Analgesic effect of vitamin E is mediated by reducing central sensitization in neuropathic pain

Hee Kee Kim, Jae Hyo Kim, Xiu Gao, Jun Li Zhou, Inhyung Lee, Kyungsoon Chung, Jin Mo Chung

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

Recent studies suggest that reactive oxygen species (ROS) are critically involved in neuropathic pain. Although vitamin E is a well-known antioxidant, its efficacy on chronic pain is not known. This study investigated the efficacy and mechanisms of vitamin E analgesia in a rat model of neuropathic pain produced by spinal nerve ligation. The effects of vitamin E were investigated using behavioral testing, electrophysiological recording of dorsal horn neurons, and determinations of phosphorylated NMDA receptor subunit 1 (pNR1) levels in the spinal dorsal horn. Results showed that a systemic single injection of a high dose or repetitive daily injections of low doses of vitamin E significantly reduced neuropathic pain behaviors. Vitamin E was also effective in producing analgesia by intrathecal injection, suggesting the importance of spinal mechanisms. In spinal dorsal horn neurons, vitamin E reduced evoked responses to mechanical stimuli as well as the sizes of their receptive fields. In addition, levels of pNR1 in neuropathic rats were also reduced by vitamin E injection. These data suggest that vitamin E produces analgesia in neuropathic rats that is, at least in part, mediated by reducing central sensitization which, in turn, is induced by peripheral nerve injury.

Original languageEnglish (US)
Pages (from-to)53-62
Number of pages10
JournalPain
Volume122
Issue number1-2
DOIs
StatePublished - May 1 2006

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Keywords

  • Analgesia
  • Antioxidant
  • Free radical scavenger
  • Mechanical allodynia
  • ROS

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine

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