■皮肤是一种屏障,可以保护免受环境危险因素的影响,这些因素可以通过DNA损伤和氧化应激使皮肤细胞癌变。核因子红系2相关因子2(NRF2)途径是一种抗应激防御系统,可通过DNA甲基化和组蛋白修饰进行调节。膳食植物化学物质具有化学预防特性,可以抑制或延迟致癌作用。荷叶是一种含有多种多酚的传统药用植物,其提取物具有多种生物活性,包括抗氧化剂,抗肥胖,和抗癌。本研究旨在研究荷叶对小鼠皮肤JB6P细胞肿瘤转化的影响。
■荷叶用水(LL-WE)和乙醇(LL-EE)提取,和LL-WE残留物进一步用乙醇(LL-WREE)提取。用不同的提取物处理JB6P+细胞。化学保护作用将通过血红素加氧酶1(HO-1)评估,NAD(P)H醌氧化还原酶(NQO1),和UDP葡糖醛酸基转移酶家族1成员A1(UGT1A1)表达。
■LL-EE在提取物中含有较高的总酚和槲皮素。在12-O-十四烷酰基佛波醇-13-乙酸酯处理的小鼠皮肤JB6P+细胞中,LL-EE显示出抑制皮肤癌变的最大潜力。LL-EE通过上调抗氧化和解毒酶激活NRF2途径,包括HO-1,NQO1和UGT1A1,并下调DNA甲基化,这可能是由较低的DNA甲基转移酶和组蛋白脱乙酰酶水平引起的。因此,我们的结果表明,LL-EE减少皮肤JB6P+细胞的肿瘤转化,可能通过激活NRF2途径和调节表观遗传DNA甲基化和组蛋白乙酰化。
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.