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Purpurin suppresses atopic dermatitis via TNF-α/IFN-γ-induced inflammation in HaCaT cells. | LitMetric

AI Article Synopsis

  • - The study explored how purpurin, a natural compound with known anti-inflammatory properties, affects inflammation pathways that can lead to atopic dermatitis.
  • - Researchers tested purpurin on human skin cells to see if it suppresses the release of inflammatory substances (cytokines and chemokines) triggered by immune signals TNF-α and IFN-γ, finding that purpurin effectively reduced their levels.
  • - Results showed that purpurin not only decreased inflammation markers but also inhibited key signaling pathways related to inflammation, suggesting its potential for treating atopic dermatitis.

Article Abstract

Objective: We investigated whether purpurin inhibits various pathways of inflammation leading to atopic dermatitis.

Introduction: 1,2,4-Trihydroxyanthraquinone, commonly called purpurin, is an anthraquinone that is a naturally occurring red/yellow dye. Purpurin is a highly antioxidative anthraquinone and previous studies have reported antibacterial, anti-tumor, and anti-oxidation activities in cells and animals. However, the skin inflammatory inhibition activity mechanism study of purpurin has not been elucidated in vitro.

Methods: In this study, we investigated the anti-inflammatory activity of purpurin in HaCaT (human keratinocyte) cell lines stimulated with a mixture of tumor necrosis factor-alpha (TNF-α)/Interferon-gamma (IFN-γ). The inhibitory effect of Purpurin on cytokines (IL-6, IL-8, and IL-1β) and chemokine (TARC, MDC, and RANTES) was confirmed by ELISA and RT-qPCR. We investigated each signaling pathway and the action of inhibitors through western blots.

Results: The expression levels of cytokines and chemokines were dose-dependently suppressed by purpurin treatment in TNF-α/IFN-γ-induced HaCaT cells from ELISA and real-time PCR. Purpurin also inhibited protein kinase B (AKT), mitogen-activated protein kinase (MAPKs), and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) activation in TNF-α/IFN-γ-stimulated HaCaT cells. Additionally, there was a synergistic effect when purpurin and inhibitor were applied together, and inflammation was dramatically reduced.

Conclusion: Therefore, these results demonstrate that purpurin exhibits anti-inflammatory and anti-atopic dermatitis activity in HaCaT cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9274433PMC
http://dx.doi.org/10.1177/03946320221111135DOI Listing

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