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
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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