Premium
Ramalin Isolated from Ramalina Terebrata Attenuates Atopic Dermatitis‐like Skin Lesions in Balb/c Mice and Cutaneous Immune Responses in Keratinocytes and Mast Cells
Author(s) -
Park HyeJin,
Jang Yeon Jeong,
Yim JoungHan,
Lee HongKum,
Pyo Suhkneung
Publication year - 2016
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5703
Subject(s) - chemokine , hacat , immunology , proinflammatory cytokine , immune system , mapk/erk pathway , tumor necrosis factor alpha , atopic dermatitis , medicine , chemistry , signal transduction , biology , inflammation , in vitro , microbiology and biotechnology , biochemistry
Atopic dermatitis (AD) is a chronic inflammatory skin disease that involves eczematous skin lesions with pruritic erythematous papules. In this study, we investigated the mitigating effects of ramalin, a component of the Antarctic lichen Ramalina terebrata against AD in vivo and in vitro . Oral administration of ramalin lessened scratching behaviors and significantly reduced both serum immunoglobulin E and IL‐4 levels, and mRNA levels of IL‐4 and IL‐10 in AD‐induced Balb/c mice. In vitro , treatment with ramalin produced significantly less inflammatory chemokines and cytokines, including TARC, MCP‐1, RANTES, and IL‐8 in TNF‐α‐stimulated HaCaT cells. In addition, ramalin inhibited the activation of nuclear factor‐kappa B as well as the phosphorylation of mitogen‐activated protein kinases (MAPK). Furthermore, ramalin treatment resulted in decreased production of β‐hexosaminidase and proinflammatory cytokines IL‐4, IL‐6, and TNF‐α in 2,4 dinitrophenyl‐human serum albumin‐stimulated RBL‐2H3 cells through blocking MAPK signaling pathways. The results suggest that ramalin modulates the production of immune mediators by inhibiting the nuclear factor‐kappa B and MAPK signaling pathways. Taken together, ramalin effectively attenuated the development of AD and promoted the mitigating effects on Th2 cell‐mediated immune responses and the production of inflammatory mediators in mast cells and keratinocytes. Thus, ramalin may be a potential therapeutic agent for AD. Copyright © 2016 John Wiley & Sons, Ltd.