Chemoprevention of lotus leaf ethanolic extract through epigenetic activation of the NRF2-mediated pathway in murine skin JB6 P+ cell neoplastic transformationopen access
- Authors
- Tung, Y.-C.; Sung, P.-H.; Chen, P.-C.; Wang, H.C.; Lee, Jong Hun; Su, Z.-Y.
- Issue Date
- Jul-2023
- Publisher
- National Taiwan University
- Keywords
- Antioxidant; Cancer transformation; DNA methylation; Herbal medicine; Skin cell
- Citation
- Journal of Traditional and Complementary Medicine, v.13, no.4, pp.337 - 344
- Journal Title
- Journal of Traditional and Complementary Medicine
- Volume
- 13
- Number
- 4
- Start Page
- 337
- End Page
- 344
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/88501
- DOI
- 10.1016/j.jtcme.2023.02.002
- ISSN
- 2225-4110
- Abstract
- Background and aim: Skin is one barrier protecting from environmental risk factors that can make skin cells cancerous through DNA damage and oxidative stress. The nuclear factor erythroid 2-related factor 2 (NRF2) pathway is an anti-stress defense system that can be regulated by DNA methylation and histone modification. Dietary phytochemicals have chemopreventive properties that can inhibit or delay carcinogenesis. The lotus leaf is a traditional medicinal plant containing many polyphenols whose extracts show many biological activities, including antioxidant, anti-obesity, and anti-cancer. This study aim to investigate the effect of lotus leaves on neoplastic transformation in murine skin JB6 P+ cells. Experimental procedure: Lotus leaves were extracted with water (LL-WE) and ethanol (LL-EE), and the LL-WE residues were further extracted with ethanol (LL-WREE). JB6 P+ cells were treated with different extracts. The chemoprotective effect would be evaluated by heme oxygenase 1 (HO-1), NAD(P)H quinone oxidoreductase (NQO1), and UDP glucuronosyltransferase family 1 member A1 (UGT1A1) expression. Results and conclusion: LL-EE contained higher total phenolics and quercetin among extracts. In mouse skin JB6 P+ cells with 12-O-tetradecanoylphorbol-13-acetate treatment, LL-EE showed the greatest potential to suppress skin carcinogenesis. LL-EE activated the NRF2 pathway by upregulating antioxidant and detoxification enzymes upregulates antioxidant and detoxification enzymes, including HO-1, NQO1, and UGT1A1, and downregulates DNA methylation, which might be caused by lower DNA methyltransferase and histone deacetylase levels. Therefore, our results show that LL-EE reduces the neoplastic transformation of skin JB6 P+ cells, potentially by activating the NRF2 pathway and regulating epigenetic DNA methylation and histone acetylation. © 2023 Center for Food and Biomolecules, National Taiwan University
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