Hyperlipidemic Microenvironment Conditionates Damage Mechanisms in Human Chondrocytes by Oxidative Stress

Overview

Journal Lipids Health Dis

Publisher Biomed Central

Specialties Biochemistry
Endocrinology

Date 2017 Jun 14

PMID 28606092

Citations 15

Authors

Daniel Medina-Luna

Monica Guadalupe Santamaria-Olmedo

Yessica Zamudio-Cuevas

Karina Martinez-Flores

Javier Fernandez-Torres

Gabriela Angelica Martinez-Nava

Denise Clavijo-Cornejo

Cristina Hernandez-Diaz

Anell Olivos-Meza

Luis Enrique Gomez-Quiroz

Maria Concepcion Gutierrez-Ruiz

Carlos Pineda

Francisco Blanco

Anthony M Reginato

Alberto Lopez-Reyes

Affiliations

Soon will be listed here.

Abstract

Background: Currently, two pathogenic pathways describe the role of obesity in osteoarthritis (OA); one through biomechanical stress, and the other by the contribution of systemic inflammation. The aim of this study was to evaluate the effect of free fatty acids (FFA) in human chondrocytes (HC) expression of proinflammatory factors and reactive oxygen species (ROS).

Methods: HC were exposed to two different concentrations of FFA in order to evaluate the secretion of adipokines through cytokines immunoassays panel, quantify the protein secretion of FFA-treated chondrocytes, and fluorescent cytometry assays were performed to evaluate the reactive oxygen species (ROS) production.

Results: HC injury was observed at 48 h of treatment with FFA. In the FFA-treated HC the production of reactive oxygen species such as superoxide radical, hydrogen peroxide and the reactive nitrogen species increased significantly in a at the two-dose tested (250 and 500 μM). In addition, we found an increase in the cytokine secretion of IL-6 and chemokine IL-8 in FFA-treated HC in comparison to the untreated HC.

Conclusion: In our in vitro model of HC, a hyperlipidemia microenvironment induces an oxidative stress state that enhances the inflammatory process mediated by adipokines secretion in HC.

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