缺血-再灌注损伤后视网膜形态学改变和Bcl-2/Bax表达

目的观察视网膜缺血-再灌注损伤后的形态学变化;探讨Bcl-2/Bax表达与视网膜神经节细胞数量的关系。方法建立Wistar大鼠视网膜缺血-再灌注模型,计数其再灌注后1、6、12、24、48、72 h的视网膜神经节细胞(RGC);免疫组化SP法检测同时段凋亡相关蛋白Bcl-2、Bax的表达。结果大鼠缺血-再灌注后RGC计数在6 h时开始大量减少,6~12 h快速减少,24 h后呈慢速减少。再灌注6、12、24、48、72h的Bcl-2、Bax蛋白阳性表达结果与正常组比较,有显著差异(P<0.05)。再灌注后6、12 h Bcl-2/Bax比率上升,24、48、72 h下降。结论视网膜缺血再灌注后RGC凋亡与Bcl-2/Bax表达有关。

Change of Morphology and Bcl-2 / Bax after Retinal Ischemia-reperfusion Injury

Objective To observe the morphological change of the retina and to study the relation be-twwen the change of Bcl-2 / Bax and that of retinal ganglion cel(lRGC)after retinal ischemia-reperfusion injuryin rat. Methods The models of retinal ischemia-reperfusion injury in rats were made. The change of RGC in dif-ferent time after retinal ischemia-reperfusion injury was observed and the expression of Bcl-2 and Bax in the retinawas studied. Results The number of RGC reduced significantly due to the retinal ischemia-reperfusion injury.The initial loss of RGC accelerated after 6 hours and then declined gradually by 24 hours. The expression of Bcl-2and Bax increased and the reaction of Bax to injury was slower than Bcl-2. Both of the expression raised first anddeclined later. There was statistical significance of the expression of Bcl-2 and Bax between the ischemia and con-trol group 6-72 hours after reperfusion (P < 0. 05).The ratio of Bcl-2/ Bax raised 6-12 hours and decreased 24-72hours after reperfusion. Conclusion Bcl-2 and Bax play an important role in the mechanism of apoptosis of re-tinal never cells, which has relative relation with the ratio of Bcl-2/ Bax at differentintervals after retinal ischemia-reperfusion injury.