The aim of the study was to investigate the anti-asthmatic effects of apigenin and the possible mechanisms. Asthma model was established by ovalbumin-induced asthma. A total of 50 mice were randomly assigned to six experimental groups: control, model, dexamethasone (2 mg/kg) and apigenin (5 mg/kg, 10 mg/kg). Airway resistance (Raw) was measured, histological studies were evaluated by hematoxylin and eosin (HE) staining, OVA-specific serum and BALF IgE levels and Th17 cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA), Th17 cells were evaluated by flow cytometry (FCM), and protein level of RORγt was measured by western blotting. Our study demonstrated that apigenin inhibited OVA-induced increases in Raw and eosinophil count; interleukin (IL)-6, TNF- and IL-17A levels were recovered. Histological studies demonstrated that apigenin substantially inhibited OVA-induced eosinophilia in lung tissue and airway tissue. Flow cytometry studies demonstrated that apigenin substantially inhibited Th17 cells. Western blotting studies demonstrated that apigenin substantially inhibited RORγt protein level. These findings suggest that apigenin may effectively ameliorate the progression of asthma and could be used as a therapy for patients with allergic asthma.