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目的 研究非促分裂haFGF(nm haFGF)对N 甲基 N 亚硝脲 (MNU)所致大鼠视网膜损伤的保护作用及其作用机制。方法 通过ipMNU(60mg·kg-1 )复制大鼠视网膜损伤模型, 0和 12h后,玻璃体腔内注射不同剂量nm haFGF。24h和 7d后,测量周边视网膜总厚度和外视网膜厚度、光感受器细胞凋亡指数及视网膜Bcl 2和Bax蛋白表达水平。结果 MNU作用 24h后,nm haFGF组周边视网膜的凋亡指数显著降低 (P<0 01); 7d后,nm haFGF组周边视网膜光感受器细胞数明显增多,且周边视网膜总厚度和外视网膜厚度增加 (P<0 01);不同剂量nm haFGF可调节Bcl 2和Bax蛋白表达水平。结论 nm haFGF能部分抑制MNU引起的SD大鼠视网膜损伤,其作用机制可能与上调Bcl 2和下调Bax蛋白表达水平有关。
Objective To investigate the protective effect of non-mitotic haFGF (nm haFGF) on retinal damage induced by N-methyl N-nitrosourea (MNU) in rats and its mechanism. Methods Rat retinal injury model was induced by ipMNU (60mg · kg-1). Different doses of nm haFGF were injected into vitreous cavity at 0 and 12 hours. After 24 and 7 days, the total peripheral retinal thickness and the thickness of the outer retina, the photoreceptor apoptosis index and the protein expression of Bcl 2 and Bax in the retina were measured. Results The apoptotic index of peripheral retinal cells in the group of nm haFGF decreased significantly after MNU treatment for 24 h (P <0.01). After 7 days, the number of peripheral retinal photoreceptor cells in the nm haFGF group increased significantly, and the total thickness of the peripheral retina and the outer retina increased P <0.01). Different doses of nm haFGF could regulate the expression of Bcl-2 and Bax proteins. Conclusion nm haFGF can partially inhibit the retinal damage induced by MNU in SD rats, and its mechanism may be related to the up-regulation of Bcl 2 and down-regulation of Bax protein expression.