【摘要】 目的研究大鼠视神经夹挫伤后视网膜神经节细胞(RGC)形态学改变及Bcl-2/Bax蛋白表达的变化,为了解视神经损伤的病理机制提供一定的依据。方法建立大鼠视神经夹挫伤动物模型,伤后1d、3d、5d、7d、9d、2周、4周处死,HE染色观察RGC的动态变化,免疫组化方法检测RGC表达Bcl-2及Bax的水平。结果视神经伤后RGC数目严重下降,2周内RGC快速减少,2周以后缓慢减少;伤后Bcl-2及Bax表达随时间而有不同程度的增加,Bax对损伤的反应较Bcl-2稍晚,两者表达均呈现先升后降的趋势,并维持一定的时间。Bcl-2和Bax蛋白表达比与RGC存活数目有一定的相关性。结论视神经损伤后RGC数目减少是其视功能下降的病理基础之一,Bcl-2和Bax在RGC死亡机制中起重要作用,Bcl-2/Bax比率与RGC的减少呈一定的相关性。更多还原

【Abstract】 Objective To observe the morphological change of retinal ganglion cell(RGC) and the change of Bax/Bcl-2 after optic nerve crush in rat.?Methods The models of optic nerve crush in rats were made.The change of RGC in different time after injury was observed and the expression of Bax and Bcl-2 in retina were studied by immunohistology.?Results The number of RGC was reduced significantly due to partial lesion of optic nerve crush. The initial loss of RGC was accelerated during one week after nerve crush and then declined gradually by 14 days,the later declines was protracted in RGC densities.The expression of Bax and Bcl-2 increased and the reaction of Bax to injury is slower than Bcl-2.Both of expression raised first and declined later.The ratio of Bcl-2/Bax is closely relative to the number of RGC.?Conclusions The secondary degeneration following optic nerve crush is morphological basis of fall of visual function,Bcl-2 and Bax play an important role in the mechanism of dead of RGC,which has relative relation with the ratio of Bcl-2/Bax at different intervals after optic injury.更多还原