Analysis of the mechanism of liquiritigenin in promoting cardiomyocyte regeneration based on miRNA-34b-TIA-1-SG molecular network-mediated autophagy

This study aims to clarify that miRNA-34b affects the autophagy through regulating TIA-1-SG and explore the role of miRNA-34b-TIA-1-SG molecular network-mediated autophagy in cardiomyocyte regeneration. 32 patients with autophagy injury caused by myocardial ischemia perfusion admitted to the hospital were included and 32 healthy controls were enrolled at the same time. ELISA was used to detect miRNA-34b level. Cardiomyocytes were isolated and cultured by adherence method and the relationship between miRNA-34b and TIA-1-SG was analyzed by dual-luciferase gene reporter assay. The correlation between myocardial autophagy and liquiritigenin treatment was assessed along with qRT-PCR analysis of the changes of genes (TIA-1, SG, ULK1, OsATG7, FAM176A, Beclin 1). miRNA-34b expression in 32 patients with myocardial autophagy injury was higher than normal group. miRNA-34b binds to the 3′-UTR of TIA-1 and transfection of miRNA-34b inhibitor increased the luciferase activity, which was not affected in pMIR-TIA-1-mut group, confirming the relationship between miRNA-34b and TIA-1. The addition of liquiritigenin can promote the reduction of expression of myocardial autophagy injury-related genes. In the absence of liquiritigenin, the expression of genes related to myocardial autophagy injury increased significantly. Autophagy imbalance plays an important role in myocardial infarction, which participates in myocardial infarction. miRNA-34b can target and regulate TIA-1 gene, promote myocardial infarction repair, and inhibit the state of autophagy by regulating autophagy-related gene TIA-1. Liquiritigenin regulates autophagy imbalance in myocardial infarction to delay myocardial remodeling and improve prognosis.