A Fermented Whole Grain Prevents Lipopolysaccharides-Induced Dysfunction in Human Endothelial Progenitor CellsReport as inadecuate




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Oxidative Medicine and Cellular Longevity - Volume 2017 2017, Article ID 1026268, 13 pages - https:-doi.org-10.1155-2017-1026268

Research Article

Section of Diabetes and Metabolic Disease, Department of Clinical and Experimental Medicine, University of Pisa and Azienda Ospedaliero-Universitaria Pisana, Via Paradisa 2, 56124 Pisa, Italy

National Research Council, Institute of Biology and Agricultural Biotechnology IBBA, Pisa Unit, Research Area of Pisa, Via Moruzzi 1, 56124 Pisa, Italy

Correspondence should be addressed to Vincenzo Longo

Received 23 November 2016; Revised 8 February 2017; Accepted 20 February 2017; Published 13 March 2017

Academic Editor: Grant N. Pierce

Copyright © 2017 Laura Giusti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Endogenous and exogenous signals derived by the gut microbiota such as lipopolysaccharides LPS orchestrate inflammatory responses contributing to development of the endothelial dysfunction associated with atherosclerosis in obesity, metabolic syndrome, and diabetes. Endothelial progenitor cells EPCs, bone marrow derived stem cells, promote recovery of damaged endothelium playing a pivotal role in cardiovascular repair. Since healthy nutrition improves EPCs functions, we evaluated the effect of a fermented grain, Lisosan G LG, on early EPCs exposed to LPS. The potential protective effect of LG against LPS-induced alterations was evaluated as cell viability, adhesiveness, ROS production, gene expression, and NF-kB signaling pathway activation. Our results showed that LPS treatment did not affect EPCs viability and adhesiveness but induced endothelial alterations via activation of NF-kB signaling. LG protects EPCs from inflammation as well as from LPS-induced oxidative and endoplasmic reticulum ER stress reducing ROS levels, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defense. Moreover, LG pretreatment prevented NF-kB translocation from the cytoplasm into the nucleus caused by LPS exposure. In human EPCs, LPS increases ROS and upregulates proinflammatory tone, proapoptotic factors, and antioxidants. LG protects EPCs exposed to LPS reducing ROS, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defenses possibly by inhibiting NF-κB nuclear translocation.





Author: Laura Giusti, Morena Gabriele, Giuseppe Penno, Monia Garofolo, Vincenzo Longo, Stefano Del Prato, Daniela Lucchesi, and Lau

Source: https://www.hindawi.com/



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