The protective effects of empagliflozin on DNA oxidative changes in a model of vascular endothelial and smooth muscle cells damaged by oxidized cholesterol.

DNA bases DNA oxidative damage Empagliflozin Oxidized cholesterol Reactive oxygen species Smooth muscle cells Vascular endothelial damage

Journal

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295

Informations de publication

Date de publication:
27 Dec 2023
Historique:
received: 17 10 2023
revised: 19 12 2023
accepted: 21 12 2023
medline: 29 12 2023
pubmed: 29 12 2023
entrez: 28 12 2023
Statut: aheadofprint

Résumé

Diabetes patients often suffer chronic vascular complications resulting from endothelial dysfunction, smooth muscle cell (SMC) proliferation, inflammation and disturbed oxidative balance. Empagliflozin is one of three approved sodium-glucose cotransporter 2 (SGLT2) inhibitors for type 2 diabetes mellitus. was to determine the protective and repairing effect of EMPA in a model of vascular endothelial and SMC damage with 25-hydroxycholesterol (25-OHC). Human umbilical vascular endothelial cells (HUVECs) and SMCs were treated with compounds which induce DNA single-strand breaks (SSBs) and subjected to comet assay. Oxidative DNA damage was detected using endonuclease III (Nth) or human 8 oxoguanine DNA glycosylase (hOOG1). Reactive oxygen species (ROS) formation was determined by the fluorescence of a 6-carboxy-2',7'-dichlorodihydrofluoresce probe in diacetate (H 25-OHC-stimulated SMCs showed greater resistance to ROS generation and DNA damage compared to HUVECs. In both experimental models, EMPA treatment was associated with lower ROS production and DNA damage, including oxidative damage to purines and pyrimidines. This effect was not dose-dependent. EMPA was found to counteract this DNA damage by inhibiting ROS production. It appears that the EMPA induced indirect repair of DNA by inhibiting ROS production.

Sections du résumé

BACKGROUND BACKGROUND
Diabetes patients often suffer chronic vascular complications resulting from endothelial dysfunction, smooth muscle cell (SMC) proliferation, inflammation and disturbed oxidative balance. Empagliflozin is one of three approved sodium-glucose cotransporter 2 (SGLT2) inhibitors for type 2 diabetes mellitus.
THE AIM OF THIS STUDY OBJECTIVE
was to determine the protective and repairing effect of EMPA in a model of vascular endothelial and SMC damage with 25-hydroxycholesterol (25-OHC).
METHODS METHODS
Human umbilical vascular endothelial cells (HUVECs) and SMCs were treated with compounds which induce DNA single-strand breaks (SSBs) and subjected to comet assay. Oxidative DNA damage was detected using endonuclease III (Nth) or human 8 oxoguanine DNA glycosylase (hOOG1). Reactive oxygen species (ROS) formation was determined by the fluorescence of a 6-carboxy-2',7'-dichlorodihydrofluoresce probe in diacetate (H
RESULTS RESULTS
25-OHC-stimulated SMCs showed greater resistance to ROS generation and DNA damage compared to HUVECs. In both experimental models, EMPA treatment was associated with lower ROS production and DNA damage, including oxidative damage to purines and pyrimidines. This effect was not dose-dependent. EMPA was found to counteract this DNA damage by inhibiting ROS production.
CONCLUSIONS CONCLUSIONS
It appears that the EMPA induced indirect repair of DNA by inhibiting ROS production.

Identifiants

pubmed: 38154272
pii: S0753-3322(23)01863-2
doi: 10.1016/j.biopha.2023.116065
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

116065

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Ewelina Woźniak (E)

Medical University of Lodz, Department of Internal Diseases and Clinical Pharmacology, Laboratory of Tissue Immunopharmacology, Kniaziewicza 1/5, 91-347 Lodz, Poland. Electronic address: ewelina.wozniak@umed.lodz.pl.

Magdalena Świstek (M)

Medical University of Lodz, Department of Internal Diseases and Clinical Pharmacology, Laboratory of Tissue Immunopharmacology, Kniaziewicza 1/5, 91-347 Lodz, Poland.

Marlena Broncel (M)

Medical University of Lodz, Department of Internal Diseases and Clinical Pharmacology, Laboratory of Tissue Immunopharmacology, Kniaziewicza 1/5, 91-347 Lodz, Poland.

Bożena Bukowska (B)

University of Lodz, Faculty of Biology and Environmental Protection, Department of Biophysics of Environmental Pollution, Pomorska 141/143, 90-236 Lodz, Poland.

Paulina Gorzelak-Pabiś (P)

Medical University of Lodz, Department of Internal Diseases and Clinical Pharmacology, Laboratory of Tissue Immunopharmacology, Kniaziewicza 1/5, 91-347 Lodz, Poland.

Classifications MeSH