Home CONTACT General Physiology and Biophysics 2018 General Physiology and Biophysics Vol.37, No.6, p.687–694, 2018

Journal info


Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.37, No.6, p.687–694, 2018

Title: Monoamine oxidase inhibition improves vascular function and reduces oxidative stress in rats with lipopolysaccharide-induced inflammation
Author: C. Rațiu, D. Uțu, A. Petruș, P. Norbert, S. Olariu, O. Duicu, A. Sturza, D. M. Muntean

Abstract: Oxidative stress and vascular inflammation are the two major pathomechanisms that contribute to the progression of both cardiovascular and metabolic diseases. We have previously demonstrated that monoamine oxidases (MAOs), mitochondrial enzymes with two isoforms (A and B), are contributors to the endothelial dysfunction associated with inflammation in mice. The present study was purported to assess the effects of MAOs on endothelial dysfunction in rats with lipopolysaccharide (LPS)-induced acute inflammation. To this aim, aortas harvested from rats treated or not with a single dose of LPS were used for organ-bath studies of vascular reactivity and hydrogen peroxide (H2O2) production assessment in the presence vs. absence of MAO inhibitors. Our results demonstrate that MAO-A and B isoforms are induced in the rat vascular system after LPS administration. Both reversible and irreversible MAOs inhibition improved vascular function and reduced oxidative stress. In conclusion, MAOs are contributors to the occurrence of endothelial dysfunction in the rat model of LPS-induced acute inflammation. MAO inhibition may become a viable therapeutic strategy for the treatment of cardiometabolic disease.

Keywords: Monoamine oxidase, Lipopolysaccharide, Acute inflammation, Endothelial dysfunction, Oxidative stress
Published online: 28-Nov-2018
Year: 2018, Volume: 37, Issue: 6 Page From: 687, Page To: 694
doi:10.4149/gpb_2018014


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.