Emodin alleviates alternatively activated macrophage and asthmatic airway inflammation in a murine asthma model

Authors: Yun-duan SONG1, Xiao-zong LI1, Ya-xian WU2, Yao SHEN3, Fang-fang LIU1, Pei-pei GAO4, Lei SUN2, Feng QIAN2,5
1 Department of Clinical Laboratory, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, China
2 Engineering Research Center of Cell & Therapeutic Antibody, Ministry of Education, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China
3 Department of Respiratory Medicine, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, China
4 Department of Pharmaceutical Preparation Section, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, China;
5 Research Center for Cancer Precision Medicine, Bengbu Medical College, Bengbu 233003, China
Corresponding to: Lei SUN:, Feng QIAN:,
DOI: 10.1038/aps.2017.147
Received: 13 July 2017
Accepted: 6 November 2017
Advance online: 8 February 2018


Alternatively activated macrophages (AAMs) are not only associated with asthma but also lead to asthmatic airway inflammation and remodeling. Inhibition of AAMs is an alternative therapeutic strategy for treating asthma. In this study we investigated whether emodin (1,3,8-trihydroxy-6-methylanthraquinone), isolated from the rhizome of Rheum palmatum, alleviated asthmatic airway inflammation and reduced AAM polarization in a murine asthma model. Mice were sensitized with a triple allergen mix containing dust mite, ragweed and aspergillus (DRA). In mice with DRA-induced asthma, asthmatic inflammation was significantly enhanced. Intraperitoneal injection of emodin (20 mg·kg-1·d-1, ip) 1 h prior to DRA challenge on days 12-14 significantly decreased pulmonary eosinophil and lymphocyte infiltration, mucus secretion and serum IgE production, as well as IL-4 and IL-5 production in bronchoalveolar lavage fluid. In response to emodin treatment, activated markers of AAM Ym-1, Fizz-1 and arginase-1 in the lung tissues were remarkably decreased. In mouse bone marrow-derived macrophages (BMDMs) in vitro, emodin (2–50 µmol/L) dose-dependently inhibited IL-4-induced AAM polarization and STAT6 phosphorylation. Collectively, our results suggest that emodin effectively ameliorates asthmatic airway inflammation and AAM polarization, and it may therefore become a potential agent for the treatment of asthma.
Keywords: asthma; emodin; alternatively activated macrophage; airway inflammation; STAT6; IL-4