dihydrolycorine and Disease-Models--Animal

In spite of early interventions to treat acute myocardial infarction (MI), the occurrence of adverse cardiac remodeling following heart failure due to acute MI remains a clinical challenge. Thus, there is an increasing demand for the development of novel therapeutic agents capable of inhibiting the development of pathological ventricular remodeling. RNA-seq data analysis of acute MI rat models from GEO revealed that Runx1 was the most differentially expressed MI-related gene. In this study, we demonstrated that increased Runx1 expression under pathological conditions results in decreased cardiac contractile function. We identified dihydrolycorine, an alkaloid lycorine, as a promising inhibitor of Runx1. Our results showed that treatment with this drug could prevent adverse cardiac remodeling, as indicated by the downregulation of fibrotic genes using western blotting (collagen I, TGF

Topics: Alkaloids; Animals; Antifibrotic Agents; Apoptosis; Cell Hypoxia; Cells, Cultured; Core Binding Factor Alpha 2 Subunit; Disease Models, Animal; Down-Regulation; Fibrosis; Male; Myocardial Infarction; Myocytes, Cardiac; Rats, Sprague-Dawley; Signal Transduction; Ventricular Function, Left; Ventricular Remodeling