title: Transcription factor Nrf2 protects the spinal cord from inflammation produced by spinal cord injury.
abstract: BACKGROUND
  Inflammation plays an important role in the pathogenesis of secondary damage after spinal cord injury (SCI). Previous studies have suggested that nuclear factor-erythroid 2-related factor 2 (Nrf2), a pleiotropic transcription factor, may play a key role in modulating inflammation in a variety of experimental models. This study evaluated the neuroprotective role of Nrf2 in the inflammatory response after SCI in mice.
  
  
  METHODS
  Nrf2-deficient (Nrf2(-/-)) and wild-type (Nrf2(+/+)) mice spinal cord compression injury was induced by the application of vascular clips (force of 10 g) to the dura. Sulforaphane (SFN) was used to activate Nrf2 after SCI. Inflammatory cytokines, NF-κB activity, histologic injury score, dying neurons count in grey matter, water content of impaired spinal cord, and Basso open-field motor score (BMS) were assessed to determine the extent of SCI-mediated damage.
  
  
  RESULTS
  The results showed that SFN activated Nrf2 in impaired spinal cord tissue, improved hindlimb locomotor function assessed by BMS, reduced inflammatory damage, histologic injury, dying neurons count, and spinal cord edema caused by SCI. Nrf2(-/-) mice demonstrated more severe neurologic deficit and spinal cord edema after SCI and did not benefit from the protective effect of SFN.
  
  
  CONCLUSIONS
  Taken together, our results suggest that Nrf2 may represent a strategic target for SCI therapies.
authors.affiliation: Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, PR China.
authors.forename: Lei
authors.initials: L
authors.lastname: Mao
authors.forename: Handong
authors.initials: H
authors.lastname: Wang
authors.forename: Xiaoliang
authors.initials: X
authors.lastname: Wang
authors.forename: Hong
authors.initials: H
authors.lastname: Liao
authors.forename: Xianzhong
authors.initials: X
authors.lastname: Zhao
mesh_terms: D000818:Animals; D016207:Cytokines / Q000096:biosynthesis; D004247:DNA / Q000378:metabolism; D004487:Edema / Q000517:prevention & control; D017879:Isothiocyanates; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009187:Myelitis / Q000517:prevention & control*; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000032:analysis; D051267:NF-E2-Related Factor 2 / Q000502:physiology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology; D013454:Sulfoxides; D013861:Thiocyanates / Q000494:pharmacology
chemical_list: D016207:Cytokines; D017879:Isothiocyanates; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; C495636:Nfe2l2 protein, mouse; D013454:Sulfoxides; D013861:Thiocyanates; D004247:DNA; D016660:NAD(P)H Dehydrogenase (Quinone); C491732:Nqo1 protein, mouse; C016766:sulforaphane