Topical dimethyl sulfoxide inhibits corneal neovascularization and stimulates corneal repair in rabbits following acid burn

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dc.contributor.authorAltan, S.
dc.contributor.authorSagsoz, H.
dc.contributor.authorOgurtan, Z.
dc.date.accessioned2024-04-24T16:24:54Z
dc.date.available2024-04-24T16:24:54Z
dc.date.issued2017
dc.departmentDicle Üniversitesien_US
dc.description.abstractNeovascularization of the cornea is characterized by the growth of blood vessels caused by imbalances between angiogenic and anti-angiogenic factors. We investigated whether the expression of Vascular endothelial growth factor (VEGF), Vascular endothelial growth factor receptor (VEGF), Vascular endothelial growth inhibitor (VEGI) receptors, as well as topical drug treatments, participate in regulating corneal neovascularization after corneal damage and remodeling. We used 72 mature male New Zealand rabbits. Corneal burns were induced by hydrofluoric acid under general anesthesia. The rabbits then were treated with indomethacin or dimethyl sulfoxide (DMSO). The animals were euthanized on days 2, 7 and 14 after injury. Each cornea was fixed with 10% neutral formalin. On days 2, 7 and 14, VEGF, flk1/KDR and flt1/fms were strongly expressed in the epithelial, stromal and inflammatory cells, but not in the corneal endothelial cells. On day 7, newly formed blood vessels were observed growing toward the center of the cornea. In the control, indomethacin treated, DMSO-treated, and indomethacin + DMSO-treated animals, VEGI, VEGF, and the receptors, flk1/KDR, flt1/fms and flt4, were expressed at different densities in the neovascular regions. This was particularly evident in the indomethacin- and indomethacin + DMSO-treated groups on days 7 and 14, compared to day 2. Treatment with VEGF and DMSO stimulated repair of corneal damage. We suggest that VEGI in the endothelial cells of neovascularized cornea may act as a signaling protein that promotes balance between cell proliferation and apoptosis. Topical administration of DMSO inhibited corneal neovascularization more effectively than indomethacin.en_US
dc.identifier.doi10.1080/10520295.2017.1371333
dc.identifier.endpage636en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue8en_US
dc.identifier.pmid29233043
dc.identifier.scopus2-s2.0-85037977161
dc.identifier.scopusqualityQ2
dc.identifier.startpage619en_US
dc.identifier.urihttps://doi.org/10.1080/10520295.2017.1371333
dc.identifier.urihttps://hdl.handle.net/11468/16891
dc.identifier.volume92en_US
dc.identifier.wosWOS:000427660100010
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofBiotechnic & Histochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAngiogenesisen_US
dc.subjectBurnsen_US
dc.subjectCorneaen_US
dc.subjectCytokineen_US
dc.subjectDimethyl Sulfoxideen_US
dc.subjectDmsoen_US
dc.subjectEyeen_US
dc.subjectHydrofluoric Aciden_US
dc.subjectIndomethacinen_US
dc.subjectNeovascularizationen_US
dc.subjectRabbiten_US
dc.subjectVegien_US
dc.titleTopical dimethyl sulfoxide inhibits corneal neovascularization and stimulates corneal repair in rabbits following acid burnen_US
dc.titleTopical dimethyl sulfoxide inhibits corneal neovascularization and stimulates corneal repair in rabbits following acid burn
dc.typeArticleen_US

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