Ginsenoside Rg1

The roots of Panax ginseng C. A. Mey.

Ginsenoside Rg1 is one of the major active components of ginseng. Ginsenoside Rg1 displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.

In Vitro:Ginsenoside Rg1 promotes the proliferation and differentiation of human dental pulp cells (hDPCs). The proliferative ability of hDPCs in Ginsenoside Rg1 is significantly enhanced (p<0.05), especially in the Ginsenoside Rg1 (5 μM) group. ALP activity and gene expressions of DSPP and DMP1 are increased in the induction group, Ginsenoside Rg1 group, and their combination group compared with the control group (p<0.05)[3]. In the RAW264.7 cells stimulated by lipopolysaccharides (LPS) , the level of p-IκBα and p-p65 is significantly higher than in controls and PPAR-γ levels are significantly lower. Treatment with Rg1 vitro inhibits IκBα phosphorylation, reduces NF-κB nuclear translocation and upregulates PPAR-γ expression[2].

In Vivo:In the inflamed joints of adjuvant-induced arthritis (AIA) rats, the level of p-IκBα and p-p65 is significantly higher than in controls and PPAR-γ levels are significantly lower. Treatment with Ginsenoside Rg1 in vivo inhibits IκBα phosphorylation, reduces NF-κB nuclear translocation and upregulates PPAR-γ expression[2]. Ginsenoside Rg1 (G-Rg1) and Ginsenoside Rg2 (G-Rg2) reduce the escape latencies on the last two training days compared to the Alzheimer's disease (AD) model group (p<0.05). In the spatial exploration test, the total time spent in the target quadrant and the number of mice that exactly crossed the previous position of the platform are clearly shorter and lower, respectively, in the AD model group mice than in the normal control group mice (p<0.01), a trend that is reversed by treatment with Ginsenoside Rg1 and Ginsenoside Rg2 (Ginsenoside Rg1, p<0.01; Ginsenoside Rg2, p<0.05). Treatment with Ginsenoside Rg1 and Ginsenoside Rg2 effectively improve cognitive function of the mice that have declined due to AD. Ginsenoside Rg1 and Ginsenoside Rg2 reduce Aβ1-42 accumulation in APP/PS1 mice. In the Ginsenoside Rg1 and Ginsenoside Rg2 treated mice, the pathological abnormalities observed in the APP/PS1 mice are gradually ameliorated. Clear nucleoli and light brown, sparsely scattered Aβ deposits are visible[1].

References:
[1]. Li N, et al. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer's disease. J Ginseng Res. 2016 Jan;40(1):9-17. [2]. Zhang L, et al. Ginsenoside Rg1 attenuates adjuvant-induced arthritis in rats via modulation of PPAR-γ/NF-κB signal pathway. Oncotarget. 2017 Jul 24;8(33):55384-55393. [3]. Wang P, et al. Effect of ginsenoside Rg1 on proliferation and differentiation of human dental pulp cells in vitro. Aust Dent J. 2012 Jun;57(2):157-65.

Involvement of IGF-I receptor and estrogen receptor pathways in the protective effects of ginsenoside Rg1 against Abeta(2)(5)(-)(3)(5)-induced toxicity in PC12 cells.[Pubmed:23603302]

Neurochem Int. 2013 Jun;62(8):1065-71.

Ginsenoside Rg1 is the main pharmacologically active compound of ginsenosides and has demonstrated pharmacological effects in the cardiovascular system, central nervous system and immune system. The involvement of insulin-like growth factor-I receptor (IGF-IR)-dependent pathway and estrogen receptor (ER)-dependent pathway in the biological effect of Ginsenoside Rg1 have been demonstrated in our previous study. The present study tested the hypothesis that the protective effects of Rg1 against Abeta25-35-induced toxicity involved activation of the IGF-IR and ER signaling pathways in PC12 cells. Treatment with Abeta25-35 decreased the cell viability in a dose-dependent manner in PC12 cells. Rg1 pretreatment resulted in an enhancement of survival and the maximum protection occurred at the concentration of 1muM. Co-treatment with IGF-IR antagonist JB-1 or ER antagonist ICI182,780 could completely block the protective effect of Rg1. The decreased Bcl-2 mRNA expression induced by Abeta25-35 could be restored by Rg1 pretreatment. Rg1 pretreatment could also restore the decreased mitochondrial membrane potential induced by Abeta25-35 and these effects could be completely blocked by JB-1 or ICI182,780. In addition, Rg1 treatment alone could significantly increase the phosphorylation level of MEK and ERK in a time-dependent manner and the functional transactivation of ERalpha in PC12 cells. The functional transactivation of ERalpha by Rg1 could be completely blocked by JB-1 or ICI182,780. Taken together, our results suggest that IGF-IR and ER signaling pathways might be involved in the protective effect of Rg1 against Abeta25-35-induced toxicity in PC12 cells.

