〔Abstract〕 Objective To study the protective effect and molecular mechanism of long non-coding RNA(lncRNA) PWAR5 on cardiomyocytes in lipopolysaccharide-induced myocarditis. Methods The primary rat cardiomyocytes were isolated and cultured, and were infected with lentivirus carrying PWAR5 sequence(PWAR5 group) and empty lentivirus(Control group). Real-time quantitative polymerase chain reaction(qRT-PCR) was used to detect infection efficiency. After lipopolysaccharide-induced myocarditis, the MTS method was used to detect the effect of PWAR5 on the viability of primary rat cardiomyocytes, and the ELISA method was used to detect the levels of interleukin(IL)-1β and tumor necrosis factor(TNF)-α in the supernatant. Flow cytometry was used to detect the effect of PWAR5 on the apoptosis of primary rat cardiomyocytes. Bioinformatics methods and dual-luciferase reporter gene experiments were used to predict and verify the target gene of PWAR5. qRT-PCR was used to detect the expression of target gene. Western blot was used to detect the expression of target gene protein and apoptosis-related proteins. Results Compared with the Control group, the expression of PWAR5 in the PWAR5 group increased(P<0.01). After lipopolysaccharide treatment, compared with the Control group, the cell viability of the PWAR5 group increased(P<0.01), the contents of IL-1β and TNF-α in the supernatant decreased(P<0.01), and the percentage of apoptosis in the PWAR5 group decreased(P<0.01). The target gene of PWAR5 might be miR-30 a-5 p, and PWAR5 could complement miR-30 a-5 p(P<0.01). Compared with the Control group, the expression of miR-30 a-5 p in the cells of the PWAR5 group decreased(P<0.01), and the expression of suppressor of cytokine signaling 3(SOCS3) mRNA increased(P<0.01). Compared with the Control group, the expression of SOCS3 and Bcl-2 protein in the PWAR5 group increased, while the expression of Bax and Caspase-3 protein decreased. Conclusion PWAR5 can reduce the damage of cardiomyocytes caused by myocarditis by targeting the miR-30 a-5 p/SOCS3 molecular axis.