Cited by 205Nitric Oxide and Endothelin EffectsMetabolism, Diabetes, and CancerDiabetes Treatment and Management

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Metformin decreases intracellular production of reactive oxygen species in aortic endothelial cells

Ouslimani, Nadjat, Peynet, Jacqueline, Bonnefont-Rousselot, Dominique, Thérond, Patrice, Legrand, Alain, Beaudeux, Jean-Louis·2005·Metabolism

DOI 10.1016/j.metabol.2005.01.029

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Abstract

Beyond its antidiabetic activity justifying its use in the treatment of the type 2 diabetes, metformin (MET [dimethylguanidine, Glucophage]) has been shown to exhibit antioxidant properties in vitro, which could contribute to limit the deleterious vascular complications of diabetes. We investigated whether MET, at the pharmacological level of 10 -5 mol/L, was able to modulate intracellular production of reactive oxygen species (ROS) both in quiescent bovine aortic endothelial cells (BAECs) and in BAECs stimulated by a short incubation with high levels of glucose (30 mmol/L, 2 hours) or angiotensin II (10 -7 mol/L, 1 hour). Intracellular ROS production was measured by fluorescence of the DCF (2,7-dichlorodihydrofluorescein) probe. Our results showed that MET was able to reduce the intracellular production of ROS in both nonstimulated BAECs (-20%, P < .05) and BAEC stimulated by high levels of glucose or angiotensin II (-28% and -72%, respectively, P < .01). Experiments performed in the presence of the nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase inhibitor apocynin or the respiratory mitochondrial chain inhibitor rotenone indicated that MET exerted its effect partly through an inhibition of the formation of ROS produced mainly by NAD(P)H oxidase and also, to a lesser extent, by the respiratory mitochondrial chain.

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Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean?
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High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C--dependent activation of NAD(P)H oxidase in cultured vascular cells
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Authors: Ouslimani, N., Peynet, J., Bonnefont-Rousselot, D., Thérond, P., Legrand, A., & Beaudeux, J.-L.
Corresponding author: Beaudeux, Jean-Louis
ORCID: Thérond, Patrice
Beaudeux, Jean-Louis
Venue: Metabolism
Publisher: Elsevier BV
Published: 2005-06
Volume: 54
Issue: 6
Pages: 829-834
ISSN: 0026-0495 (ISSN-L)
DOI: 10.1016/j.metabol.2005.01.029
OpenAlex: W2103676852
Cited by: 204
References: 54
Citations by year: 2026: 5 · 2025: 5 · 2024: 8 · 2023: 5 · 2022: 6 · 2021: 20 · 2020: 14 · 2019: 10 · 2018: 9 · 2017: 9 · 2016: 15 · 2015: 13 · 2014: 11 · 2013: 12 · 2012: 11
FWCI: 4.60
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Metabolism (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords: metformin, reactive oxygen species, aortic endothelial cells, antioxidant activity, NADPH oxidase, apocynin, mitochondrial respiratory chain, angiotensin II, high glucose, diabetic vascular complications, type 2 diabetes
MeSH terms: Animals, Aorta, Cattle, Cells, Cultured, Hypoglycemic Agents, Metformin, Reactive Oxygen Species, NADPH Oxidases, Endothelial Cells

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Metformin decreases intracellular production of reactive oxygen species in aortic endothelial cells

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