ABSTRACT
<p><b>OBJECTIVE</b>To observe the effects of electroacupuncture (EA) on the activation of microglia cells in the Lto Lspinal cord in rats with neuropathic pain, so as to investigate whether EA could inhibit the activation of spinal microglial cells and regulate the expression of brain-derived neurotrophic factor (BDNF) to achieve the analgesic effect.</p><p><b>METHODS</b>Forty male Sprague Dawley rats were randomly divided into a normal group, a sham-model group, a model group and an EA group, 10 rats in each one. The rats in the normal group received no treatment; the rats in sham-model group were treated with operation to exposure sciatic nerve for 2 to 3 min (no knot); the rats in the remaining groups were treated with model establishment of chronic constrictive injury (CCI). 7 days after model establishment, the rats in the EA group were treated with EA at "Zusanli" (ST 36) and "Yanglingquan" (GB 34), 30 min per time, once a day for consecutive 7 days. Only immobilization was used in the remaining groups the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of affected side feet were respectively measured before model establishment and 3 days, 5 days, 7 days, 10 days, 12 days and 14 days after model establishment; 14 days after model establishment, rats were sacrificed; the immunohistochemical method was used to measure the expression of Iba1 and BDNF in the sample of Lto Lspinal cord; real-time fluorescent quantitative PCR was used to measure the expression BDNF mRNA.</p><p><b>RESULTS</b>Compared with the sham-model group, the pain threshold was decreased significantly in the model group (<0.05), leading to hyperpathia. After EA treatment, compared with the model group, the pain threshold was increased significantly in the EA group (<0.05). 14 days after operation, the microglia cells in the Lto Lspinal cord, expression of BDNF and level of mRNA in the model group were significantly higher than those in the normal group and sham-model group (all<0.01); those in the EA group were significantly lower than those in the model group (all<0.01).</p><p><b>CONCLUSIONS</b>The analgesic effect on neuropathic pain is likely to be achieved by EA through inhibiting the activation of spinal microglia cells and down-regulating the expression of BDNF.</p>