Skullcapflavone II Suppresses TNF-α/IFN-γ-Induced TARC, MDC, and CTSS Production in HaCaT Cells
| Autor: | Hanon Lee, Jang Hee Oh, Dong Hun Lee, Jin Ho Chung |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Chemokine
Skullcapflavone II MDC p38 Mitogen-Activated Protein Kinases NF-κB chemistry.chemical_compound STAT1 HaCaT Cells Biology (General) anti-inflammatory activity Spectroscopy Cathepsin S biology atopic dermatitis Chemistry NF-kappa B General Medicine Computer Science Applications STAT1 Transcription Factor Phosphorylation Signal Transduction keratinocytes QH301-705.5 Cell Survival p38 mitogen-activated protein kinases p38 MAPK Catalysis Article Inorganic Chemistry Interferon-gamma Humans Physical and Theoretical Chemistry Molecular Biology QD1-999 TARC Chemokine CCL22 Flavonoids Messenger RNA Tumor Necrosis Factor-alpha Organic Chemistry CTSS Molecular biology Cathepsins HaCaT Gene Expression Regulation biology.protein Chemokine CCL17 |
| Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 6428, p 6428 (2021) Volume 22 Issue 12 |
| ISSN: | 1422-0067 |
| Popis: | Skullcapflavone II (SFII), a flavonoid derived from Scutellaria baicalensis, has been reported to have anti-inflammatory properties. However, its therapeutic potential for skin inflammatory diseases and its mechanism are unknown. Therefore, this study aimed to investigate the effect of SFII on TNF-α/IFN-γ-induced atopic dermatitis (AD)-associated cytokines, such as thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). Co-stimulation with TNF-α/IFN-γ in HaCaT cells is a well-established model for induction of pro-inflammatory cytokines. We treated cells with SFII prior to TNF-α/IFN-γ-stimulation and confirmed that it significantly inhibited TARC and MDC expression at the mRNA and protein levels. Additionally, SFII also inhibited the expression of cathepsin S (CTSS), which is associated with itching in patients with AD. Using specific inhibitors, we demonstrated that STAT1, NF-κB, and p38 MAPK mediate TNF-α/IFN-γ-induced TARC and MDC, as well as CTSS expression. Finally, we confirmed that SFII significantly suppressed TNF-α/IFN-γ-induced phosphorylation of STAT1, NF-κB, and p38 MAPK. Taken together, our study indicates that SFII inhibits TNF-α/IFN-γ-induced TARC, MDC, and CTSS expression by regulating STAT1, NF-κB, and p38 MAPK signaling pathways. |
| Databáze: | OpenAIRE |
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