Shikonin Suppresses High Glucose-Induced Cardiomyocyte Damage by Down-Regulating circ_0000491

Abstract

To probe the action of shikonin on cardiomyocyte damage triggered by high glucose and its possible mechanism. High glucose was used to induce rat cardiomyocyte H9C2 to establish a cell injury model, and different doses of shikonin were used to treat H9C2 cells. Flow cytometry tested cell apoptosis. The enzyme-labeled method and water-soluble tetrazolium salt method were used to detect superoxide dismutase and malondialdehyde content, respectively. Quantitative reverse transcription polymerase chain reaction assayed circ_0000491 levels. After shikonin treatment, the apoptosis rate of H9C2 cells, levels of malondialdehyde in cells, and circ_0000491 contents were declined, and superoxide dismutase content was increased in a dose-dependent manner. After transfection with si-circ_0000491, the apoptosis rate and malondialdehyde levels were suppressed, but superoxide dismutase content was increased in H9C2 cells. Transfection of plasmid cloning deoxyribonucleic acid-circ_0000491 could attenuate these inhibitory effects of shikonin on high glucose-induced H9C2 cell apoptosis and oxidative stress. Shikonin could inhibit cell apoptosis and oxidative stress by down-regulating circ_0000491, thereby improving high glucose-induced cardiomyocyte damage.