Objective：San＇ao Decoction（三拗汤,SAD）,as a representative Chinese medicine（CM）formula, was chosen to evaluate the effect of airway inflammation and hyperresponsiveness on the lipopolysaccharide （LPS）enhanced ...Objective：San＇ao Decoction（三拗汤,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.展开更多
基金Supported by a Grant-in-aid for Scientific Research in the 11th Five-Year Plan,the Ministry of Science and Technology of P.R. China(No.2006BAI06A02-01)Natural Science Foundation of China(No.81072748)
文摘Objective：San＇ao Decoction（三拗汤,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.
