Suppr超能文献

3-溴-4,5-二羟基苯甲醛抑制 TNF-α/IFN-γ 刺激的 HaCaT 角质形成细胞炎症和皮肤屏障损伤。

3-Bromo-4,5-dihydroxybenzaldehyde Isolated from Suppresses TNF-α/IFN-γ-Stimulated Inflammation and Deterioration of Skin Barrier in HaCaT Keratinocytes.

机构信息

Department of Food Technology and Nutrition, Chonnam National University, Yeosu 59626, Korea.

Department of Marine Bio-Food Sciences, Chonnam National University, Yeosu 59626, Korea.

出版信息

Mar Drugs. 2022 Aug 31;20(9):563. doi: 10.3390/md20090563.

Abstract

is a well-known red alga that has promising pharmacological characteristics. The current study evaluates the protective effect of 3-bromo-4,5-dihydroxybenzaldehyde (BDB) isolated from on tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated inflammation and skin barrier deterioration in HaCaT keratinocytes. The anti-inflammatory effect of BDB in TNF-α/IFN-γ-stimulated HaCaT keratinocytes is evaluated by investigating nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, inflammatory cytokines, and chemokines. Further, the interaction between BDB and the skin barrier functions in stimulated HaCaT keratinocytes is investigated. The findings of the study reveal that BDB dose-dependently increases cell viability while decreasing intracellular reactive oxygen species (ROS) production. BDB downregulates the expression of inflammatory cytokines, interleukin (IL)-6, -8, -13, IFN-γ, TNF-α, and chemokines, Eotaxin, macrophage-derived chemokine (MDC), regulated on activation, normal T cells expressed and secreted (RANTES), and thymus and activation-regulated chemokine (TARC) by modulating the MAPK and NF-κB signaling pathways in TNF-α/IFN-γ-stimulated HaCaT keratinocytes. Furthermore, BDB increases the production of skin hydration proteins and tight junction proteins in stimulated HaCaT keratinocytes by preserving skin moisturization and tight junction stability. These findings imply that BDB exhibits a protective ability against inflammation and deterioration of skin barrier via suppressing the expression of inflammatory signaling in TNF-α/IFN-γ-stimulated HaCaT keratinocytes.

摘要

是一种具有潜在药理特性的著名红藻。本研究评估了 3-溴-4,5-二羟基苯甲醛(BDB)对肿瘤坏死因子(TNF)-α/干扰素(IFN)-γ刺激的 HaCaT 角质形成细胞炎症和皮肤屏障恶化的保护作用。通过研究核因子 kappa B(NF-κB)和丝裂原活化蛋白激酶(MAPK)途径、炎症细胞因子和趋化因子来评估 BDB 在 TNF-α/IFN-γ 刺激的 HaCaT 角质形成细胞中的抗炎作用。此外,还研究了 BDB 与刺激的 HaCaT 角质形成细胞中皮肤屏障功能的相互作用。研究结果表明,BDB 呈剂量依赖性地增加细胞活力,同时降低细胞内活性氧(ROS)的产生。BDB 通过调节 TNF-α/IFN-γ 刺激的 HaCaT 角质形成细胞中的 MAPK 和 NF-κB 信号通路,下调炎症细胞因子白细胞介素(IL)-6、-8、-13、IFN-γ、TNF-α 和趋化因子 Eotaxin、巨噬细胞来源趋化因子(MDC)、调节激活正常 T 细胞表达和分泌(RANTES)和胸腺激活调节趋化因子(TARC)的表达。此外,BDB 通过维持皮肤保湿和紧密连接稳定性,增加刺激的 HaCaT 角质形成细胞中皮肤水合蛋白和紧密连接蛋白的产生。这些发现表明,BDB 通过抑制 TNF-α/IFN-γ 刺激的 HaCaT 角质形成细胞中炎症信号的表达,表现出对炎症和皮肤屏障恶化的保护能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/116d/9504623/45d4e8d2f565/marinedrugs-20-00563-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验