title: Intracranial injection of recombinant stromal-derived factor-1 alpha (SDF-1α) attenuates traumatic brain injury in rats.
abstract: OBJECTIVE
  This study was conducted to investigate the role of stromal-derived factor-1 alpha (SDF-1α) in a secondary brain injury after traumatic brain injury (TBI) in rats, and to further elucidate its underlying regulatory mechanisms.
  
  
  METHODS
  Male Sprague-Dawley rats underwent TBI for 30 min, and then received intracranial injections of recombinant SDF-1α, SDF-1α antibody, or saline as a vehicle control. At 24 h after TBI, brain tissues from the experimental animals were subjected to histology, immunohistochemistry, quantitative real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and western blot analyses.
  
  
  RESULTS
  TBI-induced brain edema and blood-brain barrier disruption were ameliorated by post-injury injections of SDF-1α. TBI-induced neuronal degradation and apoptosis, accompanied by increased cleaved caspase-3, cleaved PARP and Bax, and decreased Bcl-2 were found to be attenuated by SDF-1α injection. Nitric oxide (NO) and inducible nitric oxide synthase (iNOS) levels decreased in SDF-1α treated animals after TBI. SDF-1α repressed inflammatory responses by inhibiting the expression of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6. However, neutralizing the effect of SDF-1α with its antibody abolished these therapeutic alterations in TBI animals. Importantly, SDF-1α attenuated the brain lesion by affecting the ERK and NF-κB signaling pathways after mechanical head trauma in rats.
  
  
  CONCLUSIONS
  SDF-1α ameliorates mechanical trauma-induced pathological changes via its anti-apoptotic and anti-inflammatory action in the brain.
authors.affiliation: Department of Neurology, The First Affiliated Hospital of China Medical University, 155 North Nanjing Street, Shenyang, 110001, People's Republic of China.
authors.forename: Weifeng
authors.initials: W
authors.lastname: Sun
authors.forename: Jiafeng
authors.initials: J
authors.lastname: Liu
authors.forename: Yu
authors.initials: Y
authors.lastname: Huan
authors.forename: Chaodong
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001929:Brain Edema / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D054377:Chemokine CXCL12 / Q000494:pharmacology / Q000627:therapeutic use*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000893:Anti-Inflammatory Agents; D054377:Chemokine CXCL12; D016207:Cytokines; D011994:Recombinant Proteins; D009569:Nitric Oxide