色素上皮衍生因子对角膜碱烧伤后新生血管形成的抑制

背景：角膜新生血管导致角膜透明性降低,造成严重的视觉障碍.色素上皮衍生因子是一种内源性血管生成抑制剂,其对于角膜新生血管是否具有抑制作用尚不清楚.目的：探索局部运用色素上皮衍生因子对大鼠角膜碱烧伤后角膜新生血管的抑制作用.方法：将20只大鼠随机分为生理盐水组与色素上皮衍生因子组,每组10只.用NaOH溶液将大鼠右眼角膜烧伤诱导产生新生血管.碱烧伤后2组每日分别给予生理盐水和色素上皮衍生因子点眼,并采用裂隙灯显微镜观察和测量各组角膜新生血管生长情况.碱烧伤后12 d处死大鼠,将角膜组织固定切片,行苏木精-伊红染色观察,并进行免疫组织化学染色检测各组大鼠角膜血管内皮生长因子和 CD31的表达.结果与结论：大鼠角膜碱烧伤后3,7,12 d,色素上皮衍生因子组大鼠角膜新生血管面积均小于生理盐水组（P 〈0.05）.角膜碱烧伤后12 d,苏木精-伊红染色显示生理盐水组大鼠角膜产生大量新生血管,角膜组织结构紊乱;色素上皮衍生因子组新生血管较少,角膜组织结构趋于整齐.角膜碱烧伤后12 d,免疫组织化学染色示生理盐水组大鼠角膜上皮和基质层可见血管内皮生长因子大量表达,角膜基质层可见血管内皮生长因子和CD31大量表达;色素上皮衍生因子组新生血管稀少,CD31表达较弱.证实局部应用色素上皮衍生因子可有效抑制大鼠角膜化学伤后的血管新生.

Pigment epithelium-derived factor inhibits corneal neovascularization after corneal alkali burn

BACKGROUND： Corneal neovascularization can reduce the transparency of cornea thus causing severe visual impairment. Pigment epithelium-derived factor is an endogenous angiogenesis inhibitor, and it is unclear whether it can inhibit corneal neovascularization. OBJECTIVE： To investigate the inhibitory effect of topical y administration of pigment epithelium-derived factor on the corneal neovascularization of rats after corneal alkali burn. METHODS： Twenty rats were randomly divided into normal saline group and pigment epithelium-derived factor group, 10 rats in each group. NaOH solution was used to burn the right cornea in order to induce neovascularization. After burn, the rats in the two groups received pigment epithelium-derived factor drop and normal saline drop daily, respectively, and the growth of corneal neovascularization in each group was observed and calculated by slit lamp microscope. The rats were sacrificed at 12 days after burn, and then the histological structure of the cornea was observed with hematoxylin-eosin staining. Expression of vascular endothelial growth factor and CD31 was detected by immunohistochemistry. RESULTS AND CONCLUTION： At 3, 7 and 12 days after corneal alkali burn, the area of corneal neovascularization in the pigment epithelium-derived factor group was smal er than that in the normal saline group （P 〈 0.05）. At 12 days after corneal alkali burn, hematoxylin-eosin staining revealed that a large amount of neovascularization could be seen in the normal saline group, and the structure of corneal tissue was in disorder; the neovascularization was less in the pigment epithelium-derived factor group, and the structure of corneal tissue was in order. Immunohistochemical staining at 12 days after corneal alkali burn revealed that the expression of vascular endothelial growth factor was mainly in corneal epithelial layer and matrix layer. The expression of vascular endothelial growth factor and CD31 was massive in corneal matrix layer; while the corneal neovascularization was less in the pigment epithelium-derived factor group and the CD31 expression was weak. The experimental results indicate that topical application of pigment epithelium-derived factors can inhibit alkali-induced corneal neovascularization effectively.