牛碱性成纤维细胞生长因子对紫外线损伤角膜的修复作用

Repair Effect of Bovine Basic Fibroblast Growth Factor on UV-damaged Cornea

关键词:  bFGF  紫外线  角膜  Bcl-2  Bax

Key words:  bFGF  ultraviolet  cornea  Bcl-2  Bax

摘要:

目的 探讨牛碱性成纤维细胞生长因子（bovinebasic fibroblast growth factor，bFGF）对大鼠角膜紫外线损伤后的修复作用。方法 选取30只健康无眼疾SD大鼠（♂，200~250 g），随机分成3组，每组10只。除正常对照组常规饲养外，其余2组大鼠紫外线照射42 d，造模后，治疗组给予bFGF滴眼液；照射组给予等量生理盐水滴眼，14 d后取材。治疗期间每7 d进行裂隙灯检查、荧光素染色及泪膜破裂时间测定。TUNEL检测角膜细胞凋亡指数，免疫组化法检测Bax、Bcl-2表达。结果 造模结束后，模型大鼠角膜混浊，新生血管增生。照射组治疗后新生血管蔓延、角膜混浊严重。与照射组相比，治疗组新生血管只在角膜缘且角膜基本透明；角膜混浊程度减轻（P<0.05）；随着治疗时间延长，泪膜破裂时间平均值提高；角膜细胞凋亡指数下降（P<0.05）；Bcl-2/Bax显著升高（P<0.05）。结论 bFGF可显著减轻紫外线照射导致的角膜损伤，其作用机制可能与升高Bcl-2蛋白表达、降低Bax的蛋白表达从而上调Bcl-2/Bax比例有关。

Abstract:

OBJECTIVE To observe the repair effect of bovine basic fibroblast growth factor(bFGF) on UV-damaged corneal in rats. METHODS Thirty healthy male SD rats (♂, 200~250 g) without eye disease were randomly divided into 3 groups, 10 in each group. Normal control group was fed routinely without ultraviolet irradiation. After 42 d of ultraviolet irradiation, bFGF eye drops were given to the treatment group after modeling. Irradiation group was given the same amount of saline eye drops, the samples were taken 14 d later. Slit lamp examination, fluorescein staining, and tear film break-up time(BUT) were measured every 7 d during treatment. TUNEL was used to detect apoptosis index of corneal cells, and immunohistochemistry was used to detect the expression of Bax and Bcl-2. RESULTS The cornea of model rats had been opacity and neovascularization after ultraviolet irradiation. After treatment, the neovascularization and corneal opacity were severe in irradiation group. Compared with irradiation group, the neovascularization in irradiation treatment group was only at the limbus and the cornea was basically transparent; the degree of corneal opacity was reduced(P<0.05); the mean value of BUT increased with the prolongation of treatment time; the death index of cornea decreased(P<0.05); Bcl-2/Bax was increased significantly (P<0.05). CONCLUSION bFGF can significantly reduce corneal damage caused by ultraviolet radiation, and its mechanism may be related to increasing Bcl-2 protein expression, decreasing Bax protein expression and up-regulating Bcl-2/Bax ratio.