Ginsenoside Rc Improves Cardiomyocyte Apoptosis and Inflammation in Acute Myocardial Infarction by Regulating the TNNI3/CRP Pathway

Background: Ginsenoside Rc has been known for its promising protective effects against myocardial injury, including inflam-mation, apoptosis, oxidative stress, and related pathways. However, the underlying molecular mechanisms behind these effects still need to be explored. The purpose of this study was to explore the therapeutic effect of Ginsenoside Rc on acute myocardial infarction (MI) and the molecular mechanism behind it.Methods: MI mouse model and oxygen-glucose deprivation (OGD) cardiomyocyte injury model were established and Ginseno-side Rc was treated. Troponin I3 (TNNI3)/C-reactive protein (CRP) expression was altered by plasmid transfection or lentiviral vector injection. Myocardial histopathological changes were evaluated by hematoxylin-eosin (HE) staining and terminal de-oxynucleotidyl transferase-mediated dNTP nick end labeling (TUNEL) staining. The changes in inflammatory cytokines in cells and tissues were evaluated by enzyme-linked immunosorbent assay (ELISA). Commercial kits were used for the assessment of creatine kinase-MB (CK-MB) and lactic dehydrogenase (LDH). Western blot was used to analyze cleaved caspase-3 protein ex-pression in cells and tissues. The apoptosis rate of cardiomyocytes was measured by flow cytometry. The interaction between TNNI3 and CRP was detected by co-immunoprecipitation (CO-IP) assay.Results: TNNI3/CRP expression was abnormally high in MI, and Ginsenoside Rc decreased their relative expression (p < 0.05). Ginsenoside Rc administration reduced inflammation and apoptosis in MI mice and OGD-injured cardiomyocytes (p < 0.05). Ginsenoside Rc administration or TNNI3 knockdown improved the myocardial tissue injury in MI mice (p < 0.05). The thera-peutic effect of Ginsenoside Rc on myocardial injury in MI mice was weakened by overexpressing TNNI3 (p < 0.05). Similarly, its therapeutic effect on OGD cardiomyocyte injury was also weakened by enhancing TNNI3 and CRP (p < 0.05). TNNI3 and CRP also interacted in cardiomyocytes.Conclusions: Ginsenoside Rc improves MI-induced cardiomyocyte apoptosis and inflammation by inhibiting the TNNI3/CRP axis. The study shows that Ginsenoside Rc can serve as a potential drug for the future treatment of MI.