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Protection of the vascular endothelium in experimental situations

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Protection of the vascular endothelium in experimental situations. / Sotníková, Ružena; Nedelčevová, Jana; Navarová, Jana; Nosáĺová, Viera; Drábiková, Katarína; Szöcs, Katalin; Křenek, Peter; Kyseĺová, Zuzana; Bezek, Stefan; Knezl, Vladimír; Dřímal, Ján; Brosková, Zuzana; Kristová, Viera; Okruhlicová, Ludmila; Bernátová, Iveta; Bauer, Viktor.

in: Interdisciplinary toxicology, Jahrgang 4, Nr. 1, 03.2011, S. 20-26.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Sotníková, R, Nedelčevová, J, Navarová, J, Nosáĺová, V, Drábiková, K, Szöcs, K, Křenek, P, Kyseĺová, Z, Bezek, S, Knezl, V, Dřímal, J, Brosková, Z, Kristová, V, Okruhlicová, L, Bernátová, I & Bauer, V 2011, 'Protection of the vascular endothelium in experimental situations', Interdisciplinary toxicology, Jg. 4, Nr. 1, S. 20-26. https://doi.org/10.2478/v10102-011-0005-y

APA

Sotníková, R., Nedelčevová, J., Navarová, J., Nosáĺová, V., Drábiková, K., Szöcs, K., Křenek, P., Kyseĺová, Z., Bezek, S., Knezl, V., Dřímal, J., Brosková, Z., Kristová, V., Okruhlicová, L., Bernátová, I., & Bauer, V. (2011). Protection of the vascular endothelium in experimental situations. Interdisciplinary toxicology, 4(1), 20-26. https://doi.org/10.2478/v10102-011-0005-y

Vancouver

Sotníková R, Nedelčevová J, Navarová J, Nosáĺová V, Drábiková K, Szöcs K et al. Protection of the vascular endothelium in experimental situations. Interdisciplinary toxicology. 2011 Mär;4(1):20-26. https://doi.org/10.2478/v10102-011-0005-y

Bibtex

@article{9419d36d9399498ead4c5b79593279d1,
title = "Protection of the vascular endothelium in experimental situations",
abstract = "One of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 found in vitro were partly confirmed in vivo. Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effect in vivo.",
author = "Ru{\v z}ena Sotn{\'i}kov{\'a} and Jana Nedel{\v c}evov{\'a} and Jana Navarov{\'a} and Viera Nos{\'a}{\'l}ov{\'a} and Katar{\'i}na Dr{\'a}bikov{\'a} and Katalin Sz{\"o}cs and Peter K{\v r}enek and Zuzana Kyse{\'l}ov{\'a} and Stefan Bezek and Vladim{\'i}r Knezl and J{\'a}n D{\v r}{\'i}mal and Zuzana Broskov{\'a} and Viera Kristov{\'a} and Ludmila Okruhlicov{\'a} and Iveta Bern{\'a}tov{\'a} and Viktor Bauer",
year = "2011",
month = mar,
doi = "10.2478/v10102-011-0005-y",
language = "English",
volume = "4",
pages = "20--26",
journal = "Interdisciplinary toxicology",
issn = "1337-6853",
publisher = "Slovak Toxicology Society SETOX",
number = "1",

}

RIS

TY - JOUR

T1 - Protection of the vascular endothelium in experimental situations

AU - Sotníková, Ružena

AU - Nedelčevová, Jana

AU - Navarová, Jana

AU - Nosáĺová, Viera

AU - Drábiková, Katarína

AU - Szöcs, Katalin

AU - Křenek, Peter

AU - Kyseĺová, Zuzana

AU - Bezek, Stefan

AU - Knezl, Vladimír

AU - Dřímal, Ján

AU - Brosková, Zuzana

AU - Kristová, Viera

AU - Okruhlicová, Ludmila

AU - Bernátová, Iveta

AU - Bauer, Viktor

PY - 2011/3

Y1 - 2011/3

N2 - One of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 found in vitro were partly confirmed in vivo. Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effect in vivo.

AB - One of the factors proposed as mediators of vascular dysfunction observed in diabetes is the increased generation of reactive oxygen species (ROS). This provides support for the use of antioxidants as early and appropriate pharmacological intervention in the development of late diabetic complications. In streptozotocin (STZ)-induced diabetes in rats we observed endothelial dysfuction manifested by reduced endothelium-dependent response to acetylcholine of the superior mesenteric artery (SMA) and aorta, as well as by increased endothelaemia. Changes in endothelium-dependent relaxation of SMA were induced by injury of the nitric oxide radical (·NO)-signalling pathway since the endothelium-derived hyperpolarising factor (EDHF)-component of relaxation was not impaired by diabetes. The endothelial dysfunction was accompanied by decreased ·NO bioavailabity as a consequence of reduced activity of eNOS rather than its reduced expression. The results obtained using the chemiluminiscence method (CL) argue for increased oxidative stress and increased ROS production. The enzyme NAD(P)H-oxidase problably participates in ROS production in the later phases of diabetes. Oxidative stress was also connected with decreased levels of reduced glutathione (GSH) in the early phase of diabetes. After 10 weeks of diabetes, adaptational mechanisms probably took place because GSH levels were not changed compared to controls. Antioxidant properties of SMe1EC2 found in vitro were partly confirmed in vivo. Administration of SMe1EC2 protected endothelial function. It significantly decreased endothelaemia of diabetic rats and improved endothelium-dependent relaxation of arteries, slightly decreased ROS-production and increased bioavailability of ·NO in the aorta. Further studies with higher doses of SMe1EC2 may clarify the mechanism of its endothelium-protective effect in vivo.

U2 - 10.2478/v10102-011-0005-y

DO - 10.2478/v10102-011-0005-y

M3 - SCORING: Journal article

C2 - 21577280

VL - 4

SP - 20

EP - 26

JO - Interdisciplinary toxicology

JF - Interdisciplinary toxicology

SN - 1337-6853

IS - 1

ER -