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


RESULTS
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.
Institute of Traditional Medicine & Bioscience, Daejeon University, Daejeon, Republic of Korea.
Seung-Hyung
SH
Kim
Department of Herbology, College of Korean Medicine, Sangji University, Wonju, Republic of Korea.
Jung-Hee
JH
Hong
Department of Herbology, College of Korean Medicine, Sangji University, Wonju, Republic of Korea. Electronic address: lyc072@sangji.ac.kr.
Young-Cheol
YC
Lee
D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D053119:Benzophenanthridines / Q000494:pharmacology* / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid; D028281:Chelidonium / Q000737:chemistry*; D054423:Chemokine CCL24 / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D004802:Eosinophilia / Q000188:drug therapy; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D007073:Immunoglobulin E / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism*; D008168:Lung / Q000378:metabolism; D051379:Mice; D050800:STAT6 Transcription Factor / Q000096:biosynthesis; D015398:Signal Transduction / Q000187:drug effects
D053119:Benzophenanthridines; D054423:Chemokine CCL24; D016207:Cytokines; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D018793:Interleukin-13; D050800:STAT6 Transcription Factor; C494100:Stat6 protein, mouse; D015847:Interleukin-4; D007073:Immunoglobulin E; C062047:chelidonine
Asthma; Chelidonine; Eotaxin-2; Foxp3; STAT6