Abstract: Objective To observe the effects of nodakenin on airway inflammation in a mouse model of allergic asthma. Methods BALB/c mice were assigned randomly to one of the following four experimental groups: control, model, nodakenin and dexamethasone. All mice, except for those in control group, were sensitized and challenged by OVA to induce airway inflammation. One hour before every OVA challenge, nodakenin group was administered intragastrically with nodakenin at a dose of 10 mg/kg, and dexamethasone group was injected intraperitoneally with dexamethasone a dose of 1 mg/kg. Airway responsiveness was measured by a lung function analysis systems. The number of total leukocytes in BALF was counted using a hemocytometer, and differential cells were counted using Diff-Quick-stained smears. Histopathology of lung tissue was analyzed by Hematoxylin-eosin staining. Levels of inflammatory mediators in serum or BALFs were measured by ELISA. The activity and expression of proteins in NF- κB signaling pathway was respectively evaluated by EMSA and western blot analysis. Results Compared with control group, the model group exhibited obvious airway inflammation, airway reactivity were significantly increased, the levels of total cells and differential cells were significantly increased, levels of IL-4, IL-5, IL-13, IgE were significantly increased, levels of nuclear p65 and p-p65 protein was significantly enhanced, levels of cytoplasmic p65 and IκBα protein were significantly decreased, and the NF-κB DNA binding activity was significantly increased. Compared with model group, nodakenin significantly suppressed airway inflammation, airway hyperreactivity, reduced levels of IL-4, IL-5 and IL-13 in BALF, and IgE in serum, decreased levels of nuclear p65 and p-p65 protein, increased cytoplasmic p65 and IκBα protein, and increased the NF-κB DNA binding activity. Conclusion Nodakenin efficiently inhibited antigen-induced airway inflammation in asthmatic mouse.

Key words: Nodakenin, Peucedanum decursivum Maxim, asthma, NF-κB