Abstract
BACKGROUND This study investigated the effects and underlying mechanisms of emodin on cough variant asthma (CVA) in mice. MATERIAL AND METHODS The bronchial asthma mouse model was successfully established by use of ovalbumin (OVA) sensitization and challenge. The BALB/c mice were divided into 6 groups: a control group, an OVA model without or with emodin (15, 30, 60 mg/kg) group, and a dexamethasone (0.5 mg/g) group. The effect of the treatment was determined by measuring airway responsiveness. The levels of immunoglobulin molecules, as well as inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum, were determined by ELISA. The lung tissues were stained by hematoxylin-eosin (HE). The expressions of Notch receptors (Notch 1-3) and Delta-like (DLL) 4 in the lung tissues were detected by RT-PCR and Western blot analysis. RESULTS Compared with the model group, emodin treatment significantly increased the levels of immunoglobulin E (IgE) and IgG1/IgG2a in BALF and serum (p<0.05). HE results indicated that emodin inhibited the infiltration of inflammatory cells and that emodin reduced the levels of inflammatory cytokines, interleukin (IL)-5, IL-17, and interferon (IFN)-γ in BALF and serum (p<0.05). Furthermore, the expressions of Notch 1, 2, 3, and DLL4 in lung tissue were inhibited by emodin treatment. CONCLUSIONS The results demonstrated that emodin alleviated inflammation in CVA mice, which might be associated with suppression of the Notch pathway. Emodin might be a promising therapeutic agent for allergic asthma.