Objective To observe the effect of deep electroacupuncture(EA)at"Huantiao"(GB 30)on functional and pathological changes of the damaged sciatic nerve and apoptosis-related factors in lumbar dorsal root ganglia(DRGs)in rats

so as to study its mechanisms underlying relieving sciatica.Methods Forty-eight SD rats were randomly divided into normal

model

deep EA(DEA)and shallow EA(SEA)groups(n=12 in each group).The sciatic nerve injury model was established by silicone tube extrusion of the sciatic nerve stem.For DEA group

acupuncture needles were inserted into GB 30 about 8 mm deep to induce nerve impulse under the guidance of high-frequency ultrasound

and the needles were inserted into GB 30 about 3—5 mm in the SEA group.The EA treatment was applied to bilateral GB 30 for 20 min beginning from the 15 th day on after modeling

once daily for 14 days.The sciatic nerve function index(SFI)and motor nerve conduction velocity(MNCV)were recorded and calculated.Pathological changes of the sciatic nerve were displayed by H.E.staining.The cell apoptosis and expression of PI 3 Kand AKT proteins in lumbar 4—5 DRGs were detected by TUNEL staining

and immunohistochemistry

respectively.Results In comparison with the normal group

the SFI and MNCV were significantly decreased(P<0.01

P<0.05)

the number of neuronal apoptosis and the expression of PI 3 Kand AKT in L 4—L 5 DRGs were significantly increased in the model group(P<0.05).Following the treatment

the SFI

MNCV

and the number of neuronal apoptosis were reversed compared with the model group(P<0.01

P<0.05)

both PI 3 Kand AKT expression levels were significantly up-regulated in both DEA and SEA groups(P<0.05).The therapeutic effects were significantly better in the DEA group than in the SEA group in down-regulating cell apoptosis number and in up-regulating SFI

MNCV

and PI 3 Kand AKT protein expression on day 28 of modeling(P<0.01

P<0.05).Conclusion Deep EA at GB 30 can activate PI 3 K-AKT signaling pathway

inhibit the apoptosis of nerve cells in DRGs after sciatic nerve injury in rats

which may contribute to its effect in improving neurological impairment.