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

• Published in: Pharmacological reports Vol. 67; no. 6; pp. 1168 - 1177
• Main Authors: Kim, Seung-Hyung, Hong, Jung-hee, Lee, Young-Cheol
• Format: Journal Article
• Language: English
• Published: Cham Elsevier Urban & Partner Sp. z o.o 01.12.2015; Springer International Publishing
• Subjects: Animals; Asthma; Asthma - chemically induced; Asthma - drug therapy; Asthma - metabolism; Benzophenanthridines - pharmacology; Benzophenanthridines - therapeutic use; Bronchoalveolar Lavage Fluid; Chelidonine; Chelidonium - chemistry; Chemokine CCL24 - metabolism; Cytokines - metabolism; Drug Safety and Pharmacovigilance; Eosinophilia - drug therapy; Eotaxin-2; Female; Forkhead Transcription Factors - biosynthesis; Foxp3; Immunoglobulin E - metabolism; Interleukin-13 - metabolism; Interleukin-4 - metabolism; Lung - metabolism; Mice; Original Research Article; Pharmacotherapy; Pharmacy; Signal Transduction - drug effects; STAT6; STAT6 Transcription Factor - biosynthesis; Chelidonine; Eotaxin-2; STAT6; Foxp3; Asthma
• ISSN: 1734-1140; 2299-5684
• DOI: 10.1016/j.pharep.2015.04.013

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. 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. 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. 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.