Ginsenoside rb2 regulates tissue autophagy in the ischemic penumbra area and delays BMSC senescence by improving the ischemic-hypoxic microenvironment

Abstract

Abstract Introduction: Ischemic cardiovascular disease (CVD), is associated with high morbidity and mortality. Panax notoginseng (PNS) has some advantages in improving ischemic cardiovascular diseases, but the mechanism of action of its active ingredient ginsenoside Rb2 is not clear. Methods: In this study, network pharmacology, molecular docking, and LC-MS/MS were used to evaluate the relationship between PNS and its main active constituent and autophagy. In vivo and in vitro investigations were then used to further confirm the results. Results: In this investigation, we discovered that the primary active component of PNS, ginsenoside Rb2, might increase tissue autophagy in myocardial infarction rat models' ischemic semidark zone. In the cell model, ginsenoside Rb2 boosted the proliferation rate and decreased the apoptosis rate of bone marrow mesenchymal stem cells (BMSCs). And alleviated oxidative stress, delayed aging, raised GATA4mRNA, lowered cTNTmRNA levels, and protected BMSCs from the harm brought on by ischemic-hypoxic injury. Discussion: Our research initially established an ischemic-hypoxic cell model, which may be provided as a reference for related research. And clarified the functions of ginsenoside Rb2 in the ischemic-hypoxic microenvironment, which may be conducive to the exploration of therapeutic targets of ischemic CVD.