Objective To observe whether the IL-23/Th17 inflammatory pathway is involved in the development of calcific aortic valve disease, and whether secukinumab can delay the progression of calcific aortic valve disease by inhibiting the IL-23/Th17 inflammatory pathway. Methods Forty-seven mice were divided into a blank control group, a model group, and a secukinumab group according to the random number table method. The blank control group was fed with normal chow, the model group and the secukinumab group were fed with pro-calcification chow for 16 weeks to establish a calcific aortic valve disease model, and the peak flow velocity changes of the aortic valves were detected under Doppler ultrasonography in all the mice after 4 weeks of intervention by secukinumab on the secukinumab group; relevant indexes were determined by HE staining, Von kossa staining, immunohistochemical staining, ELISA, and PCR. PCR were used to determine the relevant indexes. Results Compared with the model group, 4 weeks of drug intervention in the secukinumab group significantly reduced peak flow velocity ( P<0.05) and serum IL-6 levels ( P<0.05) in the aortic valve; compared with the secukinumab group, the leaflet thickness in the model group was significantly increased and there were more calcium deposits; Immunohistochemical results showed that macrophages ( P<0.05), IL-17A ( P<0.05), and IL-23 ( P>0.05) infiltration in the valve leaflets were reduced in the secukinumab group compared with the model group.PCR results suggested that the expression of STAT3, BMP-2 and α-SMA mRNA were significantly reduced in the secukinumab group compared with the model group ( P<0.05).Conclusion The IL-23/Th17 inflammatory pathway is involved in the pathogenesis of calcific aortic valve disease, and the inflammation, fibrosis, osteogenic differentiation, and calcification of mouse valves were alleviated after the intervention of secukinumab, which may delay the disease progression by inhibiting the IL-23/Th17 inflammatory pathway.