Inhibitory Effects of Topical Thymoquinone on Corneal Neovascularization

Erdurmuş, Mesut; Yağcı, Ramazan; Yılmaz, Bülent; Hepşen, İbrahim F.; Turkmen, Cem; Aydın, Bahri; Karadağ, Remzi

doi:10.1097/ico.0b013e31804f5a45

Cited by 28 publications

(24 citation statements)

References 31 publications

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“…By day 7, neovascularizaiton extended to the margins of the corneal burn. Thus, the endpoint of the study was achieved because the neovascularization in control eyes has a tendency to regress gradually after day 7 [15,16] . Table 1 summarizes the length and number of new vessels in both groups.…”

Section: Resultsmentioning

confidence: 99%

“…All these treatment options used in corneal neovascularization are not ideal treatments because of side effects like thermal injury to adjacent areas, ocular hypertension, cataract formation and vessel recanalization [16] .…”

Section: Discussionmentioning

confidence: 99%

“…Various compounds like steroids [17,18] , nonsteroidal anti-inflammatory drugs [19,20] , heparin [20] , natural extracts [15,16] , cyclosporine A [21] , methotrexate [22] , and different therapies like argon laser treatment and photodynamic therapy [23] have been used in experimental and clinical studies for treatment and prevention of corneal neovascularization. All these treatment options used in corneal neovascularization are not ideal treatments because of side effects like thermal injury to adjacent areas, ocular hypertension, cataract formation and vessel recanalization [16] .…”

Section: Discussionmentioning

confidence: 99%

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Inhibitory Effects of SU5416, a Selective Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor, on Experimental Corneal Neovascularization

Keskın

Totan²,

Karadağ³

et al. 2011

Ophthalmic Res

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Purpose: Treatment of neovascularization in ocular diseases with vascular endothelial growth factor (VEGF) inhibition shows promising results. SU5416 is a low-molecular-weight tyrosine kinase inhibitor. It selectively inhibits the membrane-bound tyrosine kinase activity of VEGF-2 receptor (Flk-1/KDR) and blocks the intracellular signaling process. The aim of this study was to evaluate the effect of SU5416 on corneal neovascularization. Methods: Corneas were cauterized with silver nitrate/potassium nitrate sticks in 20 eyes of 20 BALB/C mice. In the study group (n = 10), SU5416 (25 mg/kg) dissolved in dimethyl sulfoxide was given as an intraperitoneal injection in a single daily dose for 7 days. The other group of 10 mice given intraperitoneal dimethyl sulfoxide alone served as a control group. After 7 days, corneal neovascularization was evaluated using photographs captured by fluorescein angiography. Colored photographs were taken by a biomicroscope with a digital camera. Data were expressed as mean neovascular length and mean number of new vessels for each animal. The values were computed and compared between the groups. Results: The mean burn stimulus intensities were not different between the groups. In the study group, the mean length of the vessels and the mean number of vessels were 0.49 ± 0.05 and 11.20 ± 1.69 mm, respectively. In the control group, the mean length of the vessels and the mean number of the vessels were 0.89 ± 0.11 and 17.80 ± 1.03 mm, respectively. There is a statistically significant difference in the mean length and the mean number of new vessels between the study and control groups (p < 0.001). Conclusion: Selective inhibition of VEGFR-2 (Flk-1/KDR) tyrosine kinase with SU5416 was shown to have an inhibitory effect on corneal neovascularization in this animal model. VEGFR-2 (Flk-1/KDR) tyrosine kinase inhibition may represent a different pathway for treatment of the neovascularization process in ocular pathologies. Fluorescein angiography photographs of new vessels on the cornea may provide a better evaluation of neovascularization than colored images in animal models.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibitory Effects of SU5416, a Selective Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor, on Experimental Corneal Neovascularization

Keskın

Totan²,

Karadağ³

et al. 2011

Ophthalmic Res

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“…Work with this model has demonstrated that topical antioxidants suppress the growth of blood vessels in rats [13], implicating reactive oxygen species (ROS) in corneal neovascularization. NADPH oxidase is an important source of ROS that mediates redox signalling in the wound-healing response [14].…”

