Sulodexide Prevents Hyperglycemia-Induced Endothelial Dysfunction and Oxidative Stress in Porcine Retinal Arterioles

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Abstract
<jats:p>Diabetes mellitus may cause severe damage to retinal blood vessels. The central aim of this study was to test the hypothesis that sulodexide, a mixture of glycosaminoglycans, has a protective effect against hyperglycemia-induced endothelial dysfunction in the retina. Functional studies were performed in isolated porcine retinal arterioles. Vessels were cannulated and incubated with highly concentrated glucose solution (HG, 25 mM D-glucose) +/− sulodexide (50/5/0.5 μg/mL) or normally concentrated glucose solution (NG, 5.5 mM D-glucose) +/− sulodexide for two hours. Endothelium-dependent and endothelium-independent vasodilatation were measured by videomicroscopy. Reactive oxygen species (ROS) were quantified by dihydroethidium (DHE) fluorescence. Using high-pressure liquid chromatography (HPLC), the intrinsic antioxidant properties of sulodexide were investigated. Quantitative PCR was used to determine mRNA expression of regulatory, inflammatory, and redox genes in retinal arterioles, some of which were subsequently quantified at the protein level by immunofluorescence microscopy. Incubation of retinal arterioles with HG caused significant impairment of endothelium-dependent vasodilation, whereas endothelium-independent responses were not affected. In the HG group, ROS formation was markedly increased in the vascular wall. Strikingly, sulodexide had a protective effect against hyperglycemia-induced ROS formation in the vascular wall and had a concentration-dependent protective effect against endothelial dysfunction. Although sulodexide itself had only negligible antioxidant properties, it prevented hyperglycemia-induced overexpression of the pro-oxidant redox enzymes, NOX4 and NOX5. The data of the present study provide evidence that sulodexide has a protective effect against hyperglycemia-induced oxidative stress and endothelial dysfunction in porcine retinal arterioles, possibly by modulation of redox enzyme expression.</jats:p>
Autoren
  • Alice Dauth
  • Andrzej Bręborowicz
  • Yue Ruan
  • Qi Tang
  • Jenia K Zadeh
  • Elsa W Böhm
  • Norbert Pfeiffer
  • Pratik H Khedkar
  • Andreas Patzak
  • Ksenija Vujacic-Mirski
  • Andreas Daiber
  • Adrian Gericke
DOI
10.3390/antiox12020388
eISSN
2076-3921
Ausgabe der Veröffentlichung
2
Zeitschrift
Antioxidants
Sprache
en
Online publication date
2023
Paginierung
388 - 388
Status
Published online
Herausgeber
MDPI AG
Herausgeber URL
http://dx.doi.org/10.3390/antiox12020388
Datum der Datenerfassung
2023
Titel
Sulodexide Prevents Hyperglycemia-Induced Endothelial Dysfunction and Oxidative Stress in Porcine Retinal Arterioles
Ausgabe der Zeitschrift
12

Datenquelle: Crossref

Andere Metadatenquellen:
Author's licence
CC-BY
Autoren
  • Alice Dauth
  • Andrzej Breborowicz
  • Yue Ruan
  • Qi Tang
  • Jenia K Zadeh
  • Elsa W Böhm
  • Norbert Pfeiffer
  • Pratik H Khedkar
  • Andreas Patzak
  • Ksenija Vujacic-Mirski
  • Andreas Daiber
  • Adrian Gericke
Hosting institution
Universitätsbibliothek Mainz
Sammlungen
  • DFG-491381577-G
Resource version
Published version
DOI
10.3390/antiox12020388
Funding acknowledgements
  • Deutsche Forschungsgemeinschaft (DFG)|491381577|Open-Access-Publikationskosten 2022–2024 Universität Mainz - Universitätsmedizin
File(s) embargoed
false
Open access
true
ISSN
2076-3921
Ausgabe der Veröffentlichung
2
Zeitschrift
Antioxidants
Schlüsselwörter
  • 610 Medizin
  • 610 Medical sciences
Sprache
eng
Open access status
Open Access
Paginierung
388
Datum der Veröffentlichung
2023
Public URL
https://openscience.ub.uni-mainz.de/handle/20.500.12030/9138
Herausgeber
MDPI
Datum der Datenerfassung
2023
Datum, an dem der Datensatz öffentlich gemacht wurde
2023
Zugang
Public
Titel
Sulodexide prevents hyperglycemia-induced endothelial dysfunction and oxidative stress in porcine retinal arterioles
Ausgabe der Zeitschrift
12

Files

sulodexide_prevents_hyperglyc-20230525130504545.pdf

Datenquelle: OPENSCIENCE.UB

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