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目的 :观察血管内皮生长因子 (vascularendothelialgrowthfactor,VEGF)在大鼠角膜移植术后不同时间点的表达及与角膜新生血管 (CNV)生长之间的关系。方法 :利用免疫组化方法观察同种异体大鼠角膜移植术后不同时间点VEGF的表达。结果 :角膜移植术后 ,VEGF组CNV生长面积与其它各组差异有高度显著性 (P <0 0 0 1 ) ,生长时间提前 ,高峰期持续时间长 ,VEGF表达明显增强。白介素 1受体拮抗剂 (IL 1ra)和地塞米松组CNV出现的时间迟 ,生长较慢 ,高峰持续时间短 ,约 3～ 4周时就开始减退 ,经统计学比较与其它各组差异有高度显著性 (P <0 0 1 ) ,VEGF表达较弱。生理盐水组和对照组CNV在角膜移植术后出现的时间基本相同 ,生长速度和CNV面积经统计学比较差异无显著性 (P >0 0 5) ,但与地塞米松组和IL 1ra组比较差异有显著性 (P <0 0 5) ,VEGF呈强表达。结论 :VEGF的表达和角膜新生血管增生呈正相关。外源性VEGF可促进角膜新生血管的增生 ;VEGF在角膜新生血管性疾病中起很重要的作用。IL 1ra抑制由IL 1引起的角膜炎性反应 ,使VEGF的表达减低 ,从而抑制了CNV。
Objective: To observe the relationship between the expression of vascular endothelial growth factor (VEGF) and corneal neovascularization (CNV) at different time after corneal transplantation in rats. Methods: Immunohistochemistry was used to observe the expression of VEGF at different time points after corneal transplantation in allogeneic rats. Results: After corneal transplantation, the growth area of CNV in VEGF group was highly significant compared with other groups (P <0.01), the growth time was earlier, the peak duration was longer, and the expression of VEGF was significantly increased. Interleukin-1 receptor antagonist (IL 1ra) and dexamethasone group CNV appeared later, slower growth, short duration of peak, about 3 to 4 weeks began to decline, the statistical comparison with other groups differences Highly significant (P <0.01), VEGF expression is weak. CNV in the saline group and the control group were basically the same after the corneal transplantation, and there was no significant difference in the growth rate and CNV area between the two groups (P> 0.05). However, compared with the dexamethasone group and the IL-1ra group The difference was significant (P <0 05), VEGF was strongly expressed. Conclusion: The expression of VEGF is positively correlated with corneal neovascularization. Exogenous VEGF can promote the proliferation of corneal neovascularization; VEGF plays a very important role in corneal neovascular disease. IL 1ra inhibits the corneal inflammatory response caused by IL 1, reduces the expression of VEGF, and thus suppresses CNV.