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首页> 外文期刊>The Journal of dermatology >Antioxidant soybean tar Glyteer rescues T-helper-mediated downregulation of filaggrin expression via aryl hydrocarbon receptor
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Antioxidant soybean tar Glyteer rescues T-helper-mediated downregulation of filaggrin expression via aryl hydrocarbon receptor

机译：抗氧化大豆焦油Glyteer通过芳烃受体拯救T辅助介导的丝蛋白表达下调

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摘要

Soybean tar Glyteer (Gly) has been widely used for the treatment of various inflammatory skin diseases in Japan since 1924 as an alternative to coal tar remedy. Recently, coal tar has been shown to induce barrier repair in atopic dermatitis via aryl hydrocarbon receptor (AhR). In this study, we demonstrated that Gly activated AhR by inducing its cytoplasmic to nuclear translocation in keratinocytes. The AhR ligation by Gly was biologically active, with significant and dose-dependent upregulation of CYP1A1 expression, which is a specific marker for AhR activation. Gly upregulated the expression of filaggrin in an AhR-dependent manner because its enhancing effect was completely abrogated in AhR-knockdown keratinocytes. T-helper (Th)2 cytokines inhibited the expression of filaggrin; however, Gly completely restored the Th2-mediated inhibition of filaggrin expression. Furthermore, Gly coordinately upregulated a series of epidermal differentiation complex genes, including involucrin, loricrin and hornerin. In addition, Gly exhibited potent antioxidant activity through the activation of nuclear factor-erythroid 2-related factor-2 (Nrf2) and downstream antioxidant enzymes such as NAD(P)H:quinone oxidoreductase 1 (Nqo1), which actually inhibited the generation of reactive oxygen species in keratinocytes treated with tumor necrosis factor- or benzo[]pyrene. In conclusion, antioxidant Gly rescues the downregulated expression of filaggrin (and plausibly other barrier proteins) in a Th2-skewed milieu via AhR activation, which may partly explain its empirical anti-inflammatory therapeutic effects.
机译：自1924年以来，大豆焦油Glyteer（Gly）作为煤焦油疗法的替代品，已在日本广泛用于治疗各种炎症性皮肤病。最近，已显示煤焦油可通过芳基烃受体（AhR）诱导特应性皮炎的屏障修复。在这项研究中，我们证明了Gly通过诱导其在角质形成细胞中的胞质到核转运而激活了AhR。 Gly的AhR连接具有生物活性，CYP1A1表达显着且呈剂量依赖性上调，这是AhR激活的特异性标记。甘氨酸以依赖于AhR的方式上调了丝聚蛋白的表达，因为其增强作用在AhR抑制型角质形成细胞中被完全废除。 T-helper（Th）2细胞因子抑制丝聚蛋白的表达。但是，Gly完全恢复了Th2介导的丝蛋白表达抑制。此外，Gly协同上调了一系列表皮分化复合基因，包括整合素，loricrin和hornerin。此外，Gly通过激活核因子-类胡萝卜素2相关因子2（Nrf2）和下游抗氧化酶（例如NAD（P）H：醌氧化还原酶1（Nqo1））的活化而具有强大的抗氧化活性，实际上抑制了该酶的产生。肿瘤坏死因子-或苯并[] py处理过的角质形成细胞中的活性氧总之，抗氧化剂Gly通过AhR激活来拯救Th2偏向环境中丝蛋白（以及可能的其他屏障蛋白）的下调表达，这可能部分解释了其经验性的抗炎治疗作用。

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