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

To explore the impact of artemisinin (ARS) on myocardial ischemia-reperfusion (I/R) injury and the underlying mechanism. 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 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, Hematoxylin-eosin (H&E) staining, Masson Trichrome staining, and TUNEL staining are applied to evaluate the protective effect of ARS on the myocardial injury. , we demonstrated that ARS alleviated HO-induced myocardial I/R injury, manifested by increased H9c2 viability, decreased pathological changes, apoptosis, and oxidative stress biomarker ROS, LDH, and CK-MB. Then, sequencing analysis revealed that miR-29b-3p/HMCN1 was the target of ARS for myocardial I/R injury. Notably, rescue experiments indicated that ARS inhibited myocardial I/R injury through targeted regulation miR-29b-3p/HMCN1. , we confirmed that ARS reduced myocardial injury, fibrosis, and apoptosis modulation of miR-29b-3p/HMCN1. This study demonstrated the functional role of the ARS/miR-29b-3p/HMCN1 axis in alleviating myocardial I/R injury, which provided a new direction for myocardial I/R injury therapy.