Effect of San’ao Decoction (三拗汤) on the airway inflammation and hyperresponsiveness in a murine model of lipopolysaccharide-enhanced asthma

• DOI: 10.1007/s11655-011-0788-x
• Publication Date: 2011-07-04T01:36:06Z
• Authors: Peng-cheng Gu; Xin-sheng Fan; Chen-xue Jiang; Hui-qin Xu; Jing-hua Yu; Yu-ping Tang
• Keywords: Lipopolysaccharides; 0301 basic medicine; Mice, Inbred BALB C; Cell Count; Pneumonia; Asthma; 3. Good health; Disease Models, Animal; Interferon-gamma; Mice; 03 medical and health sciences; Animals; Female; Interleukin-4; Bronchial Hyperreactivity; Interleukin-5; Bronchoalveolar Lavage Fluid; Lung; Drugs, Chinese Herbal

San'ao Decoction (, SAD), as a representative Chinese medicine (CM) formula, was chosen to evaluate the effect of airway inflammation and hyperresponsiveness on the lipopolysaccharide (LPS) enhanced asthma model.The asthma model was reproduced in the Balb/C mice sensitized by ovalbumin (OVA), challenged by OVA and LPS. After Balb/C mice's administration of a dose (0.0024 g/kg) of dexamethasone acetate, and three doses (2.2 g/kg, 4.4 g/kg and 8.8 g/kg) of SAD, airway inflammation and responsiveness were observed. The airway inflammation was detected by counting bronchoalveolar lavage fluid (BALF) cells and lung histopathology. Also, differential expressions of interferon-r (IFN-γ), interleukin-4 (IL-4), and IL-5 in the supernatants of BALF were examined. The changes in airway responsiveness indicated by lung resistance (R(L)) and stimulated by acetylcholine (Ach) were determined.Small-dose SAD hardly inhibit airway inflammation or hyperresponsiveness in the LPS-enhanced asthma, while medium-dose and high-dose SAD significantly inhibited the airway hyperresponsiveness, and to some extent, reduced airway inflammation. Meanwhile, the small-dose, medium-dose, and high-dose SAD promoted Th1-type cytokines (IFN-γ) and reduced Th2-type cytokines (IL-4, IL-5) to different extents, which led to a Th1/Th2 balance.SAD has a good therapeutic effect on airway hyperresponsiveness in the LPS-enhanced asthma model, but its definite influence on airway inflammation is not remarkable.