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目的研究遗传性视网膜变性的发生机制。方法对生后不同鼠龄ＲＣＳ（ＲｏｙａｌＣｏｌｅｇｅｏｆＳｕｒｇｅｏｎｓ）和ＳＤ（Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ）大鼠的视网膜进行光镜观察、计算机自动图象分析和凋亡细胞的ＴＵＮＥＬ（ＴｄＴ－ｍｅｄｉａｔｅｄｂｉｏｔｉｎ－ｄＵＴＰｎｉｃｋ－ｅｎｄｌａｂｅｌ－ｉｎｇ）检测。结果与同龄ＳＤ大鼠相比，ＲＣＳ大鼠出生后１５ｄ，视细胞（ｐｈｏｔｏｒｅｃｅｐｔｏｒ，ＰＲＣ）外节膜盘堆积，以后相继出现内节排列紊乱、消失，细胞核固缩，从生后３０ｄ到６０ｄ，ＰＲＣ迅速消失。从出生后４０ｄ，视网膜色素上皮（ｒｅｔｉｎａｌｐｉｇｍｅｎｔｅｐｉｔｈｅｌｉｕｍ，ＲＰＥ）细胞出现增殖和排列紊乱。１００ｄ时，ＲＰＥ层出现新生血管。ＴＵＮＥＬ检测，ＲＣＳ大鼠视网膜ＰＲＣ阳性数目从２５ｄ起开始逐渐增加，３５ｄ时达高峰。结论ＲＣＳ大鼠的视网膜变性以ＰＲＣ凋亡为主，ＲＰＥ紊乱和视网膜新生血管是视网膜变性的晚期病变。
Objective To study the mechanism of hereditary retinal degeneration. Methods The retinas of RCS (Royality of Solege of Surgeons) and SD (Sprague-Dawley) rats after birth were observed under light microscope. The images were analyzed by automatic computer and the TdT-mediated biotin-dUTPnick-end labeling . Results Compared with SD rats of the same age, RCS rats accumulated the outer membrane discs of photoreceptor (PRC) 15 days after birth, and then the internal segments appeared disorganized and disappeared one after the other. The nuclei were contracted from 30 days after birth to 60 days, PRC disappears rapidly. From 40 days after birth, retinal pigment epithelial cells (retinal pigment epithelium, RPE) cells showed proliferation and disorder. At 100 days, neovascularization occurred in the RPE layer. TUNEL detection, RCS rat retinal PRC positive number began to gradually increase from 25d, 35d reached a peak. Conclusion The retinal degeneration in RCS rats is dominated by PRC, and RPE disorder and retinal neovascularization are the advanced lesions of retinal degeneration.