Abstract

Background Myocardial infarction (MI) has a high mortality and disability rate and greatly affects human health. This study sought to explore the therapeutic effect and molecular mechanism of 3'-daidzein sulfonate (DSS) on MI. Methods A rat MI model was established and low and high doses of DSS were administered to the rats. An in vitro oxygen glucose deprivation model was used to verify the treatment role and mechanism of DSS. The establishment of the rat MI model was confirmed by electrocardiogram. The tissue changes were detected by HE, Masson’s trichrome, TUNEL and TTC staining. Cell viability was detected by CCK-8. The viable and dead cells were detected by Calcein-AM/PI. Apoptotic cells, ROS and JC-1 were detected by flow cytometry apoptosis. The level of proteins was detected by western blotting. MDA, SOD and GSH were detected by ELISA. Results The results of Hematoxylin and eosin, TUNEL, and Masson staining showed that the myocardial tissue of the MI group was repaired by DSS. The serum levels of cardiac troponin I ( CTnI ), lactate dehydrogenase ( LDH ), creatine kinase-MB ( CK-MB ), and malondialdehyde ( MDA ) were decreased by DSS, while the serum levels of superoxide dismutase and glutathione were promoted by DSS. The treatment of DSS activated the Nuclear Factor Erythroid 2-Related Factor 2 ( NRF-2 )/Heme Oxygenase 1 ( HO-1 ) pathway and inhibited the caspase-3 apoptosis pathway. The in vitro experiment showed that DSS greatly restored cell viability and reduced cell apoptosis. DSS also greatly inhibited mitochondrial membrane potential depolarization, reactive oxygen species production, and oxidative stress. The application of the NRF-2 inhibitor, C 29 H 25 N 3 O 4 S (ML385), greatly inhibited the treatment role of DSS and the NRF-2/HO-1 pathway, and activated the caspase-3 apoptosis pathway. Conclusions In conclusion, this study first identified the beneficial role of DSS in MI. DSS protected myocardial cells by activating the NRF-2/HO-1 pa