Protective Effect of Overexpression of Uqcrc1 in H2O2-Induced Myocardial Injury

Abstract

This study investigated the role of Uqcrc1 in oxidative stress and apoptosis induced by hydrogen peroxide (H2O2) in cardiomyocytes. H9c2 cells were divided into four groups: control, H2O2-treated, Lv-NC+H2O2 (negative control lentivirusinfected with H2O2), and Lv-Uqcrc1+H2O2 (Uqcrc1 overexpressed lentivirus-infected with H2O2 for 12 hours). Uqcrc1 expression was quantified using qRT-PCR and Western blotting. Cell proliferation was assessed with CCK-8, and various oxidative stress markers (LDH, MDA, SOD, CAT, GSH-Px) were measured. Apoptosis was evaluated using Tunel assays, intracellular ROS levels, and Cleaved Caspase3 and Caspase9 expression. Additionally, the impact on the Wnt/β-catenin pathway was examined. In the Lv-Uqcrc1 group, Uqcrc1 expression was notably higher. H2O2 treatment reduced cell proliferation and increased LDH leakage, MDA, ROS levels, and apoptosis. Cleaved Caspase3 and Caspase9 expression increased, indicating apoptosis. Lv-Uqcrc1+H2O2 group exhibited improved cell proliferation, decreased LDH leakage, increased CAT, SOD, GSH-Px activities, reduced MDA and ROS levels, and reduced apoptosis with lower Cleaved Caspase3 and Caspase9 expression. Uqcrc1 overexpression also inhibited Wnt/β-catenin pathway overactivation. In oxidative stress conditions, Uqcrc1 protected against myocardial cell injury, reducing apoptosis and oxidative damage. This study highlights Uqcrc1’s significance in cardiovascular diseases.