Sargassum horneri extract containing polyphenol alleviates DNCB-induced atopic dermatitis in NC/Nga mice through restoring skin barrier function
Suyama Prasansali Mihindukulasooriya1*, Duong Thi Thuy Dinh1*, Kalahe Hewage Iresha Nadeeka Madushani Herath1,2,3, Hyo Jin Kim4, Eui-Jeong Han5, Jinhee Cho2, Mi-Ok Ko2, You-Jin Jeon6, Ginnae Ahn5 and Youngheun Jee1,2
1Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, 2Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, Republic of Korea, 3Department of Biosystems Engineering, Faculty of Agriculture and Plantation Management, Wayamba University of Sri Lanka, Makandura, Sri Lanka, 4Department of Food Bioengineering, Jeju National University, Jeju, 5Department of Food Technology and Nutrition, Chonnam National University, Yeosu and 6Department of Marine Life Science, School of Marine Biomedical Sciences, Jeju National University, Jeju, Republic of Korea
*These authors equally contributed to this study
Corresponding Author: Youngheun Jee, Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 63243, Republic of Korea. e-mail: yhjee@jejunu.ac.kr
Summary. 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. Histol Histopathol 37, 839-852 (2022)
Key words: Brown alga, Thymic stromal lymphopoietin (TSLP), Filaggrin, Skin barrier
DOI: 10.14670/HH-18-473
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©The Author(s) 2022. Open Access. This article is licensed under a Creative Commons CC-BY International License. |
