ObjectiveTo investigate the effect of electroacupuncture(EA)on muscular atrophy and expression of microRNAs(Mir-1

Mir-133 a

Mir-133 b)and some proliferation-related factors of muscle satellite cells as histone deacetylase4(HDAC4)and the paired box transcription factor Pax7(Pax7)in skeletal muscle atrophy rats.Methods Twenty-four male SD rats were randomly and equally divided into sham operation

model and EA groups. The skeletal muscle atrophy model was established by transection of the right sciatic nerve. EA(2 Hz

1 mA)was applied to the right"Zusanli"(ST36)and"Huantiao"(GB30)for 10 min

once a day

seven times a week for 2 weeks. The wet weight of bilateral gastrocnemius muscles was measured to calculate the ratio of weight between the affected gastrocnemius muscle and healthy gastrocnemius muscle. The cross-sectional area(CSA)of the gastrocnemius muscle on the affected side was measured after H. E. staining. The expression levels of Mir-1

Mir-133 a

Mir-133 b

HDAC4 mRNA and Pax7 mRNA in the gastrocnemius muscle tissue were detected using quantitative real time-PCR.ResultsCompared with the sham operation group

the ratio of wet weight and CSA of the gastrocnemius muscle

and the expression levels of Mir-1 and Mir-133 a were significantly decreased in the model group(P<0. 01

P<0. 05)

while the expression levels of HDAC4 mRNA and Mir-133 b significantly up-regulated in the model group(P<0. 05). Following EA intervention

the decreased levels of the ratio of wet weight and CSA of the gastrocnemius muscle were significantly suppressed(P<0. 01)

suggesting an inhibition of the skeletal muscle atrophy

and the expression levels of Pax7 and HDAC4 mRNAs were notably upregulated(P<0. 05)

and those of Mir-1

Mir-133 a and Mir-133 b were significantly or further significantly down-regulated relevant to the model group(P<0. 05).ConclusionEA intervention can delay muscular atrophy in rats with denervated gastrocnemius muscle

which may be related with its function in up-regulating the expression of Pax7 and HDAC4 mRNAs and down-regulating the expression of Mir-1

Mir-133 a and Mir-133 b.