Inhibitory effects of catalpol coordinated with budesonide and their relationship with cytokines and Interleukin-13 expression.

In this study, the molecular mechanism for inhibitory effect of Catalpol coordinated with Budesonide (BUD) on allergic airway inflammation was investigated. A total of 30 adult SD rats were randomly divided into five groups, namely the positive control group, the model group, the Catalpol group, the BUD group, and the Catalpol+BUD group with 6 rats in each group, respectively. The pathologic changes of lung tissue were observed by HE stain method. The lung function of rats, the cell count, and the cytokine concentrations in bronchoalveolar lavage fluid (BALF) were detected. The levels of cytokines [interleukin-4 (IL-4), interleukin-5 (IL-5), and interferon gamma (IFN-γ)] in BALF were measured using enzyme-linked immunosorbent assay method. The expressions of Interleukin-13 (IL-13) and Eotaxin in lung tissue were measured by RT-PCR method. The total number of cells in the BALF of the group treated with Catalpol and BUD was significantly lower than the model group. The cytokines IL-5 and IL-4 exhibited a similar tendency: the concentrations of IL-4 and IL-5 for the Catalpol group were dramatically decreased compared with the model group. However, the IFN-γ concentration for the Catalpol and BUD groups were higher than the model group. After treatment with Catalpol+BUD, the eosinophils and neutrophils of the rats were further reduced, asthma-associated inflammation was obviously inhibited, IL-4 level was further decreased and IFN-γ level was further increased comparing the Catalpol group and the BUD group. Moreover, IL-13 expression was positively correlated with Eotaxin expression. The results indicated that Catapol could inhibit the expression of IL-13 and Eotaxin in the lung of asthmatic rats, which also exhibited a synergistically inhibitory effect with BUD on airway inflammation. It is suggested that Catalpol+BUD might be an effective and potential treatment for the clinical therapy of asthma. AJTR