title: [An experimental study of the therapeutical effect of bFGF in retinal ischemia/reperfusion injury].
abstract: OBJECTIVE
  To investigate the therapeutical effect of basic fibroblast growth factor (bFGF) on retina ischemia/reperfusion injury.
  
  
  METHODS
  Experimental retinal ischemia/reperfusion injury was induced by increasing intraocular pressure of rats eyes. 48 rats were divided into groups of control, ischemia/reperfusion and bFGF-treated, randomly. Apoptotic cells were detected using the TdT-dUTP terminal nick-end labeling at 1 hour, 6 hours, 12 hours, 24 hours, and 72 hours after reperfusion. The expression of caspase-3 at specified times was determined by Streptavidin Peroxidase immunohistochemistry. Atomic absorption spectrum method was used to evaluate the intracellular calcium changes of retinal tissues.
  
  
  RESULTS
  In ischemia group, apoptotic cells began to appear at 6th hour after reperfusion and increased progressively with time. The number of apoptotic cells reached the peak 24 hour after reperfusion, and no apoptotic cells could be found at 72 hours. Changes in caspase-3 expression followed a similar trend. The intracellular calcium level of rat retina began to increase at 1 hour after reperfusion, and continued to increase with the reperfusion time. At 24 hours after reperfusion the intracellular calcium level reached the peak, and decline thereafter up to 72 hours. The patterns of change of the three markers of treatment group were similar to the above. However, the magnitude of changes was relatively lower. A statistically significant difference (P < 0.05) between the ischemia group and treatment group at 6th, 12th and 24th after reperfusion was observed.
  
  
  CONCLUSIONS
  Apoptosis may play a vital role in ischemia-reperfusion injury of the retina. bFGF may have a therapeutical effect on ischemia-reperfusion injury by inhibiting the increase of retinal intracellular calcium stores and caspase-3 protein expression.
authors.affiliation: Department of Ophthalmology, Affiliated Hospital, Qingdao University Medical College, Qingdao 266003, China. niuyingjun@yahoo.com.cn
authors.forename: Ying-jun
authors.initials: YJ
authors.lastname: Niu
authors.forename: Yan-song
authors.initials: YS
authors.lastname: Zhao
authors.forename: Yun-xia
authors.initials: YX
authors.lastname: Gao
authors.forename: Zhan-yu
authors.initials: ZY
authors.lastname: Zhou
authors.forename: Hong-yun
authors.initials: HY
authors.lastname: Wang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000627:therapeutic use*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy*; D012164:Retinal Diseases / Q000188:drug therapy*
chemical_list: D016222:Fibroblast Growth Factor 2; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases; D002118:Calcium