Abstract
Ultraviolet B (UVB) is a major cause of skin inflammation, leading to skin damage. Our previous in vivo study revealed that a natural flavonoid silibinin had marked anti-inflammatory effect on UVB-exposed murine skin. UVB exposure caused reduced autophagy in epidermis while it promoted autophagy in dermis. Nevertheless, silibinin inhibited the inflammatory flux in the skin epidermis as well as dermis through the modulation of autophagy. In order to elucidate the underlying protective mechanisms of silibinin for UVB damage on skin, separate studies on epidermis and dermis are helpful. Derived from the normal tissue of the mouse, L929 cells are capable of representing some characteristics of dermal cells. UVB irradiation caused L929 cell apoptosis in a time- and dose-dependent manner. Ataxia-telangiectasia-mutated (ATM) protein and p53 were activated to cause cell apoptosis, accompanying upregulation of the autophagic flux. The pharmacological inhibition of ATM, p53 and autophagy or the transfection with autophagy-associated protein-targeted small interfering RNAs showed that the UVB-activated ATM-p53 axis and autophagy formed a positive feedback loop, which synergistically promoted cell apoptosis. Silibinin treatment simultaneously repressed the activation of ATM-p53 and autophagy and thereby protected UVB-irradiated L929 cells from apoptotic death.
Published Version
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 callDisclaimer: 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.
