Fulvic Acid Attenuates Atopic Dermatitis by Downregulating CCL17/22

被引：4
作者：
Wu, Chenxi [1 ]
Lyu, Anqi [1 ]
Shan, Shijun [1 ,2 ,3 ]
机构：
[1] Xiamen Univ, Xiangan Hosp, Sch Med, Dept Dermatol, Xiamen 361000, Peoples R China
[2] Zhejiang Univ, Hangzhou Peoples Hosp 3, Affiliated Hangzhou Dermatol Hosp, Sch Med, Hangzhou 310009, Peoples R China
[3] Shaoxing Cent Hosp, Chen Hongduo Academician Workstn, Shaoxing 312030, Peoples R China
来源：
MOLECULES | 2023年 / 28卷 / 08期
基金：
中国国家自然科学基金;
关键词：
atopic dermatitis (AD); fulvic acid (FA); CCL17; CCL22; INFLAMMATORY RESPONSE; SIGNALING PATHWAY; KERATINOCYTES; SKIN; SUPPRESSES; LYMPHOPOIETIN; INHIBITION; EXPRESSION; MDC/CCL22; THYMUS;
D O I：
10.3390/molecules28083507
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The main pathogenic factor in atopic dermatitis (AD) is Th2 inflammation, and levels of serum CCL17 and CCL22 are related to severity in AD patients. Fulvic acid (FA) is a kind of natural humic acid with anti-inflammatory, antibacterial, and immunomodulatory effects. Our experiments demonstrated the therapeutic effect of FA on AD mice and revealed some potential mechanisms. FA was shown to reduce TARC/CCL17 and MDC/CCL22 expression in HaCaT cells stimulated by TNF-alpha and IFN-gamma. The inhibitors showed that FA inhibits CCL17 and CCL22 production by deactivating the p38 MAPK and JNK pathways. After 2,4-dinitrochlorobenzene (DNCB) induction in mice with atopic dermatitis, FA effectively reduced the symptoms and serum levels of CCL17 and CCL22. In conclusion, topical FA attenuated AD via downregulation of CCL17 and CCL22, via inhibition of P38 MAPK and JNK phosphorylation, and FA is a potential therapeutic agent for AD.
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页数：12
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