Objective To observe the effect of electroacupuncture(EA)on expressions of nerve growth factor(NGF)and growth arrest-specific protein 7(Gas 7)in the right ventral posterolateral nucleus(VPL)in the focal cerebral ischemia(FCI)rats

so as to explore its possible mechanism underlying improvement of secondary injury of FCI.Methods Forty-eight SpragueDawley rats were randomly divided into normal group

sham operation group

model group and electroacupuncture(EA)group(n=12in each group)by random number table.The FCI model was made by occlusion of the right middle cerebral artery(MCAO)with thread embolus.One week after MCAO

EA(2Hz

2V)was performed on "Baihui"(GV 20)and left"Zusanli"(ST 36)for30min

once daily for successively 21 days.The expressions of NGF and Gas 7in the right VPL were detected by immunohistochemistry(n=6in each group)and Western blot(n=6in each group)

respectively;meanwhile Nissl staining was conducted to show VPL neurons.Results Nissl staining showed that the structure of right VPL was clear and complete

and the nuclei were centered and clear in the normal group and sham operation group;the VPL neurons were deeply stained

and the nuclei were pyknotic in the model group;the morphology of neurons in the EA group was similar to that of the normal group.The results of immunohistochemistry and Western blot were consistent.Expressions of NGF and Gas 7proteins in the right VPL were not of significant differences between the sham operation group and the normal group(P>0.05).Compared with the normal group

the expressions of NGF and Gas 7proteins in the VPL of the ischemic side were significantly increased in the model group(P<0.05).After treatment

the expression levels of NGF and Gas 7 proteins were further up-regulated in the EA group in comparison with the model group(P<0.05).Conclusion The enhanced expressions of NGF and Gas 7in the ischemic VPL of FCI rats may be involved in the neuroprotection and repairing;EA can significantly up-regulate the expressions of NGF and Gas 7in VPL of the ischemic side

which may contribute to its effect in improving secondary thalamic impairment of FCI.