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

Pain. 2006 May;122(1-2):53-62. doi: 10.1016/j.pain.2006.01.013. Epub 2006 Mar 9.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analgesics / administration & dosage
  • Animals
  • Behavior, Animal / drug effects*
  • Evoked Potentials, Somatosensory / drug effects*
  • Male
  • Neuralgia / diagnosis
  • Neuralgia / drug therapy*
  • Neuralgia / physiopathology*
  • Pain Threshold / drug effects*
  • Rats
  • Rats, Sprague-Dawley
  • Spinal Cord / drug effects*
  • Spinal Cord / physiopathology*
  • Treatment Outcome
  • Vitamin E / administration & dosage


  • Analgesics
  • Vitamin E