缺血再灌注损伤诱导大鼠视网膜细胞凋亡

目的 观察缺血再灌注大鼠视网膜损伤及细胞凋亡情况。 方法 采用升高大鼠眼压到109.725 mm Hg(1 mm Hg=0.133 kPa)持续1 h的方法制作视网膜缺血再灌注模型，采用常规眼球切片观察不同缺血和再灌注时间的视网膜损伤的组织病理改变；采用DNA琼脂糖凝胶电泳法检测视网膜神经元凋亡情况；采用DNA原位末端标记(terminal dUTP nick end labelling, TUNEL)法定位凋亡的视网膜细胞。 结果 缺血30 min 再灌注24、48 h的大鼠视网膜无明显的病理改变；缺血60 min再灌注24、48 h的大鼠视网膜神经节细胞层和内核层细胞明显变薄；缺血60 min再灌注12、24 h的大鼠视网膜有梯状条带。而正常对照组、缺血30 min再灌注24、48 h组及缺血60 min再灌注48 h组大鼠视网膜均无类似表现。TUNEL法显示视网膜内的细胞凋亡主要发生在节细胞和内核层光感受细胞。 结论 大鼠视网膜缺血再灌注主要是导致视网膜神经节细胞层和内核层细胞损伤，细胞凋亡可能是损伤的重要机制。 (中华眼底病杂志, 2002, 18: 296-298)

Ischemia-reperfusion insult induced apoptosis of rats' retinal cells

Objective To investigate the damage to the retinal cells and apoptosis of retinal cells of rats after ischemia-reperfusion insult. Methods The retinal ischemia-reperfusion model was developed by increasing intraocular pressure to 109 725 mm Hg in rat eyes. Morphological changes of the rat eyes were observed by means of routine histopathology with HE staining. Apoptosis of the retina was assayed by both DNA fragmentation gel-electrophoresis and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL). Results Compared with the normal control, no histopathological changes were revealed in the rat retinas 30 min after the ischemia and then reperfued for 24 h or 48 h. Retinal ganglion cell layer (RGL) and inner plaxiform layer (IPL) of the retina were observed, however, to become significantly thinner 60 min after the ischemia and then reperfued for 24 h or 48 h. Together with the pathological changes DNA ladder pattern was detected in the same group of the rats. Further, immunochemical stain of the eye demonstrated that TUNEL positive cells were localized in RGL and IPL of the retina. Conclusion Ischemia-reperfusion insult of the eye may remarkably damage the retina of the rat eye. The damage to the retinal cells is mainly localized within RGL and IPL and apoptosis is the important mechanism of the retinal disorder.