2026-06-14T03:43:15Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/103202024-09-27T08:24:52Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Robles-Vera, Iñaki
author
Toral, Marta
author
de la Visitación, Néstor
author
Aguilera-Sánchez, Nazaret
author
Redondo, Juan Miguel
author
Duarte, Juan
funder
Ministerio de Economía y Competitividad (España)
funder
Regional Government of Andalusia (España)
funder
Instituto de Salud Carlos III
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
2020-06-10T08:47:57Z
2020-06-10T08:47:57Z
2020-05
Front Physiol. 2020; 11:277
10.3389/fphys.2020.00277
1664-042X
Frontiers in physiology
32372967
http://hdl.handle.net/20.500.12105/10320
Short-chain fatty acids (SCFAs) are among the main classes of bacterial metabolic products and are mainly synthesized in the colon through bacterial fermentation. Short-chain fatty acids, such as acetate, butyrate, and propionate, reduce endothelial activation induced by proinflammatory mediators, at least in part, by activation of G protein-coupled receptors (GPRs): GPR41 and GPR43. The objective of the study was to analyze the possible protective effects of SCFAs on endothelial dysfunction induced by angiotensin II (AngII). Rat aortic endothelial cells (RAECs) and rat aortas were incubated with AngII (1 μM) for 6 h in the presence or absence of SCFAs (5-10 mM). In RAECs, we found that AngII reduces the production of nitric oxide (NO) stimulated by calcium ionophore A23187; increases the production of reactive oxygen species (ROS), both from the nicotinamide adenine dinucleotide phosphate oxidase system and the mitochondria; diminishes vasodilator-stimulated phosphoprotein (VASP) phosphorylation at Ser239; reduces GPR41 and GPR43 mRNA level; and reduces the endothelium-dependent relaxant response to acetylcholine in aorta. Coincubation with butyrate and acetate, but not with propionate, increases both NO production and pSer239-VASP, reduces the concentration of intracellular ROS, and improves relaxation to acetylcholine. The beneficial effects of butyrate were inhibited by the GPR41 receptor antagonist, β-hydroxybutyrate, and by the GPR43 receptor antagonist, GLPG0794. Butyrate inhibited the down-regulation of GPR41 and GPR43 induced by AngII, being without effect acetate and propionate. Neither β-hydroxybutyrate nor GLPG0794 affects the protective effect of acetate in endothelial dysfunction. In conclusion, acetate and butyrate improve endothelial dysfunction induced by AngII by increasing the bioavailability of NO. The effect of butyrate seems to be related to GPR41/43 activation, whereas acetate effects were independent of GPR41/43.
eng
Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II.
journal article
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ProtectiveEffectsShort-Chain_2020.pdf
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ProtectiveEffectsShort-Chain_2020_supplmat.pdf
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ProtectiveEffectsShort-Chain_2020.pdf.txt
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https://repisalud.isciii.es/bitstreams/770d25b0-7e76-40b3-8d9b-2a871b4eab9b/download
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ProtectiveEffectsShort-Chain_2020_supplmat.pdf.txt