We describe for the first time that andrographolide derivatives such as DDAG effectively reduced OVA-induced inflammatory cell recruitment into BAL fluid, IL-4, IL-5, IL-13 and eotaxin production, serum IgE synthesis, pulmonary eosinophilia, mucus hypersecretion and AHR in a mouse asthma model potentially via inhibition of NF-?B activity. Moreover, low dose of DDAG and glucocorticoid combination treatment synergistically attenuate inflammation in mouse asthma model. These findings support a therapeutic value for DDAG in the treatment of asthma.
