Hyperlipidemic microenvironment conditionates damage mechanisms in human chondrocytes by oxidative stress
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Hyperlipidemic microenvironment conditionates damage mechanisms in human chondrocytes by oxidative stressAutor(es)
Fecha
2017-06-12Cita bibliográfica
Medina-Luna D, Santamaría-Olmedo MG, Zamudio-Cuevas Y, Martínez-Flores K, Fernández-Torres J, Martínez-Nava GA, et al. Hyperlipidemic microenvironment conditionates damage mechanisms in human chondrocytes by oxidative stress. Lipids Health Dis. 2017;16(1): 114
Resumen
[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.
Palabras clave
Chondrocytes
Free fatty acids
Inflammation
Oxidative stress
Free fatty acids
Inflammation
Oxidative stress
Versión del editor
Derechos
Atribución 3.0 España
ISSN
1476-511X