Supression of chronic central pain by superoxide dismutase in rats with spinal cord injury: Inhibition of the NMDA receptor implicated

Xie,Yong‑Gang; Mu,Hong‑Jie; Li,Zhen; Ma,Jia‑Hai; Wang,Yue‑Lan

doi:10.3892/etm.2014.1878

Supression of chronic central pain by superoxide dismutase in rats with spinal cord injury: Inhibition of the NMDA receptor implicated

Authors:
- Yong‑Gang Xie
- Hong‑Jie Mu
- Zhen Li
- Jia‑Hai Ma
- Yue‑Lan Wang
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Affiliations: Department of Anesthesiology, Qianfoshan Hospital, Affiliated to Shandong University Medical College, Jinan, Shandong 250014, P.R. China, Department of Orthopedics, Yantaishan Hospital Affiliated to Medical College of Taishan, Yantai, Shandong 264000, P.R. China, Department of Otorhinolaryngology, Yantaishan Hospital Affiliated to Medical College of Taishan, Yantai, Shandong 264000, P.R. China, Department of Anesthesiology, Yuhuangding Hospital Affiliated to Qingdao University Medical College, Yantai, Shandong 264000, P.R. China
Published online on: August 4, 2014 https://doi.org/10.3892/etm.2014.1878
Pages: 1137-1141

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Abstract

Superoxide dismutase (SOD) is used to manage chronic pain, including neuropathic and inflammatory pain. However, data regarding the clinical effectiveness are conflicting and the neurophysiological mechanism of SOD has yet to be elucidated. The aim of the present study was to investigate whether SOD relieved chronic central pain (CCP) following spinal cord injury (SCI) and the possible underlying mechanisms. A CCP model was established using the Allen method and the CCP of the rats was measured using the paw withdrawal threshold. SOD was administered intraperitoneally following the establishment of CCP as a result of SCI. The results demonstrated that SOD relieved CCP in rats following SCI. In addition, the expression of spinal phosphorylated N‑methyl‑D‑aspartate(NMDA) receptor subunit 1 (pNR‑1) was inhibited in the CCP rats that had been treated with SOD. These observations indicated that SOD reduced mechanical allodynia and attenuated the enhancement of spinal pNR1 expression in rats with CCP. In addition, the results indicated that superoxide, produced via xanthine oxidase, and the participation of superoxide and nitric oxide (NO) as a precursor of peroxynitrite in NMDA, were involved in the mediation of central sensitization. Therefore, the observations support the hypothesis that SOD may have a potential therapeutic role for the treatment of CCP following SCI via the manipulation of superoxide and NO.

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