Emodin suppresses alkali burn-induced corneal inflammation and neovascularization by the vascular endothelial growth factor receptor 2 signaling pathway  

作　　者：ZHENG Xueying GUO Liang LAI Siyi LI Fengyue LIANG Mingli LIU Wanting MENG Chun LIU Guanghui 

机构地区：[1]Department of Bioengineering,College of Biological Science and Biotechnology,Fuzhou University,Fuzhou 350104,China [2]Eye Institute of Integrated Chinese and Western Medicine,Fujian University of Traditional Chinese Medicine,Fuzhou 350004,China [3]Department of Ophthalmology,Affiliated People's Hospital(Fujian Provincial People's Hospital),Fujian University of Traditional Chinese Medicine,Fuzhou 350004,China

出　　处：《Journal of Traditional Chinese Medicine》2024年第2期268-276,共9页中医杂志（英文版）

基　　金：Fujian Major Research Grants for Young and Middle-aged Health Professionals(No.2021ZQNZD012,Research and Development of Anti-Keratitis Protein Drug Sgp130);National Natural Science Foundation of China(No.81774369,Study on Mechanism of Yijing Decoction in Preventing Microvascular Damage of Early Diabetic Retinopathy based on MMPs/TIMPs)。

摘　　要：OBJECTIVE:To investigate the effects of emodin on alkali burn-induced corneal inflammation and neovascularization.METHODS:The ability of emodin to target vascular endothelial growth factor receptor 2(VEGFR2)was predicted by molecular docking.The effects of emodin on the invasion,migration,and proliferation of human umbilical vein endothelial cells(HUVEC)were determined by cell counting kit-8,Transwell,and tube formation assays.Analysis of apoptosis was performed by flow cytometry.CD31 levels were examined by immunofluorescence.The abundance and phosphorylation state of VEGFR2,protein kinase B(Akt),signal transducer and activator of transcription 3(STAT3),and P38 were examined by immunoblot analysis.Corneal alkali burn was performed on 40 mice.Animals were divided randomly into two groups,and the alkali-burned eyes were then treated with drops of either 10μM emodin or phosphate buffered saline(PBS)four times a day.Slitlamp microscopy was used to evaluate inflammation and corneal neovascularization(CNV)in all eyes on Days 0,7,10,and 14.The mice were killed humanely 14 d after the alkali burn,and their corneas were removed and preserved at-80℃ until histological study or protein extraction.RESULTS:Molecular docking confirmed that emodin was able to target VEGFR2.The findings revealed that emodin decreased the invasion,migration,angiogenesis,and proliferation of HUVEC in a dose-dependent manner.In mice,emodin suppressed corneal inflammatory cell infiltration and inhibited the development of corneal neovascularization induced by alkali burn.Compared to those of the PBS-treated group,lower VEGFR2 expression and CD31 levels were found in the emodintreated group.Emodin dramatically decreased the expression of VEGFR2,p-VEGFR2,p-Akt,p-STAT3,and p-P38 in VEGF-treated HUVEC.CONCLUSION:This study provides a new avenue for evaluating the molecular mechanisms underlying corneal inflammation and neovascularization.Emodin might be a promising new therapeutic option for corneal alkali burns.

关 键 词：alkali burn EMODIN corneal inflammation corneal neovascularisation vascular endothelial growth factor receptor-2 signal transduction 

分 类 号：R285[医药卫生—中药学]