Ginsenoside Rg1 as a Potential Regulator of Hematopoietic Stem/Progenitor Cells

Ginsenoside Rg1 (Rg1), a purified, active component of the root or stem of ginseng, exerts positive effects on mesenchymal stem cells (MSCs). Many recent studies have found that hematopoietic stem cells (HSCs), which can develop into hematopoietic progenitor cells (HPCs) and mature blood cells, are another class of heterogeneous adult stem cells that can be regulated by Rg1. Rg1 can affect HSC proliferation and migration, regulate HSC/HPC differentiation, and alleviate HSC aging, and these findings potentially provide new strategies to improve the HSC homing rate in HSC transplantation and for the treatment of graft-versus-host disease (GVHD) or other HSC/HPC dysplasia-induced diseases. In this review, we used bioinformatics methods, molecular docking verification, and a literature review to systematically explore the possible molecular pharmacological activities of Rg1 through which it regulates HSCs/HPCs.

Effects of Salvianolic Acid B/ginsenoside Rg1 Combination Against Chronic Pulmonary Embolism Induced by Polystyrene Microspheres

Pulmonary embolism (PE) is the most life-threatening complication of venous thromboembolism, but few effective treatments have been discovered to attenuate chronic PE currently. In this study, we investigated the protective effects of salvianolic acid B (SalB) and ginsenoside Rg1 (Rg1) combination (SalB/Rg1) on chronic PE and explored the potential mechanisms. The PE model was induced by 45 μm polystyrene microspheres and 20 mg/kg of SalB/Rg1 was administered to PE rats intraperitoneally. A histopathological analysis of the lungs and heart was performed through hematoxylin and eosin staining and immunohistochemical analysis. The pulmonary index and right ventricular cardiomyocyte cross-sectional area were evaluated. SalB/Rg1 markedly downregulated pulmonary index, attenuated pulmonary interstitial changes, suppressed neutrophil infiltration, prevented collagen deposition, and inhibited MMP-9 activities in the lung. We also found that SalB/Rg1 improved right ventricular hypertrophy accompanied by reducing the cardiomyocyte cross-sectional area. These data suggest that SalB/Rg1 played a protective role against microsphere-induced PE and holds a high potential for the treatment of PE in the future.

Ginsenoside Rg1 Prevents Cognitive Impairment and Hippocampal Neuronal Apoptosis in Experimental Vascular Dementia Mice by Promoting GPR30 Expression

This study is aimed at investigating the potential roles of G protein-coupled estrogen receptor 1 (GPER, also known as GPR30) in the preventive effect of ginsenoside Rg1 against cognitive impairment and hippocampal cell apoptosis in experimental vascular dementia (VD) in mice. The effects of bilateral common carotid artery stenosis (BCAS) on GPR30 expression at mRNA level were evaluated. Thereafter, the BCAS mouse model was utilized to evaluate the protection of Rg1 (0.1, 1, 10 mg/kg, 14 days, ip). Spatial memory was evaluated by water Morris Maze 7 days post BCAS. After behavioral tests, neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and potential mechanisms were determined using western blotting and quantitative real-time PCR. Our results showed that GPR30 expression in the hippocampal region at mRNA level was promoted 30 min, 3 h, 6 h, and 24 h following BCAS. Ginsenoside Rg1 (1 or 10 mg/kg, 14 days, ip) promoted GPR30 expression in the hippocampus of model mice (after behavioral tests) but did not alter GPR30 expression in the hippocampus of control mice. Moreover, treatment of ginsenoside Rg1 (10 mg/kg) or G1 (5 μg/kg), a GPR30 agonist, prevented BCAS-induced memory impairment and hippocampal neuronal loss and apoptosis and promoted the ratio of Bcl-2 to Bax expression in the hippocampus (after behavioral tests). On the contrary, G15 (185 μg/kg), an antagonist of GPR30, aggravated BCAS-induced hippocampal neuronal loss and apoptosis. Finally, drug-target molecular docking pointed that Rg1 had a lower binding energy with GPR30 compared with Bax and Bcl-2. Together, our data implicate that ginsenoside Rg1 prevents cognitive impairment and hippocampal neuronal apoptosis in VD mice, likely through promoting GPR30 expression. These results would provide important implications for the application of Rg1 in the treatment of VD.