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Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice

The main cause of arteriosclerosis is atherosclerosis in the aorta. Atherosclerosis is recognized as a chronic inflammatory condition that begins with the dysfunction or activation of arterial endothelium. Low-density lipoprotein (LDL) and especially its oxidized form play a key role in endothelial...

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Autores principales: Iketani, Masumi, Sekimoto, Kanako, Igarashi, Tsutomu, Takahashi, Mayumi, Komatsu, Masaki, Sakane, Iwao, Takahashi, Hiroshi, Kawaguchi, Hideo, Ohtani-Kaneko, Ritsuko, Ohsawa, Ikuroh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235982/
https://www.ncbi.nlm.nih.gov/pubmed/30429524
http://dx.doi.org/10.1038/s41598-018-35239-0
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author Iketani, Masumi
Sekimoto, Kanako
Igarashi, Tsutomu
Takahashi, Mayumi
Komatsu, Masaki
Sakane, Iwao
Takahashi, Hiroshi
Kawaguchi, Hideo
Ohtani-Kaneko, Ritsuko
Ohsawa, Ikuroh
author_facet Iketani, Masumi
Sekimoto, Kanako
Igarashi, Tsutomu
Takahashi, Mayumi
Komatsu, Masaki
Sakane, Iwao
Takahashi, Hiroshi
Kawaguchi, Hideo
Ohtani-Kaneko, Ritsuko
Ohsawa, Ikuroh
author_sort Iketani, Masumi
collection PubMed
description The main cause of arteriosclerosis is atherosclerosis in the aorta. Atherosclerosis is recognized as a chronic inflammatory condition that begins with the dysfunction or activation of arterial endothelium. Low-density lipoprotein (LDL) and especially its oxidized form play a key role in endothelial dysfunction and atherogenesis. Recent studies showed that senescent cells are involved in the development and progression of atherosclerosis, and eliminating senescent cells suppresses the senescence-associated secretory phenotype. We previously reported that molecular hydrogen-rich water (HW) has antioxidant and anti-inflammatory effects in numerous diseases. Here, we used LDL receptor-deficient mice fed a high-fat diet (HFD) for 13 weeks as a model for atherosclerosis and evaluated the effects of continuous administration of HW. The numbers of endothelial cells in the atheroma expressing the senescence factors p16(INK4a) and p21 decreased in HFD-fed mice given HW compared with HFD-fed mice given control water. Furthermore, macrophage infiltration and Tnfα expression in the atheroma were also suppressed. These results suggest that vascular aging can be suppressed by HW.
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spelling pubmed-62359822018-11-20 Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice Iketani, Masumi Sekimoto, Kanako Igarashi, Tsutomu Takahashi, Mayumi Komatsu, Masaki Sakane, Iwao Takahashi, Hiroshi Kawaguchi, Hideo Ohtani-Kaneko, Ritsuko Ohsawa, Ikuroh Sci Rep Article The main cause of arteriosclerosis is atherosclerosis in the aorta. Atherosclerosis is recognized as a chronic inflammatory condition that begins with the dysfunction or activation of arterial endothelium. Low-density lipoprotein (LDL) and especially its oxidized form play a key role in endothelial dysfunction and atherogenesis. Recent studies showed that senescent cells are involved in the development and progression of atherosclerosis, and eliminating senescent cells suppresses the senescence-associated secretory phenotype. We previously reported that molecular hydrogen-rich water (HW) has antioxidant and anti-inflammatory effects in numerous diseases. Here, we used LDL receptor-deficient mice fed a high-fat diet (HFD) for 13 weeks as a model for atherosclerosis and evaluated the effects of continuous administration of HW. The numbers of endothelial cells in the atheroma expressing the senescence factors p16(INK4a) and p21 decreased in HFD-fed mice given HW compared with HFD-fed mice given control water. Furthermore, macrophage infiltration and Tnfα expression in the atheroma were also suppressed. These results suggest that vascular aging can be suppressed by HW. Nature Publishing Group UK 2018-11-14 /pmc/articles/PMC6235982/ /pubmed/30429524 http://dx.doi.org/10.1038/s41598-018-35239-0 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Iketani, Masumi
Sekimoto, Kanako
Igarashi, Tsutomu
Takahashi, Mayumi
Komatsu, Masaki
Sakane, Iwao
Takahashi, Hiroshi
Kawaguchi, Hideo
Ohtani-Kaneko, Ritsuko
Ohsawa, Ikuroh
Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title_full Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title_fullStr Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title_full_unstemmed Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title_short Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice
title_sort administration of hydrogen-rich water prevents vascular aging of the aorta in ldl receptor-deficient mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235982/
https://www.ncbi.nlm.nih.gov/pubmed/30429524
http://dx.doi.org/10.1038/s41598-018-35239-0
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