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BACKGROUND The aim of this study was to investigate the mechanism of STAT3 in reducing the inflammatory responses in mice with viral myocarditis (VMC). METHODS Induce and generate viral myocarditis by using coxsackievirus B3 (CVB3) infected cardiomyocyte-specific STAT3 conditional knockout (STAT3cKO) mice and BALB/c mice. Use RT-PCR and western blot techniques to detect the expression of related cytokines in the uninfected wild-type mice group (Control group), myocarditis wild-type mice group (Model group) and STAT3cKO group, as well as the differentiation of spleen T cells in each group. Eukaryotic expression plasmid pcDNA3-STAT3 can reduce the expression of inflammatory factors the in vitro cultured cardiomyocytes of the STAT3cKO group. RESULTS RT-PCR showed that compared with the Control group, the expression levels of VMC-related genes (NF-κB, TNF‑α, IL-1β and IL-1) and anti-inflammation-related cytokines (IL-10 and TGF-β) in the Model group went up (*p < 0.05, **p < 0.01, ***p < 0.001); and also compared with the Control group, the rise in the expression levels of the above VMC-related genes in the STAT3cKO group was particularly significant (***p < 0.001, ****p < 0.0001) but there was no significant difference in the expression of IL-10 and TGF-β. After 4 weeks, a second RT-PCR showed that the expression of inflammation-related genes in the STAT3cKO group continued to be activated (***p < 0.001, ****p < 0.0001). Western blotting was performed to detect the expression of p65, a key protein of the NF-κB signalling pathway. The results showed that the p65 protein content was increased and the IL-10 protein content was decreased in the STAT3cKO group; the results of the T cell differentiation test showed that the T cell differentiation rate increased in the STAT3cKO group (**p < 0.01). Eukaryotic expression plasmid pcDNA3-STAT3 could reduce the expression of NF-κB, TNF-α, IL-1β and IL-17 (**p < 0.01). CONCLUSION The expression of STAT3 gene in VMC could to a certain extent inhibit the NF-κB signalling pathway and reduce the inflammatory responses of VMC.