Chelidonine, a principal isoquinoline alkaloid of Chelidonium majus, attenuates eosinophilic airway inflammation by suppressing IL-4 and eotaxin-2 expression in asthmatic mice

Pharmacol Rep. 2015 Dec;67(6):1168-77. doi: 10.1016/j.pharep.2015.04.013. Epub 2015 May 11.


Background: Chelidonine, a major bioactive, isoquinoline alkaloid ingredient in Chelidonium majus, exhibits anti-inflammatory and other pharmacological properties. However, its molecular mechanisms in asthma remain unclear. In this work we investigated chelidonine's effect and mechanism in airway inflammation in a mouse model of allergic asthma.

Methods: The mice were sensitized to ovalbumin followed by aerosol allergen challenges and determination of chelidonine's effect on enhanced pause (Penh), pulmonary eosinophilic infiltration, eotaxin-2, interleukin-4 (IL-4), IL-13, OVA-specific IgE production, and several transcription factors.

Result: Chelidonine strongly suppressed airway eosinophilia, expression of eotaxin-2, IL-4, and IL-13 cytokine production in bronchoalveolar lavage fluid (BALF). It also attenuated lung IL-17, and eotaxin-2 mRNA expression levels. Moreover, it suppressed eotaxin-2 and IL-17 production in accordance with up- and downregulation of forkhead box p3 (Foxp3), and signal transducer and activator of transcription (STAT6) expression, respectively.

Conclusions: Chelidonine has profound inhibitory effects on airway inflammation and this effect is caused by suppression of IL-4, eotaxin-2, and OVA-specific IgE production through the STAT6 and Foxp3 pathways. So chelidonine can improve allergic asthma in mice and be a novel anti-asthma therapeutic.

Keywords: Asthma; Chelidonine; Eotaxin-2; Foxp3; STAT6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / chemically induced
  • Asthma / drug therapy*
  • Asthma / metabolism*
  • Benzophenanthridines / pharmacology*
  • Benzophenanthridines / therapeutic use*
  • Bronchoalveolar Lavage Fluid
  • Chelidonium / chemistry*
  • Chemokine CCL24 / metabolism*
  • Cytokines / metabolism
  • Eosinophilia / drug therapy
  • Female
  • Forkhead Transcription Factors / biosynthesis
  • Immunoglobulin E / metabolism
  • Interleukin-13 / metabolism
  • Interleukin-4 / metabolism*
  • Lung / metabolism
  • Mice
  • STAT6 Transcription Factor / biosynthesis
  • Signal Transduction / drug effects


  • Benzophenanthridines
  • Chemokine CCL24
  • Cytokines
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Interleukin-13
  • STAT6 Transcription Factor
  • Stat6 protein, mouse
  • Interleukin-4
  • Immunoglobulin E
  • chelidonine