Baicalin, extracted and purified from the Chinese medicinal plant, ScutellariabaicalensisGeorgi(Huangqin in Chinese), exhibits potent anti-inflammatoryactivity against asthma. However, it remains unknown whether baicalin inhibits the activity of CCchemokinereceptor7(CCR7) and its ligands, which are crucial for the initiation of airway inflammation. In the present study, we investigated the effects of baicalin on CCR7 and its ligands, CCL19 andCCL21, as well as on the nuclear factor-κB(NF-κB)pathway in a mouse model of asthma. A mouse model of acute asthma was established by exposing the mice to ovalbumin(OVA) (by intraperitoneal injection and inhalational challenge). Within 24h of the final OVAchallenge, lung function was detected by direct airway resistance analysis. Lung tissues were examined for pathological changes. Inflammatory cell counts in bronchoalveolar lavage fluid(BALF) were assessed. ELISA was utilized to evaluate the OVA-IgE, CCL19 and CCL21 levels in BALF. The interleukin(IL)-6and tumor necrosis factor(TNF)-α levels in serum were also detected by ELISA. The protein expression levels of CCR7, as well as that of phosphorylatedIκBα(p-IκBα) and phosphorylatedp65(p-p65) were determined by western blot analysis and RT-qPCR was used to determine the CCR7mRNA levels. Our data demonstrated that the oral administration of baicalin significantly improved pulmonaryfunction and attenuated inflammatory cell infiltration into the lungs. Baicalin also decreased the levels of OVA-IgE, IL-6, TNF-α and CCR7, as well as those of its ligand, CCL19; the levels of NF-κB were also markedly suppressed by baicalin. The CCR7mRNA level was substantially decreased. Our results thus suggest that baicalin exerts an inhibitory effect on airwayinflammation, and this effect may be associated with the inhibition of CCR7 and CCL19/CCL21, which may provide new mechanistic insight into the anti‑inflammatoryeffects of baicalin.