title: Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats.
abstract: OBJECTIVE
  Baicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH.
  
  
  METHODS
  Subarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter-1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7.
  
  
  RESULTS
  Mortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress.
  
  
  CONCLUSIONS
  Early baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.
authors.affiliation: Department of Anesthesiology.
authors.forename: Chang-Po
authors.initials: CP
authors.lastname: Kuo
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Wen
authors.forename: Chun-Mei
authors.initials: CM
authors.lastname: Chen
authors.forename: Billy
authors.initials: B
authors.lastname: Huh
authors.forename: Chen-Hwan
authors.initials: CH
authors.lastname: Cherng
authors.forename: Chih-Shung
authors.initials: CS
authors.lastname: Wong
authors.forename: Wen-Jinn
authors.initials: WJ
authors.lastname: Liaw
authors.forename: Chun-Chang
authors.initials: CC
authors.lastname: Yeh
authors.forename: Bo-Feng
authors.initials: BF
authors.lastname: Lin
authors.forename: Ching-Tang
authors.initials: CT
authors.lastname: Wu
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D027342:Excitatory Amino Acid Transporter 2 / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology / Q000627:therapeutic use*; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D027342:Excitatory Amino Acid Transporter 2; D005419:Flavonoids; D018696:Neuroprotective Agents; C493395:Slc1a2 protein, rat; C413305:baicilein; D018698:Glutamic Acid; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase