Artemisinin relieves myocardial ischemia-reperfusion injury via modulating miR-29b-3p and hemicentin 1.

ABSTRACT: Objective: To explore the impact of artemisinin (ARS) on myocardial ischemia-reperfusion (I/R) injury and the underlying mechanism. Methods: Myocardial I/R rat model and cell model were used in this study. The cell viability, morphological changes, apoptosis, and oxidative stress were evaluated in cardiomyocytes H9c2 cells in vitro by using cell counting kit-8, microscope, flow cytometry, and commercial kits. High throughput sequencing is used to identify molecular targets of ARS on myocardial I/R injury, and then the gene-gene interaction network was constructed. MiR-29b-3p, hemicentin 1 (HMCN1), and apoptosis-related genes were tested by qRT-PCR and Western blotting. In the myocardial I/R rat model, echocardiography, (Triphenyl tetrazolium chloride) TTC staining, Hem

SUBMITTER: Han J 

PROVIDER: S-EPMC9403756 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature