【Abstract】Objective To investigate the effects of NLRP3 on myocardial inflammation and apoptosis in viral myocarditis. Methods SD rat myocardial cells were isolated and cultured. Knockdown of NLRP3 expression in the myocardial cells was conducted by the technique of gene silencing with siRNA, and the cells were randomly divided into 4 groups, including normal control group, Scrambled siRNA group, CVB3+Scrambled siRNA, CVB3+NLRP3 siRNA group. The levels of inflammatory cytokines such as IL1, IL18 and the myocardial injury markers such as CKMB, cTnI were measured by ELISA. The activation of NLRP3 inflammosome and the levels of apoptotic molecules such as caspase8, Bcl2, Bax, caspase9 and caspase3 were detected by quantitative realtime PCR and Western blot. Results Compared with control group, in CVB3 group, NLRP3 and caspase1 were activated, the expression level of IL1β and IL18 was increased (P＜005). The protein levels of caspase8, caspase3 and caspase9 were significantly higher than those in control group. The protein level of Bcl2 was decreased, but the protein level of Bax was enhanced, and Bax/Bcl2 ratio was also increased in CVB3 group (P＜005). The levels of myocardial cell apoptosis, CKMB and cTnI were higher than those in control group (P＜005). After NLRP3 expression was knocked down, compared with CVB3 group, the levels of caspase1, IL1β and IL18 was attenuated (P＜005). The levels of caspase3 and caspase9 were lower than those in CVB3 group. The degree of decline of bcl2 was weakened, and the ratio of Bax/ bcl2 was reduced (P＜005), but the protein levels of caspase8 and Bax were not significantly affected (P＞005). Conclusion NLRP3 plays an important role in the early stage of myocardial cell injury induced by virus infection. Inhibition of NLRP3 overactivation may reduce inflammatory damage and apoptosis of myocardial cells, and may be a potential target for treatment of viral myocarditis.