摘要
①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。②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。③结果 RCS大鼠生后 1 5d视网膜的感光细胞视杆层及外节增厚 ,视杆层的厚度在 2 5d达到高峰。感光细胞的数目在 2 5d时有所下降 ,到出生后 6 0d ,仅少许感光细胞存留。出生后 2 5~ 4 0d ,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 35d最多。 30~ 4 0d内核层和节细胞层可见Bcl 2蛋白免疫组化阳性表达 ,35d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。④结论 RCS大鼠视网膜变性过程中 ,感光细胞发生了凋亡。Bcl
Objective\ To investigate photoreceptor apoptosis and gene regulation in hereditary retinal degeneration of Royal College of Surgeon (RCS) rats.\ Methods\ The retina sections of RCS and SD rats in different ages were examined by light microscope, apoptosis and Bcl 2 protein by immunohistochemical method.\ Results\ The rod layer and outer segments of RCS rats became thicker at 15 days of age. The width of the rod layer reached the peak stage at 25 days. The number of photoreceptor cell(PRC) in RCS rats reduced at 25 days. At the age of 60 days, only a few PRC remained. From 25 to 40 days , the nuclei of PRC in RCS rats were stained positively by TUNEL, reached the highest level at 35 days. Positive staining of Bcl 2 protein could be seen in the ganglion cell layer and the inner nuclear layer from 30 to 40 days of age, showing the most in the inner nuclear layer at 35 days. No obvious positive granules could be detected in the outer nuclear layer at all ages.\ Conclusion\ The apoptosis of PRC occurred in the process of hereditary retinal degeneration of RCS rats, Bcl 2 protein might not have a role in the mechanism of protection for PRC apoptosis.
出处
《青岛大学医学院学报》
CAS
2003年第2期123-126,共4页
Acta Academiae Medicinae Qingdao Universitatis
基金
山东省自然科学基金资助项目 (Y99c0 8)