氟伐他汀对大鼠角膜碱烧伤后新生血管形成的影响

Effect of Fluvastatin on Corneal Neovascularization of Rats After Alkali Burn

目的:探讨氟伐他汀对大鼠角膜碱烧伤后新生血管形成的作用及其机制。方法:30只SD大鼠随机分为3组:生理盐水组、氟伐他汀组和地塞米松组,每组10只,均用1mol/L的NaOH烧伤大鼠右眼,生理盐水组、氟伐他汀组和地塞米松组分别以生理盐水、10-5 mol/L氟伐他汀和1g/L地塞米松点眼。碱烧伤后1-14d用裂隙灯观察角膜的混浊度和新生血管的生长情况,HE染色观察角膜组织病理学改变,免疫组化观察VEGF和CD31的表达情况。结果:碱烧伤后第3,7,14天,氟伐他汀组和地塞米松组的角膜混浊度评分和新生血管生长评分都显著低于生理盐水组,差异有统计学意义,P<0.05。组织病理学检查结果提示,与生理盐水组相比,氟伐他汀组和地塞米松组的角膜组织结构明显整齐,新生血管的形成明显减少,伴少量炎性细胞浸润。免疫组化结果显示氟伐他汀组和地塞米松组的VEGF和CD31的表达显著减少。结论:氟伐他汀能减轻大鼠角膜碱烧伤,其机制可能是下调VEGF和CD31的表达。

Objective： To investigate the effect of fluvastatin on neovascularization of rats after alkaliburned cornea. Methods： Thirty SD rats were randomly divided into three groups, normal saline group, fluvastatin group, and dexamethasone group. Each group had 10 rats. After 1 mol/L NaOH was used to burn the right eye of rats, normal saline group, fluvastatin group and dexam- ethasone group were treated with normal saline eye drops, fluvastatin eye drops and dexamethasone eye drops, respectively. Between 1 d and 14 d after alkali burn, slit lamp was used to observe the turbidity of the cornea and neovascularization. HE staining was performed to observe the corneal tissue pathological changes. The expression of VEGF and CD31 was detected by immunohistochemical staining. Results.. At the end of 3, 7 and 14 days after corneal burn, the scores of corneal turbidity and neovascularization in fluvastatin group and dexamethasone group were significantly lower than the normal saline group （P〈0.05）. Histopathological results suggested that comparied with that in the normal saline group, the corneal tissue structure was obviously clear and tidy in fluvastatin group and dexamethasone group. The formation of neovascularization and inflammatory cells infiltration were decreased in fluvastatin group. Immunohistochem- ical stainging showed that the expression of VEGF and CD31 was significantly reduced in fluvastatin group and dexamethasone group. Conclusion. Fluvastatin can reduce corneal alkali burn inrats and its mechanism may be related to the down-regulated expression of VEGF and CD31.