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Rutin alleviates psoriasis-related inflammation in keratinocytes by regulating the JAK2/STAT3 signaling.
Wu, Panhong; Liu, Yonghui; Zhai, Hanxue; Wu, Xiaohan; Liu, Aimin.
Afiliación
  • Wu P; Medical Beauty Department, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, China.
  • Liu Y; Surgery of Chinese Medicine, The Second Clinical Medical College of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
  • Zhai H; Surgery of Chinese Medicine, The Second Clinical Medical College of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
  • Wu X; Surgery of Chinese Medicine, The Second Clinical Medical College of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
  • Liu A; Medical Beauty Department, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, China.
Skin Res Technol ; 30(8): e70011, 2024 Aug.
Article en En | MEDLINE | ID: mdl-39167035
ABSTRACT

BACKGROUND:

Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored. MATERIALS AND

METHODS:

HaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.

RESULTS:

Rutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.

CONCLUSION:

Rutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Rutina / Transducción de Señal / Queratinocitos / Factor de Transcripción STAT3 / Janus Quinasa 2 Límite: Humans Idioma: En Revista: Skin Res Technol Asunto de la revista: DERMATOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Rutina / Transducción de Señal / Queratinocitos / Factor de Transcripción STAT3 / Janus Quinasa 2 Límite: Humans Idioma: En Revista: Skin Res Technol Asunto de la revista: DERMATOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido