4-phenylpyridine suppresses UVB-induced skin inflammation by targeting c-Src in vitro and in vivoopen access
- Authors
- Kim, Ju Gyeong; Kang, Ha Yeong; Kim, Min Jeong; Lim, Seokwon; Lee, Chang Joo; Kim, Kyung-Min; Jung, Sung Keun
- Issue Date
- Jul-2022
- Publisher
- WILEY
- Keywords
- 4-phenylpyridine; Brassica campestris L; ssp; pekinensis; COX-2; c-Src; phytochemicals; skin inflammation
- Citation
- JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, v.26, no.14, pp.3891 - 3901
- Journal Title
- JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
- Volume
- 26
- Number
- 14
- Start Page
- 3891
- End Page
- 3901
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/84997
- DOI
- 10.1111/jcmm.17422
- ISSN
- 1582-1838
- Abstract
- Acute or repetitive exposure to ultraviolet (UV) cause disruptions to the skin barrier and subsequent inflammatory skin disease. 4-phenylpyridine (4-PP) is a constituent of Brassica campestris L. ssp. Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of this study is to confirm the anti-inflammatory efficacy of 4-PP on UVB-induced skin inflammation in human keratinocytes HaCaT and mouse skin and validation of its molecular target. 4-PP also attenuated UVB-induced phosphorylation of p38/mitogen-activated protein kinase kinase (MKK) 3/6, c-Jun N-terminal kinase 1/2, MKK 4/7, extracellular-signal-regulated kinase 1/2, mitogen-activated protein kinase 1/2. Additionally, 4-PP inhibited UVB-induced phosphorylation of epidermal growth factor receptor (EGFR) Y1068, Y1045 and 854 residues but not the proto-oncogene tyrosine-protein kinase c-Src. Drug affinity responsive target stability assay revealed that 4-PP directly binds to c-Src and inhibits pronase c-proteolysis. Knockdown of c-Src inhibited UVB-induced COX-2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells. Dorsal treatment of 4-PP prevented UVB (0.5 J/cm(2))-induced skin thickness, phosphorylation of EGFR and COX-2 expression in mouse skin. Our findings suggest that 4-PP can be used as anti-inflammatory agent with an effect of skin inflammation by inhibiting the COX-2 expression via suppressing the c-Src/EGFR/MAPKs signalling pathway.
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