Oridonin is an extract obtained from a traditional Chinese medicinal herb, Xihuangcao. Previous studies have demonstrated that Oridonin exerts various pharmaceutical effects, such as anti‑tumor and immunosuppressive effects, as well as modulating cytokine balance. The present study identified that Oridonin could regulate the Th1/Th2 cytokine balance in mice. However, as the anti‑asthmatic effect of Oridonin is currently unknown a mouse model of asthma was used in the present study. BALB/c mice were sensitized using ovalbumin (OVA), then the sensitized mice were treated with Oridonin prior to OVA challenge. The in vivo study indicated that Oridonin decreased the OVA‑induced airway hyper‑responsiveness significantly (P<0.05). In addition, the results indicated that in Oridonin‑treated mice, the eosinophil number and total inflammatory cell number in bronchoalveolar lavage (BAL) fluid decreased significantly in the Oridonin group when compared with the control group. Further study indicated that Oridonin significantly decreased the level of inflammatory cytokines, which were induced by OVA, in BAL fluid. Histological studies were performed to evaluate the effect of Oridonin on eosinophilia and mucus in the airway, the results indicated that Oridonin significantly inhibited the eosinophilia and mucus production in the lungs. Therefore the present study demonstrated that Oridonin regulates Th1/Th2 balance in mice and exhibited anti‑asthmatic effects in a mouse model of asthma. These findings indicate that Oridonin may serve as a potential therapeutic compound for the treatment of asthma in future.

Neutrophilic asthma (NA) is characterized by neutrophil‑mediated inflammation and the presence of Th17 cells. However, the mechanisms underlying Th17 cell responses in NA remain unknown. The aim of the present study was to examine the effects of interleukin (IL)‑7 on Th17 cell responses in NA. A NA mouse model was sensitized by airway delivery of ovalbumin (OVA) and lipopolysaccharide and challenged with 1% OVA aerosol from day 21 for 3 consecutive days. Airway resistance was then measured to assess airway hyper‑responsiveness (AHR). Cells from bronchoalveolar lavage fluid (BALF) underwent Diff‑Quick and hematoxylin and eosin staining for classification. The levels of IL‑17 in the BALF were determined by ELISA. The effects of IL‑7 administration and STAT5 inhibition on Th17 cells were also characterized in vitro using splenic CD4+ T cells. Ki‑67, Bcl‑2 and activated caspase‑3 expression in differentiated Th17 cells were analyzed by flow cytometry. The mouse model of NA was characterized by increased AHR, elevated levels of IL‑17, high neutrophil counts in BALF, accumulated inflammatory cells in the lung and Th17 cell responses. IL‑7 promoted the expression of Ki‑67 and Bcl‑2 while reducing caspase‑3 expression. STAT5 inhibitor treatment decreased the levels of Ki‑67 and Bcl‑2, and resulted in increased expression of caspase‑3. These results suggested that the IL‑7/JAK/STAT5 signaling pathway may be involved in Th17 cell responses in NA.