Apigenin restores impairment of autophagy and downregulation of unfolded protein response regulatory proteins in keratinocytes exposed to ultraviolet B radiation
作者： Li Li , Min Li , Song Xu , Hongying Chen , Xu Chen
DOI: 10.1016/J.JPHOTOBIOL.2019.03.010
关键词: Keratinocyte 、 Cancer research 、 Autophagy 、 Downregulation and upregulation 、 Programmed cell death 、 Apoptosis 、 Unfolded protein response 、 Apigenin 、 Photoprotective agent 、 Chemistry 、 Biophysics 、 Radiological and Ultrasound Technology 、 Radiation 、 Radiology Nuclear Medicine and imaging
摘要: Abstract Ultraviolet (UV)-B radiation is a major environmental risk factor that responsible for the development and progression of many skin cancers. Apigenin, type bioflavonoid, has been reported to inhibit UVB-induced cancer. However, how apigenin functions in keratinocytes with UV damage remains unclear. In this study, by lactate dehydrogenase (LDH) release assay, we found treatment increased cell death primary human epidermal (HEKs) cutaneous squamous carcinoma line COLO-16. Apigenin reduced microtubule-associated protein 1 light chain 3 (LC3)-II turnover, acridine orange staining GFP-LC3 puncta both types, suggesting autophagy inhibition. restored inhibition UVB-challenged HEKs. Moreover, downregulation ataxia-telangiectasia mutated (ATM), ataxia-telangiectasia, Rad3-related (ATR) unfolded response (UPR) regulatory proteins, BiP, IRE1α PERK also inhibited apoptosis addition, autophagy-related gene (ATG) 5 RNA interference interrupted apigenin-induced restoration ATR, ATM which were downregulated HEKs exposed UVB radiation. Our findings indicate exhibits novel protective effect damage, potential application as photoprotective agent.
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