Anti-inflammatory effects of quercetin in a mouse model of MC903-induced atopic dermatitis

哈卡特 特应性皮炎 CCL22型 CCL17型 基因沉默 医学 免疫学 炎症 胸腺基质淋巴细胞生成素 趋化因子 肿瘤坏死因子α 药理学 体外 生物 CXCL10型 生物化学 基因
作者
Diandong Hou,Wei Zhang,Yali Gao,Yuzhe Sun,Hexiao Wang,Ruiqun Qi,Hong‐Duo Chen,Xing‐Hua Gao
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:74: 105676-105676 被引量:60
标识
DOI:10.1016/j.intimp.2019.105676
摘要

In this study, the anti-inflammatory mechanisms of Quercetin (Que) on atopic dermatitis (AD)-like skin lesions was examined. The left ear of mice was applied with MC903, followed by Que. administration daily on the ear for 8 days. Then macroscopic and histologic examination was performed to detect the severity of skin lesions. In the skin section of AD mice, we observed that Que. could reduce the expression of CCL17, CCL22, IL-4, IL-6, IFN-γ and TNF-α. In vitro, the anti-inflammatory effects of Que. were examined on human keratinocytes (HaCaT cells) treated with IFN-γ/TNF-α. To unveil the lncRNAs' regulatory role on Que-activated anti-inflammatory function, the next-generation high-throughput sequencing was performed in HaCat cells with or without Que. treatment, which profiled the expression of lncRNAs and mRNAs, the results illustrated that lnc-C7orf30-2, a lncRNA expressed differentially, was correlated with IL-6 expression. Silencing of lnc-C7orf30-2 by RiboTM lncRNA Smart Silencer proved its role on IL-6 expression. Therefore, the results here demonstrated that topical administration of Que. plays a beneficial role in controlling AD symptoms, which may serve as potential candidate for AD treatment.
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