Resveratrol Mitigates Ischemia/Reperfusion-Induced Cardiomyocyte Injury by Inhibiting the Expression of Superoxide Dismutase 2

Abstract

Resveratrol exhibits antioxidant, anti-inflammatory, and potentially cardio-protective properties. However, the effectiveness of resveratrol in acute myocardial infarction (AMI)-induced cardiomyocyte injury remains unclear. Superoxide Dismutase 2 (SOD2) is an important antioxidant enzyme in the mitochondria. However, few studies have reported the impact of SOD2 on AMI-induced cardiomyocyte injury. Therefore, we establish an in vitro model of cardiomyocyte ischemia/reperfusion (I/R) injury using oxygen-glucose deprivation/reoxygenation (OGD/R) to investigate the protective effects of resveratrol against OGD/R-induced cardiomyocyte injury and its underlying regulatory mechanism. Cell viability was assessed using the CCK-8. Apoptosis was evaluated by TUNEL staining. The levels of Cleaved cas-3, Bcl2, and SOD2 an important antioxidant enzyme in the mitochondria that is responsible for eliminating superoxide radicals were analyzed by western blot. The ROS positive rate was using a ROS/Superoxide detection assay kit. The relative abundance of the SOD2 mRNA was determined using the 2−ΔΔCT method. We demonstrated that OGD/R treatment significantly reduced AC16 cell viability while increasing apoptosis levels, oxidative stress, and inflammatory factor levels. We further confirmed the upregulation of SOD2 by OGD/R treatment, suggesting its potential involvement in modulating OGD/R-induced AC16 cell injury. Additionally, silencing SOD2 ameliorated the detrimental effects of OGD/R on AC16 cells. Moreover, we observed that upregulation of SOD2 aggravated OGD/R-induced AC16 cell injury, and resveratrol effectively reduced OGD/R-induced AC16 cell injury by down-regulating SOD2. In conclusion, this research provides a promising therapeutic strategy for mitigating I/R damage in AMI-induced cardiomyocytes, thereby identifying a potential target for therapeutic intervention.