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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。
Objective To investigate the apoptosis of photoreceptor cells and the possible gene regulation mechanism in hereditary retinitis pigmentosa. Methods The retinal structures of RCS rats and control SD rats were observed by light microscopy, apoptosis and Bcl-2 protein immunohistochemistry. Results In the RCS rats, the thickness of the photoreceptor cells in the retina became thicker on the 15th day after birth, and the thickness of the photoreceptor cells peaked at 25 days. The number of photoreceptor cells decreased at 25 days, and only a few photoreceptor cells remained after 60 days of birth. From 25 to 40 days after birth, retinal TUNEL positive cells in the outer nuclear layer of RCS rats were observed, and the number of positive cells was the highest at 35 days. The expression of Bcl-2 protein was observed in the inner nuclear layer and the ganglion cell layer from 30 to 40 days. The expression of Bcl-2 protein in the outer nuclear layer was the highest at 35 days. Conclusion During retinal degeneration in RCS rats, photoreceptor cell apoptosis occurs. Bcl-2 proto-oncogene may not participate in photoprotective mechanisms.