Abstract
ObjectiveTo 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. MethodsA 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. ResultsRats 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). ConclusionThe effect of EA on neuropathic pain might alleviate the hyperalgesia state by an inhibition of local prostaglandin E2 secretion.
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