Hyperlipidemic microenvironment conditionates damage mechanisms in human chondrocytes by oxidative stress.
Lipids Health Dis
; 16(1): 114, 2017 Jun 12.
Article
en En
| MEDLINE
| ID: mdl-28606092
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
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Osteoartritis
/
Hiperlipidemias
/
Inflamación
/
Obesidad
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Lipids Health Dis
Asunto de la revista:
BIOQUIMICA
/
METABOLISMO
Año:
2017
Tipo del documento:
Article
País de afiliación:
México