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　10　μM　emodin　or　phosphate　buffered　saline　(PBS)　four　times　a　day.　Slit-lamp　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　emodin-treated　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.　©　2024　JTCM.　All　rights　reserved.