G-Rb1

The current unavailability of efficient myocardial repair therapies constitutes a significant bottleneck in the clinical management of myocardial infarction (MI). Ginsenoside Rb1 (GRb1) has emerged as a compound with potential benefits in safeguarding myocardial cells and facilitating the regeneration of myocardial tissue. However, its efficacy in treating MI-related ischemic conditions is hampered by its low bioavailability and inadequate angiogenic properties. In this study, the therapeutic potential of GRb1 is enhanced by a mesoporous basic copper carbonate (BCC) microsphere due to its excellent drug delivery capability and steady angiogenic degradation products (copper ions, Cu²⁺). The cell experiments revealed that GRb1 and Cu²⁺ could generate synergistic impacts on anti-cardiomyocyte apoptosis and endothelial cell angiogenesis, while a mouse model of MI illustrated that GRb1 loaded BCC (BCC@GRb1) could significantly enhance cardiac function, diminish the area of infarction and myocardial hypertrophy, reduce cardiomyocyte apoptosis, and augment vascularization within myocardial tissue. This investigation is pioneering in demonstrating the beneficial outcomes of combining drugs with bioactive carriers in myocardial regeneration and introduces a novel, precisely engineered drug delivery system as a potential therapeutic strategy for ischemic heart disease.

Porcine epidemic diarrhea virus (PEDV) causes vomiting, dehydration, and diarrhea in piglets, seriously threatening their survival and development and causing huge economic losses to the global pig industry. Current PEDV control relies on vaccines, however, the high mutation rate of PEDV limits vaccine effectiveness, highlighting the need for new antiviral drugs. This study investigated the pharmacological effects of ginsenoside Rb1 (GRb1) on PEDV using network pharmacology, as well as GO and KEGG analyses, to predict its role in modulating the MAPK/ERK pathway. GRb1 downregulated the MAPK/ERK pathway activated by PEDV infection and reduced levels of the apoptotic protein cleaved-caspase-3, thus inhibiting PEDV-induced apoptosis and demonstrating antiviral properties. Further screening showed that the PEDV S1 protein promotes AP-1 nuclear entry and upregulates the MAPK/ERK pathway to induce apoptosis, a process reversed by GRb1. Further in vivo studies revealed that GRb1 treatment significantly reduced viral load in piglet intestinal tissues and anal swabs. GRb1 also alleviated clinical symptoms and intestinal damage in infected piglets, improving their survival rate while also downregulating the levels of inflammatory factors (IL-1β, IL-6, IL-8, and TNF-α). This study is the first to demonstrate that GRb1 effectively inhibits PEDV, uncovering its potential mechanism of action and providing a promising new approach for antiviral treatment in veterinary medicine.