Omega-3 fatty acids reduce lipopolysaccharide-induced abnormalities in expression of connexin-40 in aorta of hereditary hypertriglyceridemic rats

Title:

Omega-3 fatty acids reduce lipopolysaccharide-induced abnormalities in expression of connexin-40 in aorta of hereditary hypertriglyceridemic rats

Creator:

Frimmel, K., Ružena Sotníková, Jana Navarová, Iveta Bernátová, Križák, J., Zora Haviarová, Kura, B., Ján Slezák, and Ľudmila Okruhlicová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a73ea041-d6be-49ac-9bd8-7b9512b79768
uuid:a73ea041-d6be-49ac-9bd8-7b9512b79768
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, omega-3 mastné kyseliny, omega-3 fatty acids, lipopolysaccharide, connexin-40, hypertriglyceridemia, rat aorta, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Omega-3 fatty acids (Ω3FA) are known to reduce hypertriglyceridemia- and inflammation-induced vascular wall diseases. However, mechanisms of their effects are not completely clear. We examined, whether 10-day Ω3FA diet can reduce bacterial lipopolysaccharide-induced changes in expression of gap junction protein connexin40 (Cx40) in the aorta of hereditary hypertriglyceridemic (hHTG) rats. After administration of a single dose of lipopolysaccharide (LPS, 1 mg/kg, i.p.) to adult hHTG rats, animals were fed with Ω3FA diet (30 mg/kg/day) for 10 days. LPS decreased Cx40 expression that was associated with reduced acetylcholine-induced relaxation of aorta. Ω3FA administration to LPS rats had partial anti-inflammatory effects, associated with increased Cx40 expression and improved endothelium dependent relaxation of the aorta. Our results suggest that 10-day Ω3FA diet could protect endothelium-dependent relaxation of the aorta of hHTG rats against LPS-induced damage through the modulation of endothelial Cx40 expression, K. Frimmel, R. Sotníková, J. Navarová, I. Bernátová, J. Križák, Z. Haviarová, B. Kura, J. Slezák, Ľ. Okruhlicová., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:Suppl 1

Harvested from:

CDK

Metadata only:

false