Objective To explore the role of miR-199a in LPS-induced rat primary cardiomyocytes. Methods The primary rat cardiomyocytes were divided into control group (NC), LPS group, LPS+miR-199a mimic group and LPS+ miR-199a inhibitor group. CCK8 assays were used to explore the effect of miR-199a on cell viability of rat primary cardiomyocytes. ELISAs were used to detect the release of inflammatory factors such as TNF-α and IL-1β by HRNA-199a induced by LPS in rat primary cardiomyocytes. Expression of apoptotic proteins in rat primary cardiomyocyte induced by LPS by miR-199a was detected by flow cytometry. Western blot was used to study the expression of miR-199a mimic- or inhibitor-treated cells, and the expression of p-p65, p65, and p-iκBα, iκBα and apoptotic proteins in rat primary cardiomyocytes induced by LPS. Results Compared with the control group, LPS inhibited the viability of primary rat cardiomyocytes ( P < 0. 01 ). However, after LPS induction and simulant treatments, the viability of primary rat cardiomyocytes was more severely inhibited ( P < 0. 05). Therefore, miR-199a may aggravate cardiomyocyte damage in myocarditis. Compared with the mimics, inhibition of miR-199a reduced LPS-induced rat primary cardiomyocyte viability (P<0. 01). Compared with the NC group, LPS induced the release of TNF-α and IL-1β (P<0. 05). Compared with the LPS group, miR-199a mimic aggravated the release of TNF-α (P<0. 01) and IL-1β (P<0. 05). However, after treatment with miR-199a inhibitors, the release of TNF-α ( P< 0. 01) and IL-1β ( P< 0. 05) was decreased. Flow cytometry and Western blot showed that 50nmol / L miR-199a mimetics aggravate dapoptosis of primary rat cardiomyocytes induced by LPS (P<0. 05). This may be related to the further upregulation of caspase3 and bax expression through miR-199a mimetics and downregulation of bcl2 expression ( LPS) induced the activation of the NF-κB pathway in primary rat cardiomyocytes, which was specifically manifested by upregulation of p-iκBα and p-p65 expression. However, compared with the LPS group, p-p65 and p-iκBα were more upregulated after treatment with the mimics. After blocking miR-199a, expression of p- p65 and p-iκBα was downregulated compared with the mimic group. These findings indicate that treatment with mimics aggravate activation of the NF-κB signaling pathway in LPS-induced myocarditis in vivo. Further use of NF-κB pathway inhibitors showed that miR-199a mimics did not exacerbate the inhibitory effect of LPS on primary rat cardiomyocytes, which further suggested that miR-199a exacerbates cardiomyocyte damage through the NF-κB pathway. Conclusions miR- 199a aggravates damage of myocardial cells in myocarditis, which is mainly mediatedthrough the NF-κB signaling pathway.