title: [Protective effect of ginkgo biloba extract on cerebral ischemia/reperfusion injury in rats].
abstract: OBJECTIVE
  To study the effect of Ginkgo biloba extract (GbE) on dynamic equilibrium of free radicals and amino-acids in cortex of rats with cerebral ischemia/reperfusion (I/R) injury and its influence and characteristics to intracellular free calcium concentration ([Ca2+]i) in primary cultured hippocampal neuron of rats.
  
  
  METHODS
  Amino-acids were quantified by high performance liquid chromatographic (HPLC) analysis. Concentration of MDA and GSH-Px were determined by thiobarbituric acid (TBA) technique. SOD was assayed through xanthine method, and microfluoremetric technique was used to assay the change of [Ca2+]i and its characteristics.
  
  
  RESULTS
  Compared with the non-treated groups, at all time points (3 hrs after ischemia, 1 and 2 hrs after I/R separately), in the GbE treated groups, the levels of Glu, Asp and MDA were lower and SOD and GSH-Px were higher (P < 0.01 or P < 0.05), the GABA and Gly levels were lower in groups treated with middle (10 mg/kg) or high dosage (15 mg/kg) of GbE (P < 0.05). Compared with the group treated with small dosage GbE (5 mg/kg), Glu, Asp and MDA were lower and GABA, Gly, SOD and GSH-Px were higher in the groups treated with middle or high dosage of GbE (P < 0.05), while the difference in the latter two groups was insignificant. Level of [Ca2+]i in cultured neurons treated with 1 x 10(-5) mol/L glutamate combined 25 micrograms/ml GbE for 20s was lower with lower peak value and longer time for reaching the peak than that in neurons treated with 1 x 10(-5) mol/L glutamate alone. Besides, the time of decline phase was also shorter in the former, so the flatform stage was prolonged. The response was recovered by re-applying of glutamate after [Ca2+]i back to base line.
  
  
  CONCLUSIONS
  GbE can protect damaged neurons through keeping the balance of inhibitory/excitatory amino-acids, enhancing free radicals scavengers system, and inhibiting the effect of glutamate to [Ca2+]i.
authors.affiliation: Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022. hubo@hust.edu.cn
authors.forename: Bo
authors.initials: B
authors.lastname: Hu
authors.forename: Sheng-gang
authors.initials: SG
authors.lastname: Sun
authors.forename: Yuan-wu
authors.initials: YW
authors.lastname: Mei
mesh_terms: D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D020441:Ginkgo biloba / Q000737:chemistry*; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D008517:Phytotherapy; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000596:Amino Acids; D004365:Drugs, Chinese Herbal; D018696:Neuroprotective Agents; D013482:Superoxide Dismutase; D002118:Calcium