Abstract
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss among the elderly population. Vascular endothelial growth factor (VEGF) is essential for choroidal neovascularization (CNV) development in advanced, wet AMD. Chrysin (5,7-dihydroxyflavone) is a natural flavonoid with anti-inflammatory, anti-oxidative, and anti-angiogenic effects. We hypothesized that intravitreally injected chrysin may inhibit CNV due to its inhibitory effect on angiogenesis. To determine the effects of chrysin on an experimental CNV model, we induced CNV in Brown Norway rats with a diode laser. One week later, rats were injected intravitreally with chrysin in the right eye and vehicle in the left eye. The following week, we evaluated chrysin’s effects via the CNV grade assessed with fluorescein angiography and histologic analyses. Hypoxia-inducible factor-1 alpha (HIF-1α) and VEGF expression in the retina/choroid complex were also measured in both eyes. The mean CNV grade was significantly lower in chrysin-treated vs. control eyes (2.34 ± 1.14 vs. 2.97 ± 1.05, p < 0.001), as was the mean CNV thickness (33.90 ± 4.89 vs. 38.50 ± 5.43 μm, p < 0.001) and mean HIF-1α and VEGF levels (both p < 0.001). Compared to chrysin-treated eyes, the relative risk of control eyes developing high-leakage lesions was 2.03 (95% confidence interval: 1.46–2.83). Since chrysin inhibited laser-induced CNV and downregulated HIF-1α and VEGF expression, it is a candidate for treating wet AMD and other CNV-associated conditions.
Highlights
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss among people over the age of 50 in developed countries [1]
The advanced stage of wet AMD is represented by choroidal neovascularization (CNV), which is the abnormal ingrowth of new vessels under the macula
The mean CNV grade per lesion was significantly lower in the chrysin-treated group than in the control group
Summary
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss among people over the age of 50 in developed countries [1]. CNV develops following pathologic angiogenesis, including proteolysis of the extracellular matrix, endothelial cell migration and proliferation, and synthesis of new matrix components [2]. Treatments for CNV, such as laser photocoagulation, photodynamic therapy, and macular translocation, have yielded poor visual outcomes [4,5,6]. The recent development of pharmacological inhibitors of angiogenesis has focused on inhibiting vascular endothelial growth factor (VEGF) and potentially proteolytic enzymes such as matrix metalloproteinases [7,8,9]. New therapies that utilize VEGF antibodies, such as bevacizumab, ranibizumab, and aflibercept, have brought a paradigm shift to AMD treatment. These treatments have limitations [10,11,12]
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