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Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation
Hesperetin is a natural flavonoid with robust antioxidant properties. Our previous study reported that hesperetin can prevent cataract formation. However, an important consideration regarding hesperetin consumption is the limited bioavailability due to its poor solubility. The present study investig...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7003023/ https://www.ncbi.nlm.nih.gov/pubmed/32016451 http://dx.doi.org/10.3892/mmr.2020.10941 |
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author | Nakazawa, Yosuke Aoki, Miki Ishiwa, Sho Morishita, Naoki Endo, Shin Nagai, Noriaki Yamamoto, Naoki Funakoshi-Tago, Megumi Tamura, Hiroomi |
author_facet | Nakazawa, Yosuke Aoki, Miki Ishiwa, Sho Morishita, Naoki Endo, Shin Nagai, Noriaki Yamamoto, Naoki Funakoshi-Tago, Megumi Tamura, Hiroomi |
author_sort | Nakazawa, Yosuke |
collection | PubMed |
description | Hesperetin is a natural flavonoid with robust antioxidant properties. Our previous study reported that hesperetin can prevent cataract formation. However, an important consideration regarding hesperetin consumption is the limited bioavailability due to its poor solubility. The present study investigated the anti-cataract effects of α-glucosyl hesperidin in vivo and in vitro using a selenite-induced cataract model. SD rats (age, 13 days) were orally administered PBS (0.2 ml) or α-glucosyl hesperidin (200 mg/kg) on days 0, 1 and 2. Sodium selenite was subcutaneously administered to the rats 4 h after the first oral administration on day 0. Antioxidant levels in the lens and blood were measured on day 6. In vitro, human lens epithelial cells were treated with sodium selenite (10 µM) and/or hesperetin (50 or 100 mM) for 24 h and analyzed for apoptosis markers using sub-G(1) population and Annexin V-FITC/propidium iodide staining and DNA ladder formation. α-glucosyl hesperidin treatment significantly reduced the severity of selenite-induced cataract. The level of antioxidants was significantly reduced in the selenite-treated rats compared with in the controls; however, they were normalized with α-glucosyl hesperidin treatment. In vitro, hesperetin could significantly reduce the number of cells undergoing apoptosis induced by sodium selenite in human lens epithelial cell lines. Overall, oral consumption of α-glucosyl hesperidin could delay the onset of selenite-induced cataract, at least in part by modulating the selenite-induced cell death in lens epithelial cells. |
format | Online Article Text |
id | pubmed-7003023 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-70030232020-02-12 Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation Nakazawa, Yosuke Aoki, Miki Ishiwa, Sho Morishita, Naoki Endo, Shin Nagai, Noriaki Yamamoto, Naoki Funakoshi-Tago, Megumi Tamura, Hiroomi Mol Med Rep Articles Hesperetin is a natural flavonoid with robust antioxidant properties. Our previous study reported that hesperetin can prevent cataract formation. However, an important consideration regarding hesperetin consumption is the limited bioavailability due to its poor solubility. The present study investigated the anti-cataract effects of α-glucosyl hesperidin in vivo and in vitro using a selenite-induced cataract model. SD rats (age, 13 days) were orally administered PBS (0.2 ml) or α-glucosyl hesperidin (200 mg/kg) on days 0, 1 and 2. Sodium selenite was subcutaneously administered to the rats 4 h after the first oral administration on day 0. Antioxidant levels in the lens and blood were measured on day 6. In vitro, human lens epithelial cells were treated with sodium selenite (10 µM) and/or hesperetin (50 or 100 mM) for 24 h and analyzed for apoptosis markers using sub-G(1) population and Annexin V-FITC/propidium iodide staining and DNA ladder formation. α-glucosyl hesperidin treatment significantly reduced the severity of selenite-induced cataract. The level of antioxidants was significantly reduced in the selenite-treated rats compared with in the controls; however, they were normalized with α-glucosyl hesperidin treatment. In vitro, hesperetin could significantly reduce the number of cells undergoing apoptosis induced by sodium selenite in human lens epithelial cell lines. Overall, oral consumption of α-glucosyl hesperidin could delay the onset of selenite-induced cataract, at least in part by modulating the selenite-induced cell death in lens epithelial cells. D.A. Spandidos 2020-03 2020-01-14 /pmc/articles/PMC7003023/ /pubmed/32016451 http://dx.doi.org/10.3892/mmr.2020.10941 Text en Copyright: © Nakazawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Nakazawa, Yosuke Aoki, Miki Ishiwa, Sho Morishita, Naoki Endo, Shin Nagai, Noriaki Yamamoto, Naoki Funakoshi-Tago, Megumi Tamura, Hiroomi Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title | Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title_full | Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title_fullStr | Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title_full_unstemmed | Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title_short | Oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
title_sort | oral intake of α-glucosyl-hesperidin ameliorates selenite-induced cataract formation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7003023/ https://www.ncbi.nlm.nih.gov/pubmed/32016451 http://dx.doi.org/10.3892/mmr.2020.10941 |
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