Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, Republic of Korea.
Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, Republic of Korea.
Histol Histopathol. 2022 Sep;37(9):839-852. doi: 10.14670/HH-18-473. Epub 2022 May 30.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by skin barrier dysfunction. Sargassum horneri (S. horneri) is a brown alga that has been widely used in traditional medicine of eastern Asian countries. Recent studies proved that a brown alga S. horneri has anti-inflammatory activity. In this study, we investigated the effect of S. horneri ethanol extract (SHE) against AD in 2,4-dinitrobenzene (DNCB) induced AD in NC/Nga mice. We observed that SHE treatment decreased the epidermal thickness and epidermal hyperplasia that had been worsened through DNCB application. Moreover, SHE significantly inhibited the proliferation of mast cells and decreased the expression of IL-13 on CD4⁺ cells prompted by elevated thymic stromal lymphopoietin (TSLP) expression in DNCB-induced AD in mice. We also demonstrated that SHE directly inhibited the expression of keratinocyte-produced TSLP known to exacerbate skin barrier impairment. Especially, the decrease of filaggrin, an integral component of proper skin barrier function through a function in aggregating keratin filaments, observed in DNCB-induced AD mice was significantly improved when treated with SHE. More importantly, we proved that SHE was able to decrease the serum levels of IgG₁ and IgG₂ₐ, two crucial factors of AD, indicating the protective effect of SHE. Taken together, our findings suggest that SHE may protect NC/Nga mice against DNCB-induced AD via promoting skin barrier function.
特应性皮炎(AD)是一种慢性炎症性皮肤病,其特征为皮肤屏障功能障碍。半叶马尾藻(S. horneri)是一种褐藻,已被广泛应用于东亚国家的传统医学中。最近的研究证明,一种褐藻 S. horneri 具有抗炎活性。在这项研究中,我们研究了半叶马尾藻乙醇提取物(SHE)对 2,4-二硝基苯(DNCB)诱导的 NC/Nga 小鼠 AD 的影响。我们观察到,SHE 处理可减少表皮厚度和表皮增生,这些变化是通过 DNCB 应用而恶化的。此外,SHE 可显著抑制肥大细胞增殖,并降低由 DNCB 诱导的 AD 小鼠中胸腺基质淋巴细胞生成素(TSLP)表达升高所导致的 CD4⁺细胞中 IL-13 的表达。我们还证明,SHE 可直接抑制角质形成细胞产生 TSLP 的表达,已知 TSLP 可加重皮肤屏障损伤。特别是,通过聚集角蛋白丝的功能,在 DNCB 诱导的 AD 小鼠中观察到的丝聚蛋白(一种正常皮肤屏障功能的固有组成部分)的减少,在用 SHE 治疗后得到了显著改善。更重要的是,我们证明 SHE 能够降低 IgG₁和 IgG₂ₐ的血清水平,这两种都是 AD 的关键因素,表明 SHE 具有保护作用。综上所述,我们的研究结果表明,SHE 可能通过促进皮肤屏障功能来保护 NC/Nga 小鼠免受 DNCB 诱导的 AD。