Protective effect of emodin against airway inflammation in the ovalbumin-induced mouse model

• Published in: Chinese journal of integrative medicine 2015-06, Vol.21 (6), p.431-437
• Main Authors: Wang, Tan, Zhong, Xiang-gen, Li, Yu-hang, Jia, Xu, Zhang, Shu-jing, Gao, Yu-shan, Liu, Miao, Wu, Ruo-han
• Format: Article
• Language: English
• Subjects: Animals; Bronchoalveolar Lavage Fluid - cytology; Chemokines - metabolism; Disease Models, Animal; Emodin - chemistry; Emodin - pharmacology; Emodin - therapeutic use; Female; Gene Expression Regulation - drug effects; Heme Oxygenase-1 - genetics; Heme Oxygenase-1 - metabolism; Immunoglobulin E - blood; Interleukins - genetics; Interleukins - metabolism; Leukocytes - drug effects; Leukocytes - metabolism; Lung - drug effects; Lung - metabolism; Lung - pathology; Matrix Metalloproteinase 9 - genetics; Matrix Metalloproteinase 9 - metabolism; Medicine; Medicine & Public Health; Mice, Inbred C57BL; Original Article; Ovalbumin; Pneumonia - blood; Pneumonia - drug therapy; Pneumonia - pathology; Protective Agents - pharmacology; Protective Agents - therapeutic use; RNA, Messenger - genetics; RNA, Messenger - metabolism
• ISSN: 1672-0415; 1993-0402
• DOI: 10.1007/s11655-014-1898-z

Objective To investigate whether emodin exerts protective effects on mouse with allergic asthma. Methods A mouse model of allergic airway inflflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin (OVA) were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid (BALF) was measured. The levels of interleukin (IL)-4, IL-5, IL-13 and eotaxin in BALF and level of immunoglobulin E (IgE) in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4, IL-5, heme oxygenase (HO)-1 and matrix metalloproteinase-9 (MMP-9) were determined by real-time quantitative polymerase chain reaction. Results Emodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4, IL-5, IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally, emodin suppressed IL-4, IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression. Conclusion Emodin exhibits anti-inflammatory activity in the airway inflammation mouse model, supporting its therapeutic potential for the treatment of allergic bronchial asthma.