Anti-inflammatory and skin barrier regulation of cyanin chloride in TNF-α/IL-17A/IFN-γ-induced HaCaT psoriasis model

IF 2.5 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Biotechnology and Bioprocess Engineering Pub Date : 2024-07-23 DOI:10.1007/s12257-024-00134-1
Min Ji Kim, Hui Su Chung, Yea Ju Han, Jeong min Cho, Dong won Kim, Hyung Seo Hwang
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Abstract

Cyanin chloride, one of the active ingredients in figs, is a glycoside made of two sugars linked to a cyanidin aglycone. Although many studies have reported on the skin efficacy of cyanidin aglycone, there have been few reports on human psoriasis to date. Therefore, we focused on excessive inflammation and loss of skin barrier function, which are the main characteristics of psoriasis, and verified the function of cyanin chloride on the psoriasis. Cyanine chloride removed DPPH and ABTS radicals in a concentration-dependent manner and significantly inhibited NO production in LPS-induced RAW264.7 cells as well as suppressed inflammatory cytokines such as iNOS, COX-2, IL-6, and IL-1α/β. Moreover, we used TNF-α/IL-17A/IFN-γ-induced HaCaT cells, a human skin cell model of psoriasis. Cyanin chloride significantly inhibited the mRNA expression of inflammatory cytokines, such as IL-1α, IL-1β, and IL-6, and chemokines CXCL8 and CCL20 in TNF-α/IL-17A/IFN-γ-induced HaCaT cells. Cyanin chloride significantly inhibited the phosphorylation of STAT3 transcription factor in a concentration-dependent manner, confirming the regulatory function of CCL20 chemokine. Finally, cyanin chloride significantly restored the TEER value in TNF-α/IL-17A/IFN-γ-induced HaCaT cells, confirming the effect of strengthening the skin barrier function. In addition, cyanin chloride increased the mRNA levels of filaggrin which is cornified envelope proteins of the epidermal layer, in a concentration-dependent manner in normal epidermal cells. Taken together, the above results suggest that cyanin chloride can be considered a natural candidate for improving psoriasis, an incurable skin disease, not only by lowering excessive skin inflammatory reactions but also by restoring the skin barrier.

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氯化氰在 TNF-α/IL-17A/IFN-γ 诱导的 HaCaT 银屑病模型中的抗炎和皮肤屏障调节作用
氯化花青素是无花果中的活性成分之一,它是一种苷,由两种糖与花青素苷元连接而成。尽管许多研究都报道了青花素苷凝集物对皮肤的功效,但迄今为止有关人类牛皮癣的报道却很少。因此,我们将重点放在银屑病的主要特征--过度炎症和皮肤屏障功能丧失上,并验证了氯化氰对银屑病的作用。氯化氰能以浓度依赖性方式清除 DPPH 和 ABTS 自由基,并能显著抑制 LPS 诱导的 RAW264.7 细胞中 NO 的产生,还能抑制 iNOS、COX-2、IL-6 和 IL-1α/β 等炎症细胞因子。此外,我们还使用了 TNF-α/IL-17A/IFN-γ 诱导的 HaCaT 细胞(一种银屑病人皮肤细胞模型)。氯化蓝能明显抑制 TNF-α/IL-17A/IFN-γ-诱导的 HaCaT 细胞中炎性细胞因子(如 IL-1α、IL-1β 和 IL-6)以及趋化因子 CXCL8 和 CCL20 的 mRNA 表达。氯化氰以浓度依赖的方式明显抑制了 STAT3 转录因子的磷酸化,证实了 CCL20 趋化因子的调控功能。最后,氯化氰明显恢复了 TNF-α/IL-17A/IFN-γ 诱导的 HaCaT 细胞的 TEER 值,证实了氯化氰具有增强皮肤屏障功能的作用。此外,氯化氰还能以浓度依赖的方式增加正常表皮细胞中表皮层粟粒状包膜蛋白--丝胶蛋白的 mRNA 水平。综上所述,上述结果表明氯化氰不仅能降低过度的皮肤炎症反应,还能恢复皮肤屏障,因此可被视为改善银屑病(一种无法治愈的皮肤病)的天然候选药物。
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来源期刊
Biotechnology and Bioprocess Engineering
Biotechnology and Bioprocess Engineering 工程技术-生物工程与应用微生物
CiteScore
5.00
自引率
12.50%
发文量
79
审稿时长
3 months
期刊介绍: Biotechnology and Bioprocess Engineering is an international bimonthly journal published by the Korean Society for Biotechnology and Bioengineering. BBE is devoted to the advancement in science and technology in the wide area of biotechnology, bioengineering, and (bio)medical engineering. This includes but is not limited to applied molecular and cell biology, engineered biocatalysis and biotransformation, metabolic engineering and systems biology, bioseparation and bioprocess engineering, cell culture technology, environmental and food biotechnology, pharmaceutics and biopharmaceutics, biomaterials engineering, nanobiotechnology, and biosensor and bioelectronics.
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