Treatment of Corneal Neovascularization by Topical Application of Ascorbic Acid in the Rabbit Model

Lee, Mee Yon; Chung, Sung Kun

doi:10.1097/ico.0b013e318241433b

Cited by 30 publications

(26 citation statements)

References 18 publications

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“…To maintain corneal avascularity, angiogenic factors and inhibitors must maintain homeostasis. 15 Angiogenesis has been shown to be generally mediated by many angiogenic and antiangiogenic factors, and VEGF is known to play an important role in corneal neovascularization. 4,5 Bevacizumab is a humanized monoclonal IgG1 antibody to VEGF, and several studies have shown that subconjunctival injection of bevacizumab inhibits corneal neovascularization in experimental models or clinical trials.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Many studies have confirmed in animal models the effectiveness of subconjunctival bevacizumab on newly formed corneal blood vessels. 11,12 Our institute has studied corneal neovascularization and reported antiangiogenic effects of subconjunctival suramin, 13 subconjunctival triamcinolone acetonide, 14 topical ascorbic acid, 15 topical curcumin, 16 subconjunctival bevacizumab, 17 topical methotrexate, 18 thalidomide, 19 and topical infliximab. 20 Our study focused on the possibility that interleukin-6 (IL-6) directly stimulates VEGF and angiogenesis.…”

mentioning

confidence: 99%

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Effects of Subconjunctival Tocilizumab Versus Bevacizumab in Treatment of Corneal Neovascularization in Rabbits

Yoo

Chung

2014

Cornea

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of Subconjunctival Tocilizumab Versus Bevacizumab in Treatment of Corneal Neovascularization in Rabbits

Yoo

Chung

2014

Cornea

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“…Topical ascorbic acid application may be effective for CNV therapy. Both the concentration of VEGF and MMP‐9 showed a significant difference between the treated groups and control group . So far, ascorbic acid has been applied for various diseases including cardiovascular diseases, cancer, infection, and degenerative diseases.…”

Section: The Drug Treatment Of Cnvmentioning

confidence: 96%

Recent drug therapies for corneal neovascularization

Liu

Wang

et al. 2017

Chem Biol Drug Des

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Corneal neovascularization (CNV) is a common pathological change in ocular surface diseases. It is not only the factor that affects vision but also the main cause for corneal graft failure. Based on the mechanism of CNV, many achievements have been developed to suppress the formation of CNV. There are certain novel drugs such as aflibercept, gold nanoparticles, and netrins which provide us with new clues to treat CNV. However, we still need to develop more effective therapeutic drugs. It is of great significance to develop new effective drugs to suppress the occurrence of CNV. In this paper, recent drug therapies for CNV are reviewed. The electronic database (PubMed) is searched for relative basic research and randomized clinical trials that are published recently.

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“…Current methods to assess the efficacy of anti-angiogenic treatments have overwhelmingly focused on examination with slit lamp and photography (Chen et al, 2009;Cheng et al, 2012;Chung and Lee, 2012;Dastjerdi et al, 2009;Yoeruek et al, 2008), partly due to the lack of specific methods to detect early inflammation and tissue damage in corneal neovascularization. We have previously showed that it is possible to detect early signs of inflammation by in vivo confocal microscopy (IVCM) (Peebo et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Early effects of dexamethasone and anti-VEGF therapy in an inflammatory corneal neovascularization model

Mirabelli

Peebo

Xeroudaki

et al. 2014

Experimental Eye Research

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Inflammatory angiogenesis is the pathogenic mechanism of various sight-threatening eye diseases, among them corneal neovascularization. Current treatment options include steroids which have undesirable side effects, or anti-VEGF which has only limited efficacy. In an inflammatory environment, however, angiogenesis can be stimulated by numerous factors not directly targeted by anti-VEGF therapy. The aim of this study was to induce corneal inflammation leading to angiogenesis, and investigate the early, differential effects of steroid and anti-VEGF therapy at the cellular, tissue, and gene expression levels. Fifty-two Wistar rats received a single intrastromal corneal suture to induce a controlled inflammatory angiogenic response. Rats were subsequently treated with dexamethasone, rat specific anti-VEGF, or goat IgG (control), topically 4 times daily for 7 days. In vivo confocal microscopy of the cornea was performed longitudinally from 5 h up to 7 d to investigate morphology at the cellular and tissue-level. In vivo photographic vessel analysis and immunohistochemistry were also performed. RT-PCR for VEGF-A, FGF-2, IL-6, TNF-alpha, CXCL2, CCL2, CCL3 and DLL4 was performed at 24 h, and for VEGF-A, IL-6, TNF-alpha, FGF-2, CXCL2, CCL2, and CCL3 at 7 days. Early infiltration of CD11b + myeloid cells into the cornea at 5 h post-suture was delayed by both treatments relative to controls; however neither treatment was able to suppress accumulation of myeloid cells at day 2 or 7. Limbal vessel dilation was inhibited at 5 h by both treatments, but only dexamethasone showed sustained effect until day 2. Early macrophage recruitment was also suppressed by dexamethasone (but not by anti-VEGF) until day 2. Dexamethasone furthermore suppressed corneal neovascularization at day 7 by over 90%, whereas suppression by anti-VEGF was 14%. Despite differential suppression of vessel dilation, macrophage recruitment, and vascular invasion, anti-VEGF and dexamethasone both down-regulated VEGF-A and IL-6 expression at 24 h with sustained effect to 7 d. They also both down regulated FGF-2 and TNF-alpha at 24 h and CCL2 at 7 d. In conclusion, anti-angiogenic treatments influence early, pre-angiogenic tissue activity such as limbal vessel dilation, inflammatory cell infiltration of the stroma, and macrophage recruitment. Importantly, the differential effects of steroids and anti-VEGF treatment in suppressing neovascular growth could not be attributed to differential inhibition of several major angiogenic and inflammatory factors in the early pre-sprouting phase, including IL-6, VEGF-A, FGF-2, TNF-alpha, CCL2, CCL3, CXCL2, or DLL4.

Funding Agencies|Crown Princess Margaretas Foundation; County Council of Ostergotland; Swedish Research Council [2012-2472]

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Treatment of Corneal Neovascularization by Topical Application of Ascorbic Acid in the Rabbit Model

Abstract: Topical administration of ascorbic acid may be useful for the treatment of corneal neovascularization.

Cited by 30 publications

References 18 publications

Effects of Subconjunctival Tocilizumab Versus Bevacizumab in Treatment of Corneal Neovascularization in Rabbits

Effects of Subconjunctival Tocilizumab Versus Bevacizumab in Treatment of Corneal Neovascularization in Rabbits

Recent drug therapies for corneal neovascularization

Early effects of dexamethasone and anti-VEGF therapy in an inflammatory corneal neovascularization model

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