Background: Light at visible spectrum has been associated with anti-inflammatory and anti-aging effects. Ultraviolet A (UVA) radiation is the most important environmental factor associated with exogenous aging via induction of reactive oxygen species (ROS).
Objective: In this study, we focused on elucidating the molecular mechanisms involved in biological effects associated with 590 nm light delivered from light emitting diode (LED).
Methods: UVA-induced metalloproteinase-1 (MMP-1) expression in dermal fibroblast was used as a model system for investigation.
Results: Pretreating cultured human fibroblasts with 590 nm light attenuated UVA-induced ROS, phosphorylated Jun N-terminal kinases, and MMP-1 expressions in a sequential manner. Pretreatment with potent antioxidant N-acetylcysteine produced similar effect, suggesting enhanced antioxidant capacity induced by 590 nm photomodulation. Further experiments demonstrated that 590 nm photomodulation attenuated UVA-induced ROS and MMP-1 expressions via mitochondrial retrograde signaling that augments the antioxidant enzyme expression in a peroxisome proliferators-activated receptor γ coactivator-1α-dependent manner.
Conclusion: Our results provided possible mechanistic insights explaining the effect of visible light on treating clinical conditions associated with ROS-mediated dysfunctions.
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| http://dx.doi.org/10.1016/j.jdermsci.2015.02.018 | DOI Listing |
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