Section: Introductionmentioning

confidence: 99%

NADPH oxidase 2 plays a role in experimental corneal neovascularization

et al. 2016

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Corneal neovascularization, the growth of new blood vessels in the cornea, is a leading cause of vision impairment after corneal injury. Neovascularization typically occurs in response to corneal injury such as that caused by infection, physical trauma, chemical burns or in the setting of corneal transplant rejection. The NADPH oxidase enzyme complex is involved in cell signalling for wound-healing angiogenesis, but its role in corneal neovascularization has not been studied. We have now analysed the role of the Nox2 isoform of NADPH oxidase in corneal neovascularization in mice following chemical injury. C57BL/6 mice aged 8-14 weeks were cauterized with an applicator coated with 75% silver nitrate and 25% potassium nitrate for 8 s. Neovascularization extending radially from limbal vessels was observed in corneal whole-mounts from cauterized wild type mice and CD31+ vessels were identified in cauterized corneal sections at day 7. In contrast, in Nox2 knockout (Nox2 KO) mice vascular endothelial growth factor-A (Vegf-A), Flt1 mRNA expression, and the extent of corneal neovascularization were all markedly reduced compared with their wild type controls. The accumulation of Iba-1+ microglia and macrophages in the cornea was significantly less in Nox2 KO than in wild type mice. In conclusion, we have demonstrated that Nox2 is implicated in the inflammatory and neovascular response to corneal chemical injury in mice and clearly VEGF is a mediator of this effect. This work raises the possibility that therapies targeting Nox2 may have potential for suppressing corneal neovascularization and inflammation in humans.

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“…Briefly, starting on day 15 after sensitization, five drops of 0.4% (w/v) thymoquinone were instilled in the nasal cavity three times per day for 7 days. This dose was shown to be as effective as topical steroids in a model of allergic conjunctivitis [13]. The group 4 rabbits received mometasone furoate 2 puffs/day (100 μg) for 7 days after OVA sensitization.…”

Section: Methodsmentioning

confidence: 99%

Comparison of Histopathological Effects of Thymoquinone and Local Nasal Corticosteroids in Allergic Rhinitis in a Rabbit Model

Yurttaş

Şereflican

Erkoçoğlu³

et al. 2016

ORL

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Background/Aims: In this study, we aimed to evaluate the histopathological effects of thymoquinone treatment of the nasal mucosa in a rabbit model of allergic rhinitis, and we compared its effects with those of nasal mometasone furoate. Methods: A total of 24 male New Zealand rabbits were used. The animals were randomly assigned to one of four groups. Group 1 received no treatment, while group 2 underwent ovalbumin (OVA) sensitization only. Group 3 was the study group; after OVA sensitization, the rabbits were treated with intranasal thymoquinone. The group 4 rabbits received mometasone furoate for 7 days after OVA sensitization. Mucosal structures were stained with hematoxylin and eosin, while toluidine blue was used to stain mast cells. Apoptosis was evaluated using a TUNEL assay. Results: In the positive control groups, including the thymoquinone and intranasal mometasone furoate groups, intraepithelial and submucosal inflammation and goblet cell hypertrophy were significantly decreased compared to group 2 (p < 0.001). The cilial structure was normal, as was the chondrocyte structure in both treatment groups. Conclusion: This is the first study to evaluate the histopathological effects of thymoquinone in an allergic rhinitis model. Thymoquinone reduced allergic inflammation and may be valuable for treating allergic rhinitis. However, additional studies are needed.

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Inhibitory Effects of Topical Thymoquinone on Corneal Neovascularization

Abstract: Thymoquinone was shown to have an inhibitory effect, comparable with that of triamcinolone, on corneal neovascularization in this rat model. However, thymoquinone decreased corneal neovascularization in a dose-dependent manner.

Cited by 28 publications

References 31 publications

Inhibitory Effects of SU5416, a Selective Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor, on Experimental Corneal Neovascularization

Inhibitory Effects of SU5416, a Selective Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor, on Experimental Corneal Neovascularization

NADPH oxidase 2 plays a role in experimental corneal neovascularization

Comparison of Histopathological Effects of Thymoquinone and Local Nasal Corticosteroids in Allergic Rhinitis in a Rabbit Model

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