Objective:To observe whether the Nod-like receptor pyrin domain-containing protein 3 (NLRP3)-inflammasome participates in the pathologic process of herpes simplex virus-1 (HSV-1) induced viral myocarditis (VMC). Methods:Cultured neonatal rat ventricular cardiomyocytes (NRVM) of neonatal rats were infected with 0.01 and 0.1 PFU HSV-1 for 24 hours,respectively. Morphologic changes of NRVM were observed under light microscope. The gene expression of NLRP3-inflammasome and its downstream pathways were measured by quantitative real-time PCR (qRT-PCR). The expression and location of cysteinyl aspartate-specific proteases-1 (Caspase-1) were evaluated by immunofluorescent (IF) method. Moreover,creatine kinase-MB (CK-MB) content was detected by automatic biochemical analyzer and supernatant concentration of interleukin-18 (IL-18) was measured by enzyme-linked immunosorbent assay (ELISA). Results:Cytopathic effect (CPE) was observed in NRVM infected with HSV-1. The supernatant concentration of CK-MB,one of the myocardial injury biomarkers,was significantly increased (P < 0.05). Compared with the control group,the mRNA levels of NLRP3,Caspase-1,IL-1β and IL-18 were up-regulated over 5 times in HSV-1 infected NRVM. IF showed that the expression of Caspase-1 was significantly increased. The concentration of supernatant IL-18 was increased compared with that of the control group (P < 0.05). Conclusion:NLRP3-inflammasome and its downstream pathways were activated in cell model of HSV-1 infected VMC. NLRP3-inflammasome may participate in pathologic process of VMC,and became a potential target for VMC therapy.