Abstract: 　Objective　To explore the role of interleukin-23 (IL-23)/interleukin-17 (IL-17) signaling pathway in viral myocarditis (VMC) and evaluate the intervention effect of Aastragaloside. Methods Seventy-five male BALB/c mice were randomly divided into 4 groups, control group (n=15), model group (n=20), low-dose intervention group (n=20) and high-dose intervention group (n=20). Mice in control group were inoculated with 0.1 ml virus cultivation solution intraperitoneally while mice in the other 3 groups were treated with 0.1ml virus cultivation solution containing 1×10² TCID50 coxsackievirus B₃ (CVB₃) to establish VMC model. On the day of inoculation, mice in low- and high-dose intervention groups were intragastrically administered with 0.1 ml of 1% and 9% Astragaloside solution respectively, whereas those in control and model groups were treated with 0.1 ml carboxymethycellulose solution. Astragaloside or carboxymethycellulose was given once a day and continued 15 days. The number of mice death and the performance of mice were recorded in experimental period. All mice were sacrificed on day 15. The heart and blood sample were obtained. Histological cross sections of heart were stained with hematoxylin-eosin and scored for myocardial histopathologic changes under optical microscope. Th17 cells were analyzed by flow cytometry. The mRNA and protein expression levels of myocardial IL-23 and IL-17 were detected by real-time quantitative PCR and Western blotting, respectively. Results The mortality was statistically significant differences among the four groups (P = 0.013), which was the lowest in the control group. The myocardial histopathologic scores, the percen-tage of Th17 cells, as well as expression levels of myocardial IL-23 and IL-17 mRNA and protein were significantly lower in high-dose intervention group than those in model group and low-dose intervention group, but higher than those in control group (P < 0.05). The myocardial histopathologic scores, the percentage of Th17 cells, as well as expression levels of myocardial IL-23 and IL-17 mRNA and protein were significantly higher in model group and low-dose intervention group (P < 0.05). There were no significant difference in the above mentioned indicators between low-dose intervention group and model group (P > 0.05). Conclusions Astragaloside may dose-dependently protect against VMC by inhibiting IL-23/IL-17 signaling pathway.