to exPlorethe relationshiP betweenthe exPressionof Fas/FasL andthe aPoPtosis in retinal ischemia/rePerfusion injuryof rats, as well asthetheraPeutic effectsof basic fibroblast growth factor（bFGF）onthe ischemic retina. ·METHODS:the modelsof retinal ischemia/rePerfusion injury were made bytransiently elevating intraocular Pressure(IOP). Atotalof 28 rats were divided into Normal GrouP andoPerative GrouP.the latter was subdivided into 1, 6, 12, 24, 48 and 72 hours grouPs after rePerfusion, in whichthe left eyesofthe rats were inthe ischemia/ rePerfusion grouPs andthe rightones were inthetreatment grouPs(bFGF intracameral injection). APoPtosis was assessed bytheterminal deoxynucleotidyltransferase-mediated dUTP- biotin nick-end labelling (TUNEL) method, andthe exPressionof Fas/FasL was studied by strePt avidin-biotin comPlex （SABC）immunohistochemistry. ·RESULTS: No Positive cells wereobserved inthe normal rats’ retinae, butthere were a significant numberoftUNEL Positive cells in 6-24 hours aftertransient ischemia followed by a decrease at 48 hours.the numberoftUNEL Positive cells reached a maximum at 24 hours after ischemia.the exPressionof Fas gradually increased as early as at 6 hours, reached a Peak at 24 hours,then decreased at 48 hours. Similarly,the exPressionof Fas ligand was at Peak in 24 - 48 hours in ganglion cell layer(GCL) and INLof retina. bFGF administered before rePerfusion inhibited aPoPtotsis and amelioratedthetissue damage. It also diminished Fas and FasL exPression in ischemic/rePerfused retina. ·CONCLUSION: Retinal ischemia-rePerfusion aftertransiently elevated IOP induced aPoPtosisof cells inthe retina. Fas/FasL may have an imPortant role inthe early eventsofthe aPoPtotic Pathways. bFGF can rescue retinal ganglion cells from retinal ischemia/rePerfusion injurythrough down- regulationof Fas and Fas ligand exPression and may rePresent an imPortant mechanism fortheraPeutic neuroProtection.