title: Cysteinyl-leukotriene receptor antagonist montelukast decreases blood-brain barrier permeability but does not prevent oedema formation in traumatic brain injury.
abstract: BACKGROUND
  Traumatic brain injury is highly associated with the over-production of reactive oxygen species. The aim of this study was to investigate the putative neuroprotective effect of montelukast, a cysteinyl-leukotriene receptor antagonist, in a rat model of traumatic brain injury (TBI).
  
  
  METHODS
  Sprague Dawley rats were subjected to TBI with a weight-drop device using 300 g-1 m weight-height impact. The groups were: control (saline), montelukast (10 mg kg(-1) per day, ip), trauma and trauma + montelukast. Two days post-trauma, neurological examination scores were measured and animals were decapitated and the brain tissues were taken for the histologic and biochemical [malondialdehyde (MDA)-an index for lipid peroxidation, reduced glutathione (GSH), myeloperoxidase (MPO)-an index for neutrophil infiltration and Na+/K+-ATPase activity] evaluations. Brain oedema and blood-brain barrier (BBB) permeability were also evaluated.
  
  
  RESULTS
  The neurological examination scores mildly increased in trauma groups at 48 hours. Although the scores were decreased in the montelukast treated group, they were still significantly higher than the control. The trauma caused a significant increase in brain water content and Evans blue (EB) extravasation. Montelukast treatment reduced BBB permeability. It also decreased lipid peroxidation and MPO activity.
  
  
  CONCLUSIONS
  The present study suggests that montelukast may have beneficial effects against TBI-induced oxidative stress of the brain.
authors.affiliation: Department of Neurosurgery, Haydarpasa Numune Teaching and Research Hospital, Haydarpasa, Istanbul, Turkey.
authors.forename: Necat
authors.initials: N
authors.lastname: Biber
authors.forename: Hale Z
authors.initials: HZ
authors.lastname: Toklu
authors.forename: Seyhun
authors.initials: S
authors.lastname: Solakoglu
authors.forename: Mine
authors.initials: M
authors.lastname: Gultomruk
authors.forename: Tayfun
authors.initials: T
authors.lastname: Hakan
authors.forename: Zafer
authors.initials: Z
authors.lastname: Berkman
authors.forename: F Gul
authors.initials: FG
authors.lastname: Dulger
mesh_terms: D000085:Acetates / Q000494:pharmacology*; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001929:Brain Edema / Q000209:etiology / Q000517:prevention & control*; D001930:Brain Injuries / Q000150:complications*; D003521:Cyclopropanes; D007155:Immunologic Factors / Q000494:pharmacology*; D020024:Leukotriene Antagonists / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D010539:Permeability; D011804:Quinolines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides
chemical_list: D000085:Acetates; D003521:Cyclopropanes; D007155:Immunologic Factors; D020024:Leukotriene Antagonists; D018696:Neuroprotective Agents; D011804:Quinolines; D013440:Sulfides; C093875:montelukast