Ayuda
Ir al contenido

Dialnet


Scopoletin inhibits PDGF-BB-induced proliferation and migration of airway smooth muscle cells by regulating NF-κB signaling pathway

  • Zhongxiang Fan [2] ; Dan Tang [1] ; Qiang Wu [2] ; Qun Huang [3] ; Jie Song [2] ; Qiping Long [2]
    1. [1] Chengdu University of Traditional Chinese Medicine

      Chengdu University of Traditional Chinese Medicine

      China

    2. [2] Department of Pediatrics, Chengdu Wenjiang Maternal and Child Health Hospital, Chengdu, Sichuan Province, China.
    3. [3] Chengdu Wenjiang Maternal and Child Health Hospital, Chengdu, Sichuan Province, China
  • Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 50, Nº. 1, 2022, págs. 92-98
  • Idioma: inglés
  • Enlaces
  • Resumen
    • Background: Asthma is a common chronic inflammatory disease of the airway, and airway remodeling and the proliferation mechanism of airway smooth muscle cells (ASMCs) is of great significance to combat this disease.

      Objective: To assess possible effects of scopoletin on asthma and the potential signaling pathway.

      Materials and methods: ASMCs were treated PDGF-BB and scopoletin and subjected to cell viability detection by CCK-8 assay. Cell migration of ASMCs was determined by a wound closure assay and transwell assay. The protein level of MMP2, MMP9, calponin and α-SMA were measured using western blot. The levels of NF-κB signaling pathway were detected by Western blotting.

      Results: Scopoletin inhibited proliferation of PDGF-BB - induced ASMCs. Also it suppressed the migration and invasion of PDGF-BB - induced ASMCs. We further showed that Scopoletin regulated phenotypic transition of ASMCs. Mechanically, Scopoletin inhibited proliferation and invasion of ASMCs by regulating NF-κB signaling pathway.

      Conclusions: We therefore thought Scopoletin could serve as a promising drug for the treatment of asthma.


Fundación Dialnet

Dialnet Plus

  • Más información sobre Dialnet Plus

Opciones de compartir

Opciones de entorno