title: Resuscitation from experimental traumatic brain injury by magnolol therapy.
abstract: BACKGROUND
  The purpose of the present study was to determine whether magnolol, a free radical scavenger, mitigates the deleterious effects of traumatic brain injury (TBI).
  
  
  METHODS
  Traumatic brain injuries were induced in anesthetized male Sprague-Dawley rats using fluid percussion, and the rats were divided into groups treated with magnolol (2 mg/kg, intravenously) or vehicle. A group of rats that did not undergo TBI induction was also studied as controls. Biomarkers of TBI, including glycerol and 2,3-dihydroxybenzoic acid, were evaluated by microdialysis. Infraction volume, extent of neuronal apoptosis, and antiapoptosis factor transforming growth factor β1 (TGF-β1) were also measured. Functional outcomes were assessed by motor assays.
  
  
  RESULTS
  Compared with the rats without TBI, the animals with TBI exhibited higher hippocampal glycerol and 2,3-dihydroxybenzoic acid. Relative to the vehicle-treated group, the magnolol-treated group showed decreased hippocampal levels of glycerol and hydroxyl radical levels. The magnolol-treated rats also exhibited decreased cerebral infarction volume and neuronal apoptosis and increased antiapoptosis-associated factor TGF-β1 expression. These effects were translated into improved motor function post TBI.
  
  
  CONCLUSIONS
  Our results suggest that intravenous magnolol injection mitigates the deleterious effects of TBI in rats based on its potent free radical scavenging capability, and the mechanism of anti-neuronal apoptosis is partly due to an increase in TGF-β1 expression in the ischemic cortex.
authors.affiliation: Department of Neurosurgery, Chi-Mei Medical Center, Tainan, Taiwan; Institute of Imaging and Biomedical Photonics, National Chiao-Tung University, Tainan, Taiwan.
authors.forename: Che-Chuan
authors.initials: CC
authors.lastname: Wang
authors.forename: Kao-Chang
authors.initials: KC
authors.lastname: Lin
authors.forename: Bor-Shyh
authors.initials: BS
authors.lastname: Lin
authors.forename: Chung-Ching
authors.initials: CC
authors.lastname: Chio
authors.forename: Jinn-Rung
authors.initials: JR
authors.lastname: Kuo
mesh_terms: D000818:Animals; D017209:Apoptosis; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D001930:Brain Injuries / Q000188:drug therapy*; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005990:Glycerol / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D062385:Hydroxybenzoates / Q000378:metabolism; D017705:Lignans / Q000627:therapeutic use*; D008297:Male; D023421:Models, Animal; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D001713:Biphenyl Compounds; D016166:Free Radical Scavengers; D062385:Hydroxybenzoates; D017705:Lignans; D018696:Neuroprotective Agents; D053773:Transforming Growth Factor beta1; C005498:magnolol; C009135:2,3-dihydroxybenzoic acid; D005990:Glycerol
keywords: Free radical scavenger; Magnolol; Neuronal apoptosis; Transforming growth factor β1; Traumatic brain injury