OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: Hai Yong Chen; Chun Ho Ma; Ke-Jian Cao; James Chung-Man Ho; Eric Ziea; Vivian Taam Wong; Zhang-Jin Zhang Journal: Evid Based Complement Alternat Med Date: 2014-03-26 Impact factor: 2.629