Molecular mechanism of the inhibition effect of Lipoxin A4 on corneal dissolving pathology process
Molecular mechanism of the inhibition effect of Lipoxin A4 on corneal dissolving pathology process作者机构：Department of Ophthalmology China-Japan Union Hospital of Jilin University Department of Ophthalmologythe Second Hospital of Jilin University
出 版 物：《International Journal of Ophthalmology(English edition)》 (国际眼科杂志（英文版）)
年 卷 期：2013年第6卷第1期
页 面：39-43页
核心收录：
学科分类：1002[医学-临床医学] 100212[医学-眼科学] 10[医学]
基 金：Jilin University Basic Scientific Research Operating Expenses Fund, China (Research Fund of the Bethune B Plan of Jilin University, 2012 No.2012230) Research Fund of Jilin Provincial Science and Technology Department, China (international cooperation item, No.20120726)
主 题：lipoxin A4 IL-1β cornea collagen dissolution
摘 要：AIM:Excessive dissolve of corneal tissue induced by MMPs which were activated by cytokins and chemokines will lead to corneal ulcer. The molecular mechanism of Lipoxin A4 (LXA4) on corneal collagen degradation in three dimensions was investigated. ·METHODS:Rabbit corneal fibroblasts were harvested and suspended in serum -free MEM. Type I collagen, DMEM, collagen reconstitution buffer and corneal fibroblast suspension were mixed on ice. The resultant mixture solidified in an incubator, after which test reagents and plasminogen was overlaid and the cultures were returned to the incubator. The supernatants from collagen gel incubations were collected and the amount of hydroxyproline in the hydrolysate was measured. Immunoblot analysis of MMP-1,-3 and TMMP-1,-2 was performed. MMP-2, -9 was detected by the method of Gelatin zymography. Cytotoxicity assay was measured. RESULTS:LXA4 inhibited corneal collagen degradation in a dose and time manner. LXA4 inhibited the IL -1β induced increases in the pro-MMP-1, -2, -3, -9 and active MMP -1,-2,-3,-9 in a concentration dependent manner. LXA4 also inhibited the IL-1β induced increases in TIMP-1, -2. CONCLUSION:As a potent anti-inflammation reagent, LXA4 can inhibit corneal collagen degradation induced by IL-1β in corneal fibroblasts thus inhibiting corneal dissolving pathology process.
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