PeiTuQingXin formula alleviated atopic dermatitis symptoms via inhibiting TRADD/TRAF2/RIP1 complex mediated NF-κB signaling pathway activation.

培土清心方通过抑制TRADD/TRAF2/RIP1复合物介导的NF-κB信号通路激活来缓解特应性皮炎症状

阅读:19
作者:Cheng Zixuan, Ma Xin, Luo Feng, Mo Xiumei, Liu Junfeng, Chen Dachan, Yan Fenggen
Atopic dermatitis (AD) is a chronic inflammatory skin disease with recurrent course, and traditional Chinese medicine (TCM) is regarded as an effective treatment. In this study, we aim to evaluate the potential effects and elucidate the mechanism of PTQX formula in alleviating a house dust mite (HDM)-induced AD model. NC/Nga mice were divided into Control, AD model and PTQX-treated and stimulated with HDM oinment. PTQX formula exerted significant anti-inflammatory effects, alleviated dermatitis performance, decreased the serum IgE by more than 2-fold, reduced the secretion level of other inflammatory cytokines and downregulated the Th2 cells ratio in lymph nodes. Treatment with PTQX formula reduced the level of inflammatory cytokines, which was measured by an inflammatory cytokine array kit (RayBio(®)). Kyoto Encyclopedia of Genes and Genomes pathway enrichment revealed the anti-inflammatory effect was exerted via regulation NF-κB and Toll-like receptor signaling pathway. Data independent acquisition (DIA) proteomics analysis results showed that the expression of totally 149 proteins were regulated by PTQX formula, while the expression of TRADD was significantly downregulated. According to the western blotting analysis, the PTQX group exhibitied an over 2-fold decreased expression of TRADD, TRAF2 and RIP1 compared with the AD group, accompanied by the inhibition of NF-κB signaling pathway activity. Collectively, this finding suggested that PTQX formula may exert effects by inhibiting the expression of the TRADD/TRAF2/RIP1 complex and downregulating the activity of the NF-κB signaling pathway.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。