[摘要]目的 研究视网膜缺血再灌注损伤(RIRI)中凋亡相关基因野生型p53(WTp53)、bax和bcl-2表达的变化,探讨其作用机制。方法将28只Wistar大鼠随机分为正常组、缺血组,其中缺血组又分为再灌注后1、6、12、24、48和72 h等6个组。建立RIRI动物模型,用免疫组织化学链霉亲和素-生物素-过氧化物酶复合物(SABC)法检测再灌注后不同时段视网膜组织中WTp53、bax和bcl-2基因表达的变化。结果 缺血组视网膜再灌注后WTp53、Bax蛋白表达增加,与正常组比较,再灌注6~72 h差异有显著意义( F=487.19、281.97,q=11.526~ 52.401 ,P lt;0.05)。缺血组视网膜再灌注后Bcl-2蛋白表达无明显变化,与正常组比较,差异无显著性( P gt;0.05)。结论 缺血再灌注损伤引起WTp53、bax基因在视网膜神经节细胞层、神经纤维层与内核层表达增高;WTp53和bax可能通过诱导或促进神经节细胞凋亡参与了视网膜缺血再灌注损伤的发生。
[关键词] 视网膜;再灌注损伤;基因,WTp53;基因,bax;基因,bcl-2;大鼠,Wistar
[ABSTRACT]ObjectiveTo investigate the expression of WTp53,bax and bcl-2 in retina ischemia/reperfusion injury and explore the mechanism. MethodsTwenty-eight rats were randomly divided into normal (4 rats) and ischemia group, and the latter was subdivided into 1,6,12,24,48,and 72h after reperfusion, respectively. The rat model of experimental retina ischemia/reperfusion injury was made by increasing the intraocular pressure. The expression of WTp53, bax and bcl-2 was determined by streptavidin-biotin complex (SABC) immunohistochemistry. Results In ischemia group, WTp53 expression and bax expression increased significantly ( F=487.19,281.97;q=11.526-52.401; P lt;0.05),while the bcl-2 expression had little change. Conclu-sionWTp53 and bax expression increase in RIRI. WTp53 and bax may play a part in RIRI by promoting apoptosis.
[KEY WORDS]retina; reperfusion injury; genes,WTp53; genes, bax; genes, bcl-2; rats, Wistar
视网膜缺血再灌注损伤是眼科常见的病理过程,严重影响病人视功能。其发生机制十分复杂,已成为近年眼科的研究热点之一。目前研究发现,视网膜缺血再灌注损伤中存在着神经细胞凋亡现象,且凋亡是视网膜神经细胞丢失的重要因素之一[1]。本实验通过建立大鼠视网膜缺血再灌注损伤模型,研究凋亡相关基因野生型p53(WTp53)、bax和bcl-2的表达变化,探讨视网膜缺血再灌注损伤的发生机制。现将结果报告如下。
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