Formula PSORI-CM01 inhibits the inflammatory cytokine and chemokine release in keratinocytes via NF-κB expression

Formula PSORI-CM01 inhibits the inflammatory cytokine and chemokine release in keratinocytes via NF-κB expression
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DOI:
10.1016/j.intimp.2017.01.023
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发表时间:
2017-03-01
影响因子:
5.6
通讯作者:
Wei, Jian-an
Wei, Jian-an
中科院分区:
医学2区
文献类型:
--
作者:
Han, Ling;Sun, Jing;Wei, Jian-an

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银屑病是一种常见的慢性炎症性疾病,辅助性T细胞I(Th1)和辅助性T细胞17(Th17)在其病理学中发挥重要作用。 PSORI-CM01方剂是一种用于治疗牛皮癣的新型中药。先前已证明PSORI-CM01和含有PSORI-CM01配方(PCMO1CS)的血清可以通过抑制上皮增生来改善银屑病,但PSORI-CM01如何影响真皮中的炎症细胞因子和趋化因子仍不清楚。在这项研究中,我们发现在 IMQ 涂漆前 3 天预处理 PSORI-CM01 可以改善 IMQ 引起的小鼠皮肤损伤,因为 PASI 评分明显降低。分别使用Th1相关细胞因子IFN-γ和Th17相关细胞因子IL-17/IL-22在体外诱导人角质形成细胞系HaCaT炎症模型。 PCMO1CS 显着降低 IFN-γ 诱导的 IL-6、IL-12 和 CXCL-10 mRNA 表达,减少 IL-6 和 CXCL-10 释放到 HaCaT 上清液中。 20 ng/ml IL-17/IL22 共刺激显着上调 HaCaT 细胞中 IL-6、IL-8 和 CCL20 mRNA 的表达,PCMO1CS 在 mRNA 和蛋白水平上显着抑制这些细胞因子的表达。最后,PCMO1CS可以明显抑制由IFN-γ和IL-17/1L-22刺激激活的核NF-κB p65表达。因此,我们的新发现表明,PSORI-CM01 配方可能通过抑制皮肤环境内的炎症来对牛皮癣具有治疗作用。 (C) 2017 年由 Elsevier B.V. 出版
Psoriasis is a common chronic inflammatory disease in which T-helper I (Th1) and T-helper 17(Th17) cells play an important role in its pathology. Formula PSORI-CM01 was a novel formulated Chinese medicine used for psoriasis therapy. It had been demonstrated previously that PSORI-CM01 and serum contained Formula PSORI-CM01 (PCMO1CS) could improve psoriasis by inhibiting the epithelial hyperplasia, how PSORI-CM01 affects inflammatory cytokine and chemokine in dermis is still unknown. In this study we found PSORI-CM01 pre-treated 3 days before IMQ painting could ameliorated IMQ-induced mice skin lesion as PASI score was apparently reduced. Th1 related cytokine IFN-gamma and Th17 related cytokine IL-17/IL-22 was used to induce inflammatory models on human keratinocyte cell line HaCaT in vitro, respectively. PCMO1CS significantly reduced IFN-gamma induced mRNA expression of IL-6, IL-12 and CXCL-10, reduced IL-6 and CXCL-10 release into HaCaT supernatant. 20 ng/ml IL-17/IL22 co-stimulation significantly upregulated expression of IL-6, IL-8 and CCL20 mRNA expression in HaCaT cells, PCMO1CS significantly inhibit these cytokines expression both in mRNA and in protein levels. Finally, PCMO1CS could obviously inhibit nuclear NF-kappa B p65 expression which activated by IFN-gamma and IL-17/1L-22 stimulation. Thus, our new findings reveal that Formula PSORI-CM01 may possess therapeutic action on psoriasis by inhibiting inflammatory within skin environments. (C) 2017 Published by Elsevier B.V.