Abietic acid attenuates allergic airway inflammation in a mouse allergic asthma model

• Published in: International immunopharmacology 2016-09, Vol.38, p.261-266
• Main Authors: Gao, Yi, Zhaoyu, Liu, Xiangming, Fang, Chunyi, Lin, Jiayu, Pan, Lu, Shen, Jitao, Chen, Liangcai, Chen, Jifang, Liu
• Format: Article
• Language: English
• Subjects: Abietic acid; Adult; Animals; Anti-Inflammatory Agents - therapeutic use; Asthma; Asthma - drug therapy; Bronchial Hyperreactivity - drug therapy; Cell Movement - drug effects; Cytokines - metabolism; Disease Models, Animal; Diterpenes, Abietane - therapeutic use; Female; Humans; Immunoglobulin E - blood; Lung - drug effects; Lung - pathology; Lung - physiology; Male; Mice; Mice, Inbred BALB C; Middle Aged; NF-kappa B - metabolism; NF-κB; OVA; Pimenta - immunology; Pneumonia - drug therapy; Young Adult
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2016.05.029

Abietic acid (AA), one of the terpenoids isolated from Pimenta racemosa var. grissea, has been reported to have anti-inflammatory and immunomodulatory effects. However, the anti-allergic effects of AA remain unclear. The aim of this study was to investigate the anti-allergic effects of AA in an ovalbumin (OVA)-induced asthma murine model. The model of mouse asthma was established by induction of OVA. AA (10, 20, 40mg/kg) was administered by oral gavage 1h after the OVA treatment on days 21 to 23. At 24h after the last challenge, bronchoalveolar lavage fluid (BALF) and lung tissues were collected to assess pathological changes, cytokines production, and NF-κB expression. The results showed that AA attenuated lung histopathologic changes, inflammatory cells infiltration, and bronchial hyper-responsiveness. AA also inhibited OVA-induced the nitric oxide (NO), IL-4, IL-5, IL-13, and OVA-specific IgE production, as well as NF-κB activation. In conclusion, the current study demonstrated that AA exhibited protective effects against OVA-induced allergic asthma in mice and the possible mechanism was involved in inhibiting NF-κB activation. •AA attenuates lung histopathologic changes, inflammatory cells infiltration, and bronchial hyper-responsiveness.•AA inhibits OVA-induced the nitric oxide (NO), IL-4, IL-5, IL-13, and OVA-specific IgE production.•AA inhibits OVA-induced NF-κB activation.