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 ZHENG Xueying;GUO Liang;LAI Siyi;LI Fengyue;LIANG Mingli;LIU Wanting;MENG Chun;LIU Guanghui

作者机构：Department of BioengineeringCollege of Biological Science and BiotechnologyFuzhou UniversityFuzhou 350104China Eye Institute of Integrated Chinese and Western MedicineFujian University of Traditional Chinese MedicineFuzhou 350004China Department of OphthalmologyAffiliated People's Hospital(Fujian Provincial People's Hospital)Fujian University of Traditional Chinese MedicineFuzhou 350004China 

出 版 物：《Journal of Traditional Chinese Medicine》 (中医杂志（英文版）)

年 卷 期：2024年第44卷第2期

页      面：268-276页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

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) 

主　　题：alkali burn emodin corneal inflammation corneal neovascularisation vascular endothelial growth factor receptor-2 signal transduction 

摘      要：OBJECTIVE:To investigate the effects of emodin on alkali burn-induced corneal inflammation and ***:The ability of emodin to target vascular endothelial growth factor receptor 2(VEGFR2)was predicted by molecular *** 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 *** of apoptosis was performed by flow ***31 levels were examined by *** abundance and phosphorylation state of VEGFR2,protein kinase B(Akt),signal transducer and activator of transcription 3(STAT3),and P38 were examined by immunoblot *** alkali burn was performed on 40 *** 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 *** microscopy was used to evaluate inflammation and corneal neovascularization(CNV)in all eyes on Days 0,7,10,and *** mice were killed humanely 14 d after the alkali burn,and their corneas were removed and preserved at-80℃ until histological study or protein ***:Molecular docking confirmed that emodin was able to target *** findings revealed that emodin decreased the invasion,migration,angiogenesis,and proliferation of HUVEC in a dose-dependent *** mice,emodin suppressed corneal inflammatory cell infiltration and inhibited the development of corneal neovascularization induced by alkali *** to those of the PBS-treated group,lower VEGFR2 expression and CD31 levels were found in the emodintreated *** dramatically decreased the expression of VEGFR2,p-VEGFR2,p-Akt,p-STAT3,and p-P38 in VEGF-treated ***:This study provides a new avenue for evaluating the molecular mechanisms underlying corneal inflammation and *** might be a promising new therapeutic option for corneal alkal