Topical application of glycolic acid suppresses the UVB induced IL-6, IL-8, MCP-1 and COX-2 inflammation by modulating NF-κB signaling pathway in keratinocytes and mice skin

Background: Glycolic acid (GA), commonly present in fruits, has been used to treat dermatological diseases. Extensive exposure to solar ultraviolet B (UVB) irradiation plays a crucial role in the induction of skin inflammation. The development of photo prevention from natural materials represents an effective strategy for skin keratinocytes. Objective: The aim of this study was to investigate the molecular mechanisms underlying the glycolic acid (GA)-induced reduction of UVB-mediated inflammatory responses. Methods: We determined the effects of different concentrations of GA on the inflammatory response of human keratinocytes HaCaT cells and C57BL/6J mice dorsal skin. After GA was topically applied, HaCaT and mice skin were exposed to UVB irradiation. Results: GA reduced the production of UVB-induced nuclear factor kappa B (NF-kappa B)-dependent inflammatory mediators [interleukin (IL)-1 beta, IL-6, IL-8, cyclooxygenase (COX)-2, tumor necrosis factor-alpha, and monocyte chemoattractant protein (MCP-1)] at both mRNA and protein levels. GA inhibited the UVB-induced promoter activity of NF-kappa B in HaCaT cells. GA attenuated the elevation of senescence associated with beta-galactosidase activity but did not affect the wound migration ability. The topical application of GA inhibited the genes expression of IL-1 beta, IL-6, IL-8, COX-2, and MCP-1 in UVB-exposed mouse skin. The mice to UVB irradiation after GA was topically applied for 9 consecutive days and reported that 1-1.5% of GA exerted anti-inflammatory effects on mouse skin. Conclusion: We clarified the molecular mechanism of GA protection against UVB-induced inflammation by modulating NF-kappa B signaling pathways and determined the optimal concentration of GA in mice skin exposed to UVB irradiation. (C) 2017 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.