP 1)and cell division-cycle 42(Cdc 42)in the cortex of rats with cerebral ischemic injury(CIRI)

so as to explore the mechanism of EA in the management of cerebral infarction.Methods A total of 48 male Sprague Dawley(SD)rats were randomly and equally divided into control

model

non-acupoint EA and EA groups(n=12/group).The CIRI model was established based on the modified Zea Longa method.EA intervention was applied for 30 min

once a day for 14 days.Modified neurologic severity scores(mNSS)were assessed on day 1

3

7and 14 after modeling.Immunofluorescence assay was used to detect the immunoactivity and distribution of srGAP 1and Cdc 42 in the cortical ischemic region.Western blot was employed to detect the expression of srGAP 1and Cdc 42 in the affected cortex.Results The mNSS displayed that the neurological score in the EA group was significantly lower than that in the model group and non-acupoint EA group at the 7th d and 14 th d(P<0.01).Immunofluorescence results showed that cerebral srGAP 1and Cdc 42 were expressed mainly in the cytoplasm.The fluorescence intensity of srGAP 1of the EA group was significantly lower than that of the model group and non-acupoint EA group(P<0.01).Meanwhile the fluorescence intensity of Cdc 42 of the EA group was markedly higher than that in the model group and non-acupoint EA group(P<0.01).Western blot assay indicated that the expression level of srGAP 1in the model group was significantly higher than that of the control group(P<0.01)

and that of the EA group was much lower than those of the model group and non-acupoint EA group(P<0.01).There was no significant difference of srGAP 1expression levels between the non-acupoint EA group and the model group(P>0.05).Additionally

the protein expression of Cdc 42 in the model group was slightly higher than that of the control group(P>0.05)

and that of the EA group was significantly higher than those of the model group and non-acupoint EA group(P<0.01).There was no significant difference of Cdc 42 expression levels between the non-acupoint EA group and the model group(P>0.05).Conclusion Cerebral infarction induced increase of cerebral srGAP 1and decrease of Cdc 42 can be reversed by acupoint EA intervention in CIRI rats

which may be responsible for its effect in improving impaired neurological function after cerebral infarction.