Ginsenoside Rg1 enhances CD4(+) T-cell activities and modulates Th1/Th2 differentiation.[Pubmed:14996415]

Int Immunopharmacol. 2004 Feb;4(2):235-44.

Panax ginseng is commonly used as a tonic medicine in Asian countries such as Korea, China, and Japan. It has been reported that Ginsenoside Rg1 in P. ginseng increases the proportion of T helper (Th) cells among the total number of T cells and promotes IL-2 gene expression in murine splenocytes. This implies that Ginsenoside Rg1 increases the immune activity of CD4(+) T cells, however, the exact mechanism remains unknown. The present study elucidated the direct effect of Rg1 on helper T-cell activities and on Th1/Th2 lineage development. The results demonstrated that Ginsenoside Rg1 had no mitogenic effects on unstimulated CD4(+) T cells, but augmented CD4(+) T-cell proliferation upon activation with anti-CD3/anti-CD28 antibodies in a dose-dependent manner. Rg1 also enhanced the expression of cell surface protein CD69 on CD4(+) T cells. In Th0 condition, Ginsenoside Rg1 increases the expression of IL-2 mRNA, and enhances the expression of IL-4 mRNA on CD4(+) T cells, suggesting that Rg1 prefers to induce Th2 lineage development. In addition, Ginsenoside Rg1 increases IL-4 secretion in CD4(+) T cells under Th2 skewed condition, while decreasing IFN-gamma secretion of cells in Th1 polarizing condition. Thus, Rg1 enhances Th2 lineage development from the naive CD4(+) T cell both by increasing Th2 specific cytokine secretion and by repressing Th1 specific cytokine production. Therefore, these results suggest that Ginsenoside Rg1 is a desirable agent for enhancing CD4(+) T-cell activity, as well as the correction of Th1-dominant pathological disorders.

Ginsenoside Rg1 promotes endothelial progenitor cell migration and proliferation.[Pubmed:19262553]

Acta Pharmacol Sin. 2009 Mar;30(3):299-306.

AIM: To investigate the effect of Ginsenoside Rg1 on the migration, adhesion, proliferation, and VEGF expression of endothelial progenitor cells (EPCs). METHODS: EPCs were isolated from human peripheral blood and incubated with different concentrations of Ginsenoside Rg1 (0.1, 0.5, 1.0, and 5.0 micromol/L) and vehicle controls. EPC migration was detected with a modified Boyden chamber assay. EPC adhesion was determined by counting adherent cells on fibronectin-coated culture dishes. EPC proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In vitro vasculogenesis was assayed using an in vitro vasculogenesis detection kit. A VEGF-ELISA kit was used to measure the amount of VEGF protein in the cell culture medium. RESULTS: Ginsenoside Rg1 promoted EPC adhesion, proliferation, migration and in vitro vasculogenesis in a dose- and time-dependent manner. Cell cycle analysis showed that 5.0 micromol/L of Ginsenoside Rg1 significantly increased the EPC proliferative phase (S phase) and decreased the resting phase (G(0)/G(1) phase). Ginsenoside Rg1 increased vascular endothelial growth factor production. CONCLUSION: The results indicate that Ginsenoside Rg1 promotes proliferation, migration, adhesion and in vitro vasculogenesis.

Ginsenoside Rg1 facilitates neural differentiation of mouse embryonic stem cells via GR-dependent signaling pathway.[Pubmed:23063465]

Neurochem Int. 2013 Jan;62(1):92-102.

