摘要
目的检测大鼠角膜碱烧伤后缺氧诱导因子-1α(HIF-1α)的表达变化,探讨其在角膜碱烧伤损伤机制中的作用。方法建立大鼠角膜碱烧伤模型,采用免疫组织化学与原位杂交技术,检测角膜碱烧伤后不同时间HIF-1α在角膜各层中的表达变化。结果在正常角膜组织中,角膜各层均未见HIF-1α免疫染色,碱烧伤后1d时HIF-1α免疫活性增强,且3d时表达最强,15d时明显下降,30d时仍有高于正常水平的弱表达。原位杂交检测中正常角膜组织有极弱的HIF-1α mRNA表达,碱烧伤后HIF-1α mRNA表达增强,在伤后3d、7d时表达最明显,15d后表达强度恢复至正常组织水平。结论HIF-1α参与碱烧伤后角膜的损伤病理机制,其表达变化影响新生血管形成过程,为寻找角膜碱烧伤新的治疗途径提供了理论依据。
Objective Hypoxia can increase the expression of vascular endothelial growth factor（VEGF） ,which induces ocular neovascularization. Aim of this study was to observe the expression of HIF-1 in rat corneas with alkali burns and explore its role in pathomechanism. Methods Corneal neovascularization （CNV） model was established by putting the 3.0 mm filter paper sacking 1 mol/L NaOH solution. Thirty six Sprague-Dawley （SD） rats were randomly divided into 6 groups（ n = 6 in each） ： normal control group and post-operation 1 day,3,7,15 and 30 days groups. The expression level of HIF-1 protein and mRNA was determined at 1 day, 3,7, 15,30 days following establishment of model by in situ hybridization and immunohistochemical technique. Results There was no evident HIF-let immunoreactivity in normal cornea. However,brown-yellow particles mainly in cell nucleus appeared in the burned corneas and showed a dynamic changes in HIF-let protein expression as follows： the immunoreactivity of HIF-let protein was increased at 1 day,peaked at 3 days and reduced evidently at 15 days until weakly expressed at 30 days after modeling（ F = 1 153. 347 ,P =0. 000）. Very lower HIF-let mRNA expression was seen in normal cornea and showed an altering tendency similar to the expression of HIF-1 et protein following alkaline injury of cornea（ F = 320. 426,P = 0. 000） ,showing brown-yellow staining particles mainly in cytoplasm. Expression level of HIF-1 mRNA was gradually returned to the normal level 15 days later. Conclusion HIF-let is involved in the pathomechanism of corneal alkali burning. It may play an important role in corneal neovascularization.
出处
《眼科研究》
CAS
CSCD
北大核心
2007年第8期575-578,共4页
Chinese Ophthalmic Research
关键词
缺氧诱导因子-1Α
角膜
碱烧伤
免疫组织化学
原位杂交
新生血管
hypoxia inducible factor-let
cornea
alkaline injury
immunohistochemistry
in situ hybridization
neovascularization
