Biotechnology and Bioprocess Engineering 2024; 29(6): 1048-1060  
Anti-infl ammatory and skin barrier regulation of cyanin chloride in TNF-α/IL-17A/IFN- γ -induced HaCaT psoriasis model
Min Ji Kim 1 · Hui Su Chung 1 · Yea Ju Han 1 · Jeong min Cho 2 · Dong won Kim 2 · Hyung Seo Hwang 1
1School of Cosmetic Science and Beauty Biotechnology, Semyung University, Jechon 27136, Korea
2School of Bio-Pharmaceutical Engineering, Dongseo University, Busan 47011, Korea
Correspondence to: ✉ Hyung Seo Hwang
hshwang@semyung.ac.kr
Received: January 29, 2024; Revised: July 9, 2024; Accepted: July 17, 2024; Published online: July 23, 2024.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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-1 α/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.
Keywords: Anti-infl ammation · Cyanin chloride · Filaggrin · Psoriasis · Skin barrier · STAT3


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