Objective To investigate the effect of miRNA210 on primary myocardial cells in lipopolysaccharide(LPS)-induced myocarditis.Methods CCK8 method was used to detect the effect of miRNA210 on the viability of primary myocardial cells in normal or LPS-induced myocarditis rats.ELISA was performed to detect the secretion of tumor necrosis factor(TNF)-α and interleukin(IL)-1β after miRNA210 treatment.Flow cytometry was used to detect the apoptosis of primary myocardial cells before and after the intervention.Western blotting was used to detect the expression of TNF-α and IL-1β.The expression of apoptosis-related proteins bcl-2,bax,caspase-3,and hypoxia inducible factor 1 (HIF1)-vascular endothelial growth factor(VEGF)were detected by Western blotting.Results CCK8 detection results showed that,compared with the control group,the effect of miRNA210 mimic( t =0.000, P =1.000)and siRNA( t =0.686, P =0.500)interference had no significant difference on primary rat cardiomyocytes.The viability of rat primary cardiomyocytes significantly decreased after LPS treatment( t =8.764, P <0.001);compared with LPS group,the viability of rat primary cardiomyocytes significantly increased after inhibition of miRNA210( t =3.576, P =0.012).ELISA showed that,compared with the control group,the expressions of IL-1 β( t =4.166, P =0.014)and TNF-α( t =6.309, P =0.003)were significantly up-regulated after LPS induction;compared with the LPS group,the expressions of IL-1 β( t =4.096, P =0.015)and TNF-α( t =4.424, P =0.011)were significantly increased after application of miRNA210 mimic.After silencing miRNA210,IL-1 β( t =4.287, P =0.012)and TNF-α( t =3.577, P =0.023)were significantly down-regulated.Flow cytometry showed that,compared with the control group,the apoptosis of primary cardiomyocytes induced by LPS was significantly increased( t =32.780, P <0.001);compared with LPS group,the apoptosis induced by LPS was significantly aggravated by miRNA210 mimic( t =7.412, P = 0.002),and the apoptosis rate of primary cardiomyocytes was significantly decreased after miRNA210 was silenced( t =11.720, P <0.001).Western blot analysis showed that,compared with the control group,LPS significantly down-regulated the expression of bcl-2( t =8.346, P =0.001)and increased the expressions of bax( t =12.890, P <0.001)and caspase-3( t =4.331, P =0.012).Compared with LPS group,the expression of bcl-2( t =6.074, P <0.001)was significantly decreased,and the expressions of bax( t =5.376, P =0.022)and caspase-3( t =5.859, P =0.004)were increased after miRNA210 mimic.After silencing miRNA210,the expression of bcl-2 significantly increased( t =3.873, P =0.017),the expressions of bax( t =5.205, P =0.006)and caspase-3( t =2.800, P =0.040)significantly decreased.Compared with the control group,the expressions of HIF1( t =10.380, P =0.001)and VEGF( t =4.973, P =0.008)were significantly up-regulated in LPS group.Compared with LPS group,the expressions of HIF1( t =8.952, P <0.001)and VEGF( t =11.203, P =0.001)were significantly up-regulated after miRNA210 mimic was applied,while HIF1( t =3.893, P =0.017)and VEGF expression( t =3.181, P =0.033)were decreased after miRNA210 was silenced.Compared with LPS group,the expressions of bax( t = 4.899, P =0.008),HIF1( t =2.833, P =0.047),caspase-3( t =2.877, P =0.045),and VEGF( t = 2.994, P =0.040)were significantly decreased,and the expression of bcl-2 was increased( t =3.392, P =0.017).Conclusion Silencing miRNA210 can attenuate LPS-induced cardiomyocyte injury through HIF1-VEGF-mediated apoptotic pathway.