effect of electroacupuncture at distal–proximal acupoint combinations on spinal interleukin-1 beta in a rat model of neuropathic pain

Abstract

Objective: Pain from herniated disc is a common type of neuropathic pain. This study investigated whether electroacupuncture (EA) stimulation at distal–proximal combinations of acupoints in the rat model of neuropathic pain modulates spinal interleukin-1 beta (IL-1β) to induce acupuncture analgesia and possibly serve as a pain-relief modality for herniated disc. 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. EA 1 rats were needled at bilateral Ex-B2, BL25, BL40, and BL60 acupoints. EA 2 rats were needled at bilateral BL40 and BL60. EA 3 rats were needled at bilateral L5 Ex-B2 and BL25. EA stimulation was administered once daily over 7 days. Mechanical withdrawal threshold from noxious mechanical stimulation was measured 1 day preoperatively and at 3, 5, and 7 days postoperatively. After 7 days of intervention, enzyme-linked immunosorbent assay (ELISA) was used to quantify IL-1β in the spinal cord. Results: Mechanical withdrawal threshold of rats in the model group decreased at 3 days postoperatively when compared with the normal group (P < 0.01), lasting 7 days postoperatively. Mechanical withdrawal thresholds in the EA 1, EA 2, and EA 3 groups were elevated over the model group (P < 0.05; P < 0.01). No obvious differences were found between EA 1, EA 2, and EA 3 groups. ELISA demonstrated an increase in IL-1β in the spinal cord of rats in the model group compared with the normal group (P < 0.01). EA treatment attenuated the increase in spinal IL-1β in the model group. Expression of spinal IL-1β was significantly lower in EA 1, EA 2, and EA 3 groups. Conclusion: EA at distal + proximal acupoints, distal points, as well as proximal points attenuated upregulation of spinal IL-1β, alleviated the extent of neuropathic pain hypersensitivity, and promoted mechanical withdrawal threshold, resulting in EA analgesia.