OBJECTIVE: To investigate the role of spinal prostaglandin E2 (PGE2) in electroacupuncture (EA) analgesia and assess the theoretical basis for selection of acupoints in the treatment of neuropathic pain. METHODS: A rat model of neuropathic pain was established. Rats were randomly divided into normal, model, sham, EA 1, EA 2, and EA 3 groups. In EA 1 group, the rats were needled at bilateral L5 Jiaji (EX-B2), Dachangshu (BL 25), Weizhong (BL 40) and Kunlun (BL 60). In EA 2 group, the rats were needled at bilateral Weizhong (BL 40) and Kunlun (BL 60). In EA 3 group, the rats were needled at bilateral L5 Jiaji (EX-B2) and Dachangshu (BL 25). EA stimulation was administered once daily over 7 days. Motor function and thermal withdrawal latencies were evaluated at 1 day preoperatively and at 3, 5, and 7 days postoperatively. After 7 days of intervention, enzyme-linked immunosorbnent assay (ELISA) was used to quantify the expression of the spinal PGE2. RESULTS: Rats in the model group exhibited evident hyperalgesia in responses to thermal withdrawal latencies compared with those in the control group (P < 0.01), and EA reversed thermal withdrawal latencies (P < 0.01). The expression level of the spinal PGE2 was significantly higher in the model group than that in the control group and was reversed by EA (P < 0.01; P < 0.05). CONCLUSION: The effect of EA on neuropathic pain might alleviate the hyperalgesia state by an inhibition of local prostaglandin E2 secretion.
OBJECTIVE: To investigate the role of spinal prostaglandin E2 (PGE2) in electroacupuncture (EA) analgesia and assess the theoretical basis for selection of acupoints in the treatment of neuropathic pain. METHODS: A rat model of neuropathic pain was established. Rats were randomly divided into normal, model, sham, EA 1, EA 2, and EA 3 groups. In EA 1 group, the rats were needled at bilateral L5 Jiaji (EX-B2), Dachangshu (BL 25), Weizhong (BL 40) and Kunlun (BL 60). In EA 2 group, the rats were needled at bilateral Weizhong (BL 40) and Kunlun (BL 60). In EA 3 group, the rats were needled at bilateral L5 Jiaji (EX-B2) and Dachangshu (BL 25). EA stimulation was administered once daily over 7 days. Motor function and thermal withdrawal latencies were evaluated at 1 day preoperatively and at 3, 5, and 7 days postoperatively. After 7 days of intervention, enzyme-linked immunosorbnent assay (ELISA) was used to quantify the expression of the spinal PGE2. RESULTS:Rats in the model group exhibited evident hyperalgesia in responses to thermal withdrawal latencies compared with those in the control group (P < 0.01), and EA reversed thermal withdrawal latencies (P < 0.01). The expression level of the spinal PGE2 was significantly higher in the model group than that in the control group and was reversed by EA (P < 0.01; P < 0.05). CONCLUSION: The effect of EA on neuropathic pain might alleviate the hyperalgesia state by an inhibition of local prostaglandin E2 secretion.