Abstract: Objective　To explore the targeting relationship between miR-30a-3p and NOD1, and its effect on Hypoxia/Reoxygenation induced injury of cardiomyocytes and its mechanism.　Methods　Cells were divided into Ctrl, H/R, miR-30a-3p mimic and miR-30a-3p inhibitor groups. After treatment with Hypoxia/Reoxygenation, cells in each group were transfected with corresponding miRNA. RT-PCR was performed for measuring the gene levels of miR-30a-3p and NOD1, luciferase reporter assay was performed for measuring the relationship between miR-30a-3p and NOD1, Western blot was used to determine the protein levels of NOD1, p-RPI2, p38 MAPK, NF-κB (p65), cl-caspase-3, cell viability was measured by CCK8, cell apoptosis was determined by Hoechst, and LDH, CK, MDA, T-SOD levels were detected by kit.  Results　The expression level of miR-30a-3p decreased with the hypoxia-reoxygenation treatment time, and the expression level of NOD1 gene increased with the hypoxia-reoxygenation treatment time. In the luciferase reporter assay, the luciferase activity of NOD1 WT+miR-30a-3p mimic group was significantly lower than that of the NOD1 WTR+NC group. Compared with the Ctrl group, the gene level of miR-30a-3p, cell viability, T-SOD level were decreased, and the protein levels of NOD1, p-RPI2, p38 MAPK, NF-κB (p65), cl-caspase-3, expression levels of LDH, CK, MDA, cell apoptosis rate were increased in the H/R group. Compared with the H/R group, the gene level of miR-30a-3p, cell viability, T-SOD level were increased, and the protein levels of NOD1, p-RPI2, p38 MAPK, NF-κB（p65）, cl-caspase-3, expression levels of LDH, CK, MDA, and cell apoptosis rate were decreased in the miR-30a-3p mimic group. Meanwhile, the gene level of miR-30a-3p, cell viability, and T-SOD level were decreased, and the protein levels of NOD1, p-RPI2, p38 MAPK, NF-κB（p65）, cl-caspase-3, expression levels of LDH, CK, MDA, cell apoptosis rate were increased in the miR-30a-3p inhibitor group.　Conclusion　miR-30a-3p can target NOD1, alleviate the Hypoxia/Reoxygenation induced injury of carddiomyocytes, and  the mechanism may be related to regulation of the NF-κB signaling pathway.

Key words: Hypoxia/Reoxygenation induced injury, 　Myocardial ischemia reperfusion, 　NOD1, 　miR-30a-3p