Sulfuretin alleviates atopic dermatitis-like symptoms in mice via suppressing Th2 cell activity
- PDF / 830,851 Bytes
- 9 Pages / 595.276 x 790.866 pts Page_size
- 23 Downloads / 138 Views
ORIGINAL ARTICLE
Sulfuretin alleviates atopic dermatitis-like symptoms in mice via suppressing Th2 cell activity Pingdong Jiang 1 & Hui Sun 1
# Springer Science+Business Media, LLC, part of Springer Nature 2018
Abstract Atopic dermatitis (AD) is a chronic skin inflammatory disease characterized by uncontrolled Th2 cells response to environmental allergens. Long-term topical application of corticosteroids for treating AD may induce severe side effects. Sulfuretin is a major flavonoid found in Rhus verniciflua and carries antioxidant and anti-inflammatory properties. Its therapeutic effect on AD has not been characterized. We first studied the cytotoxic and regulatory effects of sulfuretin on differentiated Th2 cells. Next, we evaluated therapeutic effect of sulfuretin on AD-like damages caused by 2,4-dinitrochlorobenzene (DNCB) in a mouse model. Serum IgE level, overall symptomatic score, and cytokine accumulation at the lesions were measured. Lastly, we investigated the regulatory mechanism of sulfuretin on GATA3 pathway in primary mouse CD4+ cells. Study on in vitro differentiated Th2 cells showed sulfuretin inhibited IL4 production in dose-dependent manner without any cytotoxicity. In vivo study showed 10 μM sulfuretin alleviated the AD symptoms including skin lesion severity, scratching incidence, IgE serum level, and proinflammatory cytokine accumulation at local skin lesion site. Mechanistic study suggested sulfuretin attenuated Th2 cytokine production by suppressing GATA3 expression. Our results demonstrate that sulfuretin could be used as therapeutic application for treating AD. Keywords Sulfuretin . Atopic dermatitis . Th2 cell . GATA3 . DNCB
Introduction Atopic dermatitis (AD) is a common pruritic skin inflammatory disease primarily due to cutaneous hyperreactivity to environmental triggers. AD commonly occurs during early childhood, but is also found in adulthood. In children, the lifetime prevalence of AD is 10~20% as compared with 1~3% in adults. And its prevalence is on the rise all over the world, particularly in the industrialized societies. Although it is not a life-threatening disease, AD is still considered as a major skin disease that causes significant burdens upon patients’ life quality, work productivity, and health outcomes [1–3].
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12026-018-9025-4) contains supplementary material, which is available to authorized users. * Hui Sun [email protected] 1
Department of Dermatology, Wuxi No.2 People’s Hospital, Wuxi 214002, Jiangsu, China
The interplay among skin barrier dysfunction, environmental allergic triggers, and allergic inflammation is at the critical stage in the AD pathogenesis. Dysfunction in skin barrier, as primary defect, results in itchy dry skin that leads to scratching. Frequent scratching inflicts mechanical damage to skin barrier that eventually leads to allergic sensitization to environmental antigens and allergic skin inflammation. And the secondary defect is the immune response a
Data Loading...
