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J Dermatol Sci. 2017 Jun;86(3):238-248. doi: 10.1016/j.jdermsci.2017.03.004. Epub 2017 Mar 11.

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.

Author information

1
Department of Dermatology, Buddhist Tzu Chi General Hospital, Hualien 97004, Taiwan; Department of Biochemistry, School of Medicine, Tzu Chi University, Hualien 97004, Taiwan.
2
Department of Dermatology, Buddhist Tzu Chi General Hospital, Hualien 97004, Taiwan; Institute of Medical Sciences, Tzu Chi University, Hualien 97004, Taiwan.
3
Department of Dermatology, Buddhist Tzu Chi General Hospital, Hualien 97004, Taiwan.
4
Research Assistant Center, Chang Hua Show Chwan Health, Care System, Changhua 50008, Taiwan.
5
Institute of Medicine, School of Medicine, Chung Shan Medical University, Taichung 40244, Taiwan; Department of Dermatology, Chung Shan Medical University Hospital, Taichung 40244, Taiwan.
6
Department of Dermatology, Buddhist Tzu Chi General Hospital, Hualien 97004, Taiwan; Department of Biochemistry, School of Medicine, Tzu Chi University, Hualien 97004, Taiwan; Institute of Medicine, School of Medicine, Tzu Chi University, Hualien 97004, Taiwan. Electronic address: jh.med.edu@gms.tcu.edu.tw.

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.

KEYWORDS:

Glycolic acid (GA); cyclooxygenase (COX)-2; interleukin (IL)-1β; monocyte chemoattractant protein (MCP-1); nuclear factor kappa B (NF-κB); ultraviolet B (UVB)

PMID:
28330776
DOI:
10.1016/j.jdermsci.2017.03.004
[Indexed for MEDLINE]

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