| [Objective] To study the therapeutic effects of basic fibroblast growth factor (bFGF) on the ischemia-reperfusion injury of retina by exploring the effects on the expression of Fas, FasL, caspase-2 and apoptosis occurs in retinal ischemia-reperfusion injury of rats. [ Methods ] Rat models of retinal ischemia-reperfusion injury was made by transient elevating introcular pressure. 28 rats were divided into normal groups and disposal groups. The latter were then subdivided into 1,6, 12,24,48 and 72h after reperfusion groups, in which the left eyes of rats was ischemia-reperfusion groups and the right ones was bFGF treatment groups. The expression of Fas, FasL and caspase-2 was studied by strept avidin-biotin complex (SABC) immunohistochemistry. [Results] No Fas positive cells were observed in the normal retina, Fas expression gradually increased as early as 6 h, reached a peak at 24 h, then decreased at 48 h. Similarly, FasL expression was at peak in 24-48h in GCL and INL of retina. And the peak of caspase-2 expression was reached at 24h, then decreased gradually. bFGF ministered before reperfusion ameliorated the retinal tissue damage. It also diminished Fas, FasL and caspase-2 expression in ischemic-reperfused retina remarkably. Fas expression decreased markedly 'in 6,12, 24h treatment groups. bFGF diminished FasL expression at 12, 24, 48h, caspase-2 expression at 6,12, 24, 48 and 72h. [Conclusions] Retinal ischemia-reperfusion after transient IOP induced elevated expression of Fas, FasL and caspase-2 in the retina. Fas, FasL and caspase-2 may have a pivotal role in the early events of the retinal ganglion cells(RGCs) apoptotic pathway(s) in ischemia-reperfusion injury. FGF can rescue RGCs from retinal ischemia-reperfusion injury through downregulation of Fas, FasL and caspase-2 expression and may represent an important mechanism for therapeutic neuroprotection.
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