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Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy

PURPOSE: Ocular neovascularization is a leading cause of blindness in ischemic retinopathies. Hypericin is an active ingredient in the medical herb St. John’s Wort (SJW). Because hypericin inhibits intracellular signaling pathways that are believed to participate in the regulation of angiogenesis, w...

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Autores principales: Higuchi, Akiko, Yamada, Haruhiko, Yamada, Eri, Jo, Nobuo, Matsumura, Miyo
Formato: Texto
Lenguaje:English
Publicado: Molecular Vision 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2255059/
https://www.ncbi.nlm.nih.gov/pubmed/18334941
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author Higuchi, Akiko
Yamada, Haruhiko
Yamada, Eri
Jo, Nobuo
Matsumura, Miyo
author_facet Higuchi, Akiko
Yamada, Haruhiko
Yamada, Eri
Jo, Nobuo
Matsumura, Miyo
author_sort Higuchi, Akiko
collection PubMed
description PURPOSE: Ocular neovascularization is a leading cause of blindness in ischemic retinopathies. Hypericin is an active ingredient in the medical herb St. John’s Wort (SJW). Because hypericin inhibits intracellular signaling pathways that are believed to participate in the regulation of angiogenesis, we investigated the actions of hypericin and SJW in retinal neovascularization, using a mouse model of oxygen-induced retinopathy (OIR). METHODS: C57BL/6 neonatal mice were exposed to a 75% concentration of oxygen from postnatal day 7 (P7) to P12 and returned to room air from P12 to P17 to induce retinal neovascularization. SJW (15 mg/kg/day), hypericin (15, 45, or 135 μg/kg/day), or vehicle was given by gavage once a day for five days from P12 to P17. To quantify the area of retinal neovascularization and vasoobliteration, we stained retinas with isolectin B4 at P17. Phosphorylation of extracellular signal-regulated kinase (ERK) in ischemic retinas was determined by western blot analysis. To estimate retinal vascularization, we stained retinas with isolectin B4 at P7 after treatment with SJW, hypericin, or vehicle from P3 to P7. RESULTS: Gavage administration of hypericin or SJW significantly inhibited the degree of retinal neovascularization, but did not affect the area of retinal vasoobliteration in a mouse model of OIR. Both SJW and hypericin had no effect on normal vascularization over the treatment time course. Treatment with SJW or hypericin reduced phosphorylation of ERK in the retina. CONCLUSIONS: These data suggest that hypericin and SJW reduce pathological retinal neovascularization and that administration of these agents could have clinical utility for treatment of ischemic retinopathies.
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spelling pubmed-22550592008-03-11 Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy Higuchi, Akiko Yamada, Haruhiko Yamada, Eri Jo, Nobuo Matsumura, Miyo Mol Vis Research Article PURPOSE: Ocular neovascularization is a leading cause of blindness in ischemic retinopathies. Hypericin is an active ingredient in the medical herb St. John’s Wort (SJW). Because hypericin inhibits intracellular signaling pathways that are believed to participate in the regulation of angiogenesis, we investigated the actions of hypericin and SJW in retinal neovascularization, using a mouse model of oxygen-induced retinopathy (OIR). METHODS: C57BL/6 neonatal mice were exposed to a 75% concentration of oxygen from postnatal day 7 (P7) to P12 and returned to room air from P12 to P17 to induce retinal neovascularization. SJW (15 mg/kg/day), hypericin (15, 45, or 135 μg/kg/day), or vehicle was given by gavage once a day for five days from P12 to P17. To quantify the area of retinal neovascularization and vasoobliteration, we stained retinas with isolectin B4 at P17. Phosphorylation of extracellular signal-regulated kinase (ERK) in ischemic retinas was determined by western blot analysis. To estimate retinal vascularization, we stained retinas with isolectin B4 at P7 after treatment with SJW, hypericin, or vehicle from P3 to P7. RESULTS: Gavage administration of hypericin or SJW significantly inhibited the degree of retinal neovascularization, but did not affect the area of retinal vasoobliteration in a mouse model of OIR. Both SJW and hypericin had no effect on normal vascularization over the treatment time course. Treatment with SJW or hypericin reduced phosphorylation of ERK in the retina. CONCLUSIONS: These data suggest that hypericin and SJW reduce pathological retinal neovascularization and that administration of these agents could have clinical utility for treatment of ischemic retinopathies. Molecular Vision 2008-02-04 /pmc/articles/PMC2255059/ /pubmed/18334941 Text en Copyright © 2008 Molecular Vision. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Higuchi, Akiko
Yamada, Haruhiko
Yamada, Eri
Jo, Nobuo
Matsumura, Miyo
Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title_full Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title_fullStr Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title_full_unstemmed Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title_short Hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
title_sort hypericin inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2255059/
https://www.ncbi.nlm.nih.gov/pubmed/18334941
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