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Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia

Chronic hyperglycemia is associated with oxidative stress and vascular inflammation, both leading to endothelial dysfunction and cardiovascular disease that can be weakened by antioxidant/anti-inflammatory molecules in both healthy and diabetic subjects. Among natural molecules, ovothiol A, produced...

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Autores principales: Castellano, Immacolata, Di Tomo, Pamela, Di Pietro, Natalia, Mandatori, Domitilla, Pipino, Caterina, Formoso, Gloria, Napolitano, Alessandra, Palumbo, Anna, Pandolfi, Assunta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5932987/
https://www.ncbi.nlm.nih.gov/pubmed/29849868
http://dx.doi.org/10.1155/2018/2087373
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author Castellano, Immacolata
Di Tomo, Pamela
Di Pietro, Natalia
Mandatori, Domitilla
Pipino, Caterina
Formoso, Gloria
Napolitano, Alessandra
Palumbo, Anna
Pandolfi, Assunta
author_facet Castellano, Immacolata
Di Tomo, Pamela
Di Pietro, Natalia
Mandatori, Domitilla
Pipino, Caterina
Formoso, Gloria
Napolitano, Alessandra
Palumbo, Anna
Pandolfi, Assunta
author_sort Castellano, Immacolata
collection PubMed
description Chronic hyperglycemia is associated with oxidative stress and vascular inflammation, both leading to endothelial dysfunction and cardiovascular disease that can be weakened by antioxidant/anti-inflammatory molecules in both healthy and diabetic subjects. Among natural molecules, ovothiol A, produced in sea urchin eggs to protect eggs/embryos from the oxidative burst at fertilization and during development, has been receiving increasing interest for its use as an antioxidant. Here, we evaluated the potential antioxidative/anti-inflammatory effect of purified ovothiol A in an in vitro cellular model of hyperglycemia-induced endothelial dysfunction employing human umbilical vein endothelial cells (HUVECs) from women affected by gestational diabetes (GD) and from healthy mothers. Ovothiol A was rapidly taken up by both cellular systems, resulting in increased glutathione values in GD-HUVECs, likely due to the formation of reduced ovothiol A. In tumor necrosis factor-α-stimulated cells, ovothiol A induced a downregulation of adhesion molecule expression and decrease in monocyte-HUVEC interaction. This was associated with a reduction in reactive oxygen and nitrogen species and an increase in nitric oxide bioavailability. These results point to the potential antiatherogenic properties of the natural antioxidant ovothiol A and support its therapeutic potential in pathologies related to cardiovascular diseases associated with oxidative/inflammatory stress and endothelial dysfunction.
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spelling pubmed-59329872018-05-30 Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia Castellano, Immacolata Di Tomo, Pamela Di Pietro, Natalia Mandatori, Domitilla Pipino, Caterina Formoso, Gloria Napolitano, Alessandra Palumbo, Anna Pandolfi, Assunta Oxid Med Cell Longev Research Article Chronic hyperglycemia is associated with oxidative stress and vascular inflammation, both leading to endothelial dysfunction and cardiovascular disease that can be weakened by antioxidant/anti-inflammatory molecules in both healthy and diabetic subjects. Among natural molecules, ovothiol A, produced in sea urchin eggs to protect eggs/embryos from the oxidative burst at fertilization and during development, has been receiving increasing interest for its use as an antioxidant. Here, we evaluated the potential antioxidative/anti-inflammatory effect of purified ovothiol A in an in vitro cellular model of hyperglycemia-induced endothelial dysfunction employing human umbilical vein endothelial cells (HUVECs) from women affected by gestational diabetes (GD) and from healthy mothers. Ovothiol A was rapidly taken up by both cellular systems, resulting in increased glutathione values in GD-HUVECs, likely due to the formation of reduced ovothiol A. In tumor necrosis factor-α-stimulated cells, ovothiol A induced a downregulation of adhesion molecule expression and decrease in monocyte-HUVEC interaction. This was associated with a reduction in reactive oxygen and nitrogen species and an increase in nitric oxide bioavailability. These results point to the potential antiatherogenic properties of the natural antioxidant ovothiol A and support its therapeutic potential in pathologies related to cardiovascular diseases associated with oxidative/inflammatory stress and endothelial dysfunction. Hindawi 2018-04-19 /pmc/articles/PMC5932987/ /pubmed/29849868 http://dx.doi.org/10.1155/2018/2087373 Text en Copyright © 2018 Immacolata Castellano et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under 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
Castellano, Immacolata
Di Tomo, Pamela
Di Pietro, Natalia
Mandatori, Domitilla
Pipino, Caterina
Formoso, Gloria
Napolitano, Alessandra
Palumbo, Anna
Pandolfi, Assunta
Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title_full Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title_fullStr Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title_full_unstemmed Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title_short Anti-Inflammatory Activity of Marine Ovothiol A in an In Vitro Model of Endothelial Dysfunction Induced by Hyperglycemia
title_sort anti-inflammatory activity of marine ovothiol a in an in vitro model of endothelial dysfunction induced by hyperglycemia
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5932987/
https://www.ncbi.nlm.nih.gov/pubmed/29849868
http://dx.doi.org/10.1155/2018/2087373
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