Herbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, Korea.
Molecules. 2019 Jan 11;24(2):265. doi: 10.3390/molecules24020265.
Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. The use of immunomodulatory corticosteroids in AD treatment causes adverse side effects. Therefore, novel natural anti-inflammatory therapeutics are needed. The aim of the present study was to investigate the anti-allergic and anti-inflammatory activities of kuwanon G and morusin. To investigate the effect of kuwanon G and morusin on skin inflammation, enzyme-linked immunosorbent assays (ELISA) to quantitate secreted (RANTES/CCL5), thymus- and activation-regulated chemokine (TARC/CCL17), and macrophage-derived chemokine (MDC/CCL22) were performed, followed by Western blotting to measure the phosphorylation of signal transducer and activator of transcription 1 (STAT1) and nuclear transcription factor-κB (NF-κB) p65 in tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-stimulated HaCaT keratinocytes. In order to evaluate the anti-allergic effects, ELISA to quantify histamine and leukotriene C₄ (LTC₄) production and Western blotting to measure 5-lipoxygenase (5-LO) activation were performed using PMA and A23187-stimulated MC/9 mast cells. Kuwanon G reduced the release of RANTES/CCL5, TARC/CCL17, and MDC/CCL22 via down-regulation of STAT1 and NF-κB p65 signaling in TNF-α and IFN-γ-stimulated HaCaT keratinocytes. Kuwanon G also inhibited histamine production and 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Morusin inhibited RANTES/CCL5 and TARC/CCL17 secretion via the suppression of STAT1 and NF-κB p65 phosphorylation in TNF-α and IFN-γ-stimulated HaCaT keratinocytes, and the release of histamine and LTC₄ by suppressing 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Kuwanon G and morusin are potential anti-inflammatory mediators for the treatment of allergic and inflammatory skin diseases such as AD.
特应性皮炎（AD）是一种常见的慢性炎症性皮肤病。在 AD 的治疗中使用免疫调节皮质类固醇会引起不良反应。因此，需要新型的天然抗炎疗法。本研究旨在研究昆诺酮 G 和桑辛的抗过敏和抗炎活性。为了研究昆诺酮 G 和桑辛对皮肤炎症的影响，通过酶联免疫吸附试验（ELISA）定量测定分泌的（RANTES/CCL5）、胸腺激活调节趋化因子（TARC/CCL17）和巨噬细胞衍生趋化因子（MDC/CCL22），然后通过 Western blot 测量肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）刺激的 HaCaT 角质形成细胞中信号转导和转录激活因子 1（STAT1）和核转录因子-κB（NF-κB）p65 的磷酸化。为了评估抗过敏作用，通过 ELISA 定量测定组胺和白三烯 C₄（LTC₄）的产生，并通过 Western blot 测量 PMA 和 A23187 刺激的 MC/9 肥大细胞中 5-脂氧合酶（5-LO）的激活，进行了实验。昆诺酮 G 通过下调 TNF-α 和 IFN-γ 刺激的 HaCaT 角质形成细胞中 STAT1 和 NF-κB p65 信号通路，减少了 RANTES/CCL5、TARC/CCL17 和 MDC/CCL22 的释放。昆诺酮 G 还抑制了 PMA 和 A23187 刺激的 MC/9 肥大细胞中组胺的产生和 5-LO 的激活。桑辛通过抑制 TNF-α 和 IFN-γ 刺激的 HaCaT 角质形成细胞中 STAT1 和 NF-κB p65 磷酸化，抑制 RANTES/CCL5 和 TARC/CCL17 的分泌，并通过抑制 PMA 和 A23187 刺激的 MC/9 肥大细胞中 5-LO 的激活，抑制组胺和 LTC₄ 的释放。昆诺酮 G 和桑辛是治疗特应性皮炎等过敏性和炎症性皮肤病的潜在抗炎介质。
