Abstract: Objective To investigate the role and mechanism of microRNA（miR）-139-5 p in cardiomyocytes apoptosis induced by hypoxia. Methods The primary cardiomyocytes of newborn Wistar rats were isolated and cultured, and the cells were subjected to control, transfect mimic, transfect inhibitor,hypoxia, transfect mimic and hypoxia treatment,transfect inhibitor and hypoxia treatment. After transfection of miR-139-5 p mimics in cardiomyocytes, reverse transcription-polymerase chain reaction（RT-PCR） was used to detect the expression of miR-139-5 p in cardiomyocytes; flow cytometry was used to detect the apoptosis rate of cells; Western blot was used to quantify the protein expression of wnt signaling pathway wnt1, β-catenin and bcl-2 in cardiomyocytes. Results The relative expression of miR-139-5 p was significantly increased after transfection of miR-139-5 p mimic（14.01±0.50 vs 1.51±0.16, P＜0.05）. The expression of wnt1, β-catenin and bcl-2 protein were increased after hypoxia in comparison with control and transfected cells（all P＜0.05）, the apoptosis rate of hypoxia was significantly increased （20.70±0.40）% vs（0.88±0.18）%,（1.00±0.14）%, P＜0.05. Compared with hypoxic cells, the expression of wnt1, β-catenin and bcl-2 protein in hypoxic+transfect mimic cells were significantly decreased（both P＜0.05）, they were significantly increased in hypoxic+transfect inhibitor cells（both P＜0.05）, and the apoptosis rate after hypoxia+transfect mimic treatment was significantly elevated（36.10±2.30）% vs（20.70±0.40）%, P＜0.05. Apoptosis rate after hypoxia+transfect inbibitor treatment was significantly decreased（14.5±1.10）% vs（20.70±0.40）%, P＜0.05. There was no significant difference in apoptosis rate and protein expression between control and transfected cells（P＞0.05）. There was an interaction effect of transfect mimic and hypoxia on the expression of wnt1（F=53.887, P-interaction＜0.05）, β-catenin（F=19.112, P-interaction＜0.05）, and bcl-2（F=15.368, P-interaction=0.001）. Conclusion miR-139-5 p increases the apoptosis of myocardial cells in the hypoxia state by inhibiting the wnt/β-catenin signaling pathway and reducing the expression of cardiac protective factor bcl-2.