Prunella vulgaris extract and rosmarinic acid prevent UVB-induced DNA damage and oxidative stress in HaCaT keratinocytes
Language English Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Antioxidants pharmacology MeSH
- Apoptosis drug effects radiation effects MeSH
- Cell Membrane drug effects radiation effects MeSH
- Cinnamates pharmacology MeSH
- Depsides pharmacology MeSH
- Interleukin-6 metabolism MeSH
- Keratinocytes drug effects metabolism pathology radiation effects MeSH
- Rosmarinic Acid MeSH
- Humans MeSH
- Plant Components, Aerial MeSH
- Oxidative Stress drug effects radiation effects MeSH
- DNA Damage drug effects MeSH
- Sunscreening Agents pharmacology MeSH
- Cell Proliferation drug effects radiation effects MeSH
- Prunella * MeSH
- Reactive Oxygen Species metabolism MeSH
- Plant Extracts pharmacology MeSH
- Cell Line, Transformed MeSH
- Ultraviolet Rays * MeSH
- Dose-Response Relationship, Drug MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- Cinnamates MeSH
- Depsides MeSH
- IL6 protein, human MeSH Browser
- Interleukin-6 MeSH
- Sunscreening Agents MeSH
- Reactive Oxygen Species MeSH
- Plant Extracts MeSH
Solar radiation is a very important exogenous factor in skin pathogenesis and can lead to the development of a number of skin disorders. UVB irradiation is known to induce oxidative stress, inflammation and especially DNA lesions in exposed cells. It is important, therefore, to identify agents that can offer protection against UVB-caused skin damage. Natural compounds have been studied for their possible ability to control/modulate various lifestyle-related diseases. The application of plant compounds/extracts with screening, antioxidant and anti-inflammatory activities may also successfully protect the skin against UV-caused injury. We assessed the potency of Prunella vulgaris extract (PVE) and its main phenolic acid component, rosmarinic acid (RA), to suppress UVB-induced (295-315 nm) alterations to human keratinocytes HaCaT using a solar simulator. Pre- and post-treatment of HaCaT cells with PVE (5-50 mg/l) and RA (0.18-1.8 mg/l) reduced breakage together with the apoptotic process. PVE and RA also significantly eliminated ROS production and diminished IL-6 release. Taken together, both PVE and RA prevent UVB-caused injury to keratinocytes. However their efficacy needs to be demonstrated in vivo.
References provided by Crossref.org
