title: Effect of ginkgolide B on striatal extracellular amino acids in middle cerebral artery occluded rats.
abstract: BACKGROUND
  Ginkgo biloba leaves are traditionally used in China for its health-promoting properties. There is substantial experimental evidence to support the view that Ginkgo biloba extracts have neuroprotective properties under conditions such as hypoxia/ischemia. Although a number of studies have investigated that ginkgolide B, a purified terpene lactone component extracted from Ginkgo biloba leaves, is available "platelet activating factor (PAF) receptors antagonist", "antioxidant" with a variety of actions, very little has been performed to explore the effect of ginkgolide B on extracellular amino acids in experimental animal of focal cerebral ischemia/reperfusion. In this study, the effect of ginkgolide B on the striatal extracellular levels of glutamate (Glu), aspartic acid (Asp), glycine (Gly) and γ-aminobutyric acid (GABA) was evaluated in rats undergone middle cerebral artery occlusion (MCAO) for 1h followed by 23 h reperfusion.
  
  
  METHODS
  The Sprague-Dawley (SD) rats received intraperitoneal injections of ginkgolide B dissolved at a dose of 10 mg kg(-1)d(-1), 20 mg kg(-1)d(-1), or normal saline (NS) of same volume 3d before the middle cerebral artery occlusion model establishment. Extracellular concentrations of glutamate, aspartic acid, glycine and GABA in striatum were monitored using in vivo microdialysis and analyzed using high-performance liquid chromatography. Excitotoxic index (EI) was calculated. Twenty-four hours after MCAO, the cerebral infarct volume was detected on 2,3,5-triphenyltetrazolium chloride-stained coronal sections.
  
  
  RESULTS
  The result showed that administration of ginkgolide B (10 or 20 mg kg(-1)) before ischemia reduced the ischemia-induced elevation of levels of glutamate, aspartic acid and glycine, increased the elevation of extracellular GABA, decreased the excitotoxic index and diminished the volume of cerebral infarction, although a clear concentration-response relationship was not found.
  
  
  CONCLUSIONS
  The present work provides the first evidence that ginkgolide B protects against cerebral ischemic injury by inhibiting excitotoxicity by modulating the imbalance of excitatory amino acids versus inhibitory amino acids, which may support the traditional use of Ginkgo biloba leaves for the treatment of stroke.
authors.affiliation: Ophthalmological Hospital of Xingtai, Xingtai 054001, China.
authors.forename: Zan Zhang
authors.initials: ZZ
authors.lastname: Yang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Shan Xue
authors.initials: SX
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Feng
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
mesh_terms: D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D020441:Ginkgo biloba / Q000737:chemistry*; D046934:Ginkgolides / Q000494:pharmacology / Q000627:therapeutic use*; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000378:metabolism; D007783:Lactones / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000596:Amino Acids; D046934:Ginkgolides; D007783:Lactones; D010936:Plant Extracts; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; C045856:ginkgolide B; D005998:Glycine