4.5 Article

Involvement of α7nAChR in electroacupuncture relieving neuropathic pain in the spinal cord of rat with spared nerve injury

期刊

BRAIN RESEARCH BULLETIN
卷 137, 期 -, 页码 257-264

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2018.01.002

关键词

Electroacupuncture; alpha 7nAChR; IL-1 beta; CD11b; Neuropathic pain

资金

  1. National Natural Science Foundation of China [31060144]
  2. Talent Program of Department of Scientific and Technology, Jiangxi Province, China [20142BCBC22008]

向作者/读者索取更多资源

Alpha-7 nicotinic acetylcholine receptor (alpha 7nAChR) was reported to be involved in the modulation of neuropathic pain. Electroacupuncture (EA) has therapeutic effects on neuropathic pain induced by nerve injury, but the underlying mechanisms remain unclear. The present study was designed to investigate whether a7nAChR participates in the relieving effects of 2 Hz EA on neuropathic pain. Paw withdrawal threshold (PWT) was measured to study the EA-mediated analgesic effect in a rat model of spared nerve injury (SNI). The spinal alpha 7nAChR and IL-1 beta expression levels were determined by RT-PCR, Western blot analysis, and immunofluorescence staining. Additionally, immunofluorescence targeting the expression of CD11b, which is a molecular indicator of microglial activation. The results showed that 2 Hz EA stimulation significantly improved the expression of alpha 7nAChR and reduced the production of IL-1 beta and CD11b in the spinal cord of rats with SNI-induced neuropathic pain, along with the relief of mechanical hypersensitivity after EA treatment. Moreover, intrathecal injection of alpha-bungarotoxin (alpha-Bgtx), a selective antagonist for alpha 7nAChR, at the dosage of 1.0 mu g/kg, not only suppressed the analgesic effect of EA in SNI rats, but also inhibited the enhancement of alpha 7nAChR expression and the reduction of IL-1 beta expression induced by EA. In conclusion, our study indicated that 2 Hz EA reduces SNI-induced mechanical hypersensitivity via upregulating alpha 7nAChR and downregulating IL-1 beta and CD11b in the spinal cord of SNI rats, which might be one of the mechanisms underlying its effectiveness in the neuropathic pain.

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