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. Issue 3 (June 2017)

• Record Type: Journal Article
• Authors: Tang, Sheau-Chung; Liao, Pei-Yun; Hung, Sung-Jen; Ge, Jheng-Siang; Chen, Shiou-Mei; Lai, Ji-Ching; Hsiao, Yu-Ping; Yang, Jen-Hung
• Is Part Of: Journal of dermatological science. Volume 86:Issue 3(2017:Jun.)
• Page Start: 238
• Page End: 248
• Publication Date: 2017-06
• Subjects: Glycolic acid (GA) -- ultraviolet B (UVB) -- cyclooxygenase (COX)-2 -- interleukin (IL)-1β -- monocyte chemoattractant protein (MCP-1) -- nuclear factor kappa B (NF-κB); AHAs alpha hydroxy acids -- COX-2 cyclooxygenase-2 -- GA glycolic acid -- GM-CSF granulocyte-macrophage colony-stimulating factor -- HRP horseradish peroxidase -- IL-1β interleukin-1β -- MCP-1 monocyte chemoattractant protein -- NHEKs normal human epidermal keratinocytes -- NF-κB nuclear factor kappa B -- ROS reactive oxygen species -- SA-β-gal senescence-associated-β-gal -- TNF-α tumor necrosis factor-α -- UVB ultraviolet B; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2017.03.004
• Languages: English
• ISSNs: 0923-1811

Abstract

Graphical abstract: Highlights: Glycolic acid (GA) protects against UVB-induced inflammation by modulating NF-κB signaling pathways. 1–1.5% of GA is the most appropriate concentration for reducing inflammation in mouse skin. GA providing a safe and natural strategy for developing novel topical anti-inflammatory agents. Abstract: 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-κB)-dependent inflammatory mediators [interleukin (IL)-1β, IL-6, IL-8, cyclooxygenase (COX)-2, tumor necrosis factor-α, and monocyte chemoattractant protein (MCP-1)] at both mRNA and protein levels. GA inhibited the UVB-induced promoter activity of NF-κB in HaCaT cells. GA attenuated the elevation of senescence associated with β-galactosidase activity but did not affect the wound migration ability. The topical application of GA inhibited the genes expression of IL-1β, 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-κB signaling pathways and determined the optimal concentration of GA in mice skin exposed to UVB irradiation.