Mechanisms of Ischemia Cardioprotection by Lactobacillus plantarum-Fermented American Ginseng

Panax quinquefolius L. (American ginseng), which is rich in bioactive saponins but has low bioavailability, was fermented by Lactobacillus plantarum for a period of 40 hours. The substance was transformed into a potent cardiac protector. The diversity of saponins and flavor substances has been demonstrated to increase twofold through the implementation of time-course liquid deep fermentation analysis utilizing QE-MS and GC‒MS. The component transformation rules during fermentation were determined through the integration of proteomics with mass spectrometry. The efficacy of the extract in treating myocardial ischemia was demonstrated in both cell and animal models. We confirmed that fermentation-enriched ginsenosides (CK, Rk2, and F1) are pivotal for cardioprotection, demonstrating their ability to mitigate hypoxic injury in cardiomyocytes at low concentrations by reducing ROS and stabilizing the mitochondrial membrane potential. Transcriptional profiling revealed that fermented American ginseng inhibited PINK1-Parkin-mediated mitochondrial autophagy, reduced mitochondrial reactive oxygen species, and stabilized the membrane potential. In a rat ischemia model, this substance was found to restore cardiac output and ion homeostasis. The present study investigated the effects of regulating mitochondrial autophagy in the context of ischemic injury, with a particular focus on the role of fermented American ginseng in achieving this regulatory function. The findings of this study suggest that the aforementioned intervention can alleviate ischemic injury and stabilize the mitochondrial electron respiratory chain, thereby indicating its potential as a promising functional food for cardiovascular health.