OBJECTIVE To explore the improvement effect and mechanism of vitexin on asthmatic model mice based on Notch signaling pathway. METHODS Asthma model of mice was established by intraperitoneal injection of ovalbumin and aluminum hydroxide suspension and nebulization stimulation of ovalbumin， and randomly divided into model group， vitexin group （40 mg/kg）， Notch activator group （1 mg/kg Jagged1）， vitexin+Notch activator group （40 mg/kg vitexin+1 mg/kg Jagged1）， with 12 mice in each group. Another 12 mice were selected as the control group. Each group received intragastric/intraperitoneal injection of relevant medicine or normal saline， once a day， for consecutive 14 days. After the last medication， minute ventilation at rest （VE） and peak expiratory flow （PEF） were detected in mice； the pathological morphology of lung tissue and fibrosis degeneration were observed and determined. The proportion of T helper cell 17 （Th17） and T regulatory cell （Treg） in peripheral blood were detected， and the Th17/Treg ratio was calculated. The levels of serum inflammatory factors interleukin （IL）-18， IL-6， IL-17 and IL-10 were determined， and the expressions of Notch1， Delta-like ligand 4 （DLL4）， hairy and enhancer of split 1 （Hes1） in lung tissue were detected. RESULTS Compared with the control group， serious pathological injury and inflammatory cell infiltration occurred in the lung tissue of mice in the model group， while VE， PEF， the proportion of Treg cells in peripheral blood and serum level of IL-10 were significantly reduced （P＜0.05）； collagen volume fraction （CVF） in lung tissue， Th17 cells proportion and Th17/Treg ratio in peripheral blood， serum levels of IL-18， IL-6 and IL-17， and the protein expressions of Notch1， DLL4 and Hes1 in lung tissue were significantly increased （P＜0.05）. Compared with the model group， the pathological injury of lung tissue in vitexin group was significantly improved compared with model group， and the changing trend of the above indexes was reversed （P＜0.05）； Notch activator Jagged1 could significantly reverse the pharmacological effects of vitexin on asthmatic mice （P＜0.05）. CONCLUSIONS Vitexin can improve lung function， Th17/Treg immune imbalance and inflammatory response， and alleviate pathological injury and fibrosis of lung tissue in asthmatic mice by inhibiting the Notch signaling pathway.