【摘要】 目的探讨遗传性视网膜色素变性中感光细胞凋亡及其可能的基因调控机制。方法对RCS大鼠及对照SD大鼠的视网膜组织结构进行光镜观察、细胞凋亡及Bcl-2蛋白免疫组织化学检测。结果RCS大鼠生后15 d视网膜的感光细胞视杆层及外节增厚,视杆层的厚度在25 d达到高峰。感光细胞的数目在25 d时有所下降,到出生后60 d,仅少许感光细胞存留。出生后25~40 d,RCS大鼠视网膜可见外核层TUNEL染色阳性的感光细胞,阳性细胞数35 d最多。30~40 d内核层和节细胞层可见Bcl-2蛋白免疫组化阳性表达细胞,35 d时内核层阳性表达细胞数最多,外核层一直未见明显Bcl-2蛋白阳性表达细胞。结论RCS大鼠视网膜变性过程中,感光细胞发生了凋亡。Bcl-2原癌基因可能不参与感光细胞的保护机制。更多还原

【Abstract】 ObjectiveTo investigate photoreceptor apoptosis and gene regulation in hereditary retinal degeneration of Royal College of Surgeon(RCS) rats. MethodsThe retinal sections of RCS rats of different ages were examined by a light microscope,TUNEL and Bcl-2 protein immunohistochemical method.ResultsCompared with age matched SD rats,the photoreceptor cells(PRC) in RCS rats,15 days after birth,showed outer segment membrane accumulation,inner segment disorder,nuclei pycnosis,and cell disappearance.PRC death peaked at postnatal day 30 to 40.From 25 to 40 days,the nuclei of PRC in RCS rats were stained positively by TUNEL and the retina at day 35 had the largest amount of stained nuclei.Positive staining of Bcl-2 protein could be seen in the ganglion cell layer and the inner nuclear layer from 30 to 40 days,and showed the most in the inner nuclear layer at 30 days.No obvious positive granules could be detected in the outer nuclear layer at any ages.ConclusionIt is through apoptosis that PRCs die in hereditary retinal degeneration of RCS rats.Bcl-2 protein might not have a role in the regulation of photoreceptor apoptosis.更多还原