Abstract

Chronic stress-induced oxidative damage and protease synthesis cause a loss of extracellular matrix components promoting human skin ageing. The administration of antioxidant compounds, such as those observed in olive oil, may attenuate stress-induced ageing signs in human skin. Thus, the aim of this study was to investigate the effect of olive oil administration in exvivo stressed human skin. Explants of human skin were treated with high levels of epinephrine (as observed in stressed patients) and olive oil in medium for 13days. Cultures treated with medium alone were used as controls. Olive oil reversed the high epinephrine level-induced reduction in epidermis and dermis thickness and collagen fibre content in exvivo human skin. The increase in the production of reactive oxygen species (ROS) and malondialdehyde levels (an index of lipid peroxidation) promoted by high levels of epinephrine were also attenuated by olive oil in exvivo human skin. Moreover, olive oil was able to reverse the high epinephrine level-induced increase in extracellular signal-related kinase 1/2 (ERK 1/2) and c-JUN (a major component of transcription factor AP-1) phosphorylation and protein matrix metalloproteinase-2 (MMP-2) expression in exvivo human skin. Olive oil attenuates stress-induced ageing signs (thinner dermis and collagen fibre loss) in exvivo human skin by reducing MMP-2 expression, ROS production, and ERK 1/2 and c-JUN phosphorylation.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.