Objective To observe the effect of electroacupuncture(EA)on morphological changes of denervated gastrocnemius(GS)and the expression of fork-head protein(FOXO3 A)

muscle atrophy F-box(MAFbx)and myogenic differentiation antigen(Myod1)in sciatic nerve injury rats

so as to reveal its mechanism underlying improvement of myoatrophy.Methods Eighteen male Sprague-Dawley rats were randomly divided into sham operation

model and EA groups(n=6 per group).The model of gastrocnemius atrophy was established by crushing the right sciatic nerve.Then

EA(2 Hz)was applied to the right"Zusanli"(ST36)and"Huantiao"(GB30)for 10 min

once a day for 14 successive days.The wet weight of the GS on both sides was weighted to calculate the wet weight ratio(the injured side/the healthy side)

and the cross-sectional area(CSA)and diameter of GS fibers were measured after H.E.staining.The expressions of FOXO3 A

MAFbx and Myod1 protein and mRNA in the GS tissue were tested using Western blot and fluorescence quantitative PCR

separately.Results Following modeling

the GS wet weight ratio

CSA and fiber diameter were smaller in the model group than those in the sham group(P<0.01)

and were significantly higher in the EA group than in the model group(P<0.01).H.E.staining showed that the GS fibers became smaller and the myocyte got round in the model group

while the GS fibers were bigger and the myocyte was relatively regular in morphology in the EA group.After modeling

the expression levels of FOXO3 A

MAFbx and Myod1 mRNA and protein were evidently higher in the model group(P<0.01);Moreover

after EA treatment

modeling-induced increasing of expression levels of FOXO3 Aand MAFbx mRNA and protein were revised(P<0.01)

while the increased expression level of Myod1 was further up-regulated relavant to that in the model group(P<0.01).Conclusion EA of ST36 and GB30 can suppress the up-regulated expression of FOXO3 Aand MAFbx mRNA and protein and further promote the expression of Myod1 mRNA and protein in the GS tissue in rats with denervated GS atrophy

which may contribute to its function in relieving the myoatrophy

promoting the skeletal muscle protein hydrolysis and differentiation of satellite cells.