title: Effects of secretome obtained from normoxia-preconditioned human mesenchymal stem cells in traumatic brain injury rats.
abstract: BACKGROUND
  The aim of the present study was to investigate whether secretome obtained from normoxia-preconditioned human mesenchymal stem cells causes attenuation of traumatic brain injury (TBI), induced by fluid percussion injury.
  
  
  METHODS
  Anaesthetized male Sprague-Dawley rats, immediately after the onset of fluid percussion TBI, were divided into two major groups and given the vehicle solution (1 mL) or secretome (500 µg) intravenously. Another group of rats was used as sham-operated controls. The functional outcome such as motor (maximum grasp angle) was evaluated by an inclined plane test. Cellular infarction volume was calculated by triphenyltetrazolium chloride staining. Neuronal loss, apoptosis, and neurotrophic factor such as vascular epithelial growth factor (VEGF) expression in the cortex were measured by immunofluorescence staining. All the parameters were assessed on Day 3 after injury.
  
  
  RESULTS
  Compared with those of the sham-operated controls, the motor deficits and cerebral infarction of rats after TBI were significantly attenuated by secretome therapy. The TBI-induced neuronal loss and apoptosis were also significantly reduced by secretome therapy. Furthermore, VEGF-positive cells in the ischemic cortex after TBI were further significantly increased by secretome therapy.
  
  
  CONCLUSIONS
  Our results demonstrate that intravenous injection of secretome from normoxia-preconditioned human mesenchymal stem cells may ameliorate TBI-induced rats by reducing neuronal cell loss and apoptosis and promoting VEGF production, resulting in functional outcome improvement. We also recommend that secretome from normoxia-preconditioned human mesenchymal stem cells could be a promising treatment strategy for traumatic brain injury.
authors.affiliation: Department of Intensive Care Unit, Liou-Ying Chi-Mei Medical Center, Southern Taiwan University, Tainan, Taiwan.
authors.forename: Tai-Jen
authors.initials: TJ
authors.lastname: Chuang
authors.forename: Kao-Chang
authors.initials: KC
authors.lastname: Lin
authors.forename: Chung-Ching
authors.initials: CC
authors.lastname: Chio
authors.forename: Che-Chuan
authors.initials: CC
authors.lastname: Wang
authors.forename: Chin-Ping
authors.initials: CP
authors.lastname: Chang
authors.forename: Jinn-Rung
authors.initials: JR
authors.lastname: Kuo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000150:complications / Q000473:pathology* / Q000628:therapy*; D002544:Cerebral Infarction / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D017077:Culture Media, Conditioned; D006801:Humans; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation / Q000379:methods*; D059630:Mesenchymal Stem Cells / Q000378:metabolism*; D009043:Motor Activity / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D017077:Culture Media, Conditioned; D042461:Vascular Endothelial Growth Factor A