Anti-apoptotic Mechanism of Deep Electroacupuncture at "Huantiao" (GB 30) in Repair of the Injured Sciatic Nerve in Rats

Abstract

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. Forty-eight SD rats were randomly divided into normal, mo-del, 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 15th 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 K and AKT proteins in lumbar 4-5 DRGs were detected by TUNEL staining, and immunohistochemistry, respectively. 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 K and 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 K and 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 K and AKT protein expression on day 28 of modeling (P<0.01，P<0.05). 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.