Ginsenoside Rg1, a steroidal saponin of high abundance in ginseng, possesses the neuroprotective effects. In this study, we tried to explore the effect of Rg1 on promoting differentiation of mouse embryonic stem (ES) cells towards the neuronal lineage and its potential role involved in glucocorticoid receptor (GR) activation. Rg1 treatment induced a remarkable increase in the population of neuron-like cells in a time-dependent manner. More than 80% of Rg1-treated embryoid bodies (EBs) differentiated into neuron-like cells on d 8+10. Furthermore, the gradually increased protein expression of neurofilament (NEFM) and beta-tubulin III (a neuronal specific protein) was determined. GR expression gradually increased during the differentiation course. RU486, an antagonist of GR, could efficiently block the neurogenesis-promoting activity of Rg1. On the other side, Rg1 stimulated the phosphorylation of ERK1/2 and Akt at different time points through GR activation-dependent mechanisms. Treatment of both U0126 (an inhibitor of MEK) and LY294002 (an inhibitor of PI3 K), hampered the neuronal differentiation induced by Rg1. Meantime, U0126 further decreased Rg1-induced p-Akt expression. In conclusion, Rg1 possesses the effects on inducing differentiation of mouse ES cells into neurons in vitro via the GR-MEK-ERK1/2-PI3 K-Akt signaling pathway.

Ginsenoside Rg1 inhibits platelet activation and arterial thrombosis.[Pubmed:24196231]

Thromb Res. 2014 Jan;133(1):57-65.

INTRODUCTION: Derived from the root of Panax ginseng C.A.Mey, Panax notoginsenosides (PNS) is a widely used herbal medicine to treat atherothrombotic diseases in Asian medicine. Ginsenoside Rg1 is one of the main compounds responsible for the pharmaceutical actions of PNS. As platelets play pivotal roles in atherothrombogenesis, we therefore studied the effect of Rg1 on platelet activation and its underlying mechanisms. MATERIALS AND METHODS: Human platelets are obtained from healthy subjects. Platelet activation and the inhibition of Rg1 were assessed by Born aggregometer, flow cytmetry, flow chamber and western blot. The in vivo thrombosis model was induced by 10% FeCl3 on mesenteric arterioles of wild type B57/b6 mice. RESULTS: Rg1 significantly inhibited platelet aggregation induced by thrombin, ADP, collagen and U46619, e.g., aggregation rate stimulated by 0.1UmL(-1) thrombin was decreased 46% by Rg1. Rg1 also reduced thrombin (0.1UmL(-1))-enhanced fibrinogen binding and P-selectin expression of single platelet by 81% and 66%, respectively. Rg1 affected alphaIIbbeta3-mediated outside-in signaling as demonstrated by diminished platelet spreading on immobilized fibrinogen. Rg1 also decreased the rate of clot retraction in platelet rich plasma. Furthermore, Rg1 decreased platelet adhesion on collagen surface under a shear rate correlated to the arterial flow (1000s(-1)) by approximately 70%. Western blot showed that Rg1 potently inhibited ERK phosphrylation. The in vitro findings were further evaluated in the mouse model of in vivo arterial thrombosis, and Rg1 was found to prolong the mesenteric arterial occlusion time (34.9+/-4.1min without and 64.3+/-4.9min with Rg1; p<0.01). CONCLUSIONS: Rg1 inhibits platelet activation via the inhibition of ERK pathway, and attenuates arterial thrombus formation in vivo.

Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice.[Pubmed:23833204]

J Gerontol A Biol Sci Med Sci. 2014 Mar;69(3):282-94.

In aging individuals, age-related cognitive decline is the most common cause of memory impairment. Among the remedies, Ginsenoside Rg1, a major active component of ginseng, is often recommended for its antiaging effects. However, its role in improving cognitive decline during normal aging remains unknown and its molecular mechanism partially understood. This study employed a scheme of Rg1 supplementation for female C57BL/6J mice, which started at the age of 12 months and ended at 24 months, to investigate the effects of Rg1 supplementation on the cognitive performance. We found that Rg1 supplementation improved the performance of aged mice in behavior test and significantly upregulated the expression of synaptic plasticity-associated proteins in hippocampus, including synaptophysin, N-methyl-D-aspartate receptor subunit 1, postsynaptic density-95, and calcium/calmodulin-dependent protein kinase II alpha, via promoting mammalian target of rapamycin pathway activation. These data provide further support for Rg1 treatment of cognitive degeneration during aging.

Ginsenoside Rg1 is one of the major active components of ginseng. Ginsenoside Rg1 displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.

Ginsenoