非促分裂haFGF对MNU所致大鼠视网膜损伤的保护作用

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ip MNU (60 mg·kg^-1)复制大鼠视网膜损伤模型，0和12 h后，玻璃体腔内注射不同剂量nm-haFGF。24 h和7 d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24 h后，nm-haFGF组周边视网膜的凋亡指数显著降低(P<0.01)；7 d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。

Protective effect of non-mitogenic haFGF on retinal injury induced by N-methyl-N-nitrosourea in Sprague-Dawley rats

AIM: To study the effect of non-mitogenic human acidic fibroblast growth factor (nm-haFGF) on retinal injury induced by N-methyl-N-nitrosourea (MNU) in Sprague-Dawley rats and its mechanism. METHODS: Female rats of 50-days-old were injected with MNU (60 mg x kg(-1)) intraperitoneally, and three doses of nm-haFGF (1.25 microg, 2.5 microg and 5 microg in one eye of each rat) were injected, separately, into vitreous body of one eye of each rat twice a day at 0 and 12 h after MNU treatment. 24 h later, apoptotic index of photoreceptor cells was detected by TUNEL labeling and the expressions of Bcl-2 and Bax were analyzed by Western blotting. At the 7th day, retinal injury was evaluated based on retinal thickness. RESULTS: Compared with model group, apoptotic index of photoreceptor cells was significantly reduced in nm-haFGF groups at the dose of 1.25 microg and 2.5 microg in one eye of each rat at 24 h, and the total retinal thickness as well as the outer retinal thickness markedly increased 7 days after MNU, respectively. The expressions of Bcl-2 increased and that of Bax decreased adversely after being injected with different doses of nm-haFGF. CONCLUSION: nm-haFGF partially suppressed retinal injury induced by MNU in Sprague-Dawley rats. The mechanism could be related to up-regulation of Bcl-2 and down-regulation of Bax.