Abstract: Objective To investigate the protective function and mechanism of microRNA-1 (miR-1) downregulation in H2O2 injured cardiomyocytes. Methods The experiment was divided into 4 groups:Blank, NC, H2O2 and H2O2+AS-miR-1. Blank cells had no treatment, NC cells transfected with random miRNA fragement, H2O2 and H2O2+AS-miR-1 group were defined as H2O2 injured cardiomyocytes without or with transfected antisense miR-1 oligonucleotide（AS-miR-1）. The real time PCR was used to test miR-1 expression, cell vitality and apoptosis were analyzed by MTT and flow cytometry. The target gene of miR-1 was predicted by bioinformatics, and then, the mRNA and protein expression level of Bcl-2 were detected by real time PCR and western blot. Results All index had no significant changes in Blank and NC groups. H2O2 can induce cardiomyocyte injury, increase the miR-1 level and apoptosis rate, reduce cell vitality and Bcl-2 expression level. Transfection AS-miR-1 can decrease cell apoptosis, increase cell vitality and Bcl-2 expression level. Conclusion Downregulation microRNA-1 can protect H2O2 injured cardiomyocytes by increasing anti-apoptosis factor Bcl-2 expression.

Key words: miR-1, cell cycles, transfection, microRNAs, myocytes, cardiac, oxidative stress, 过氧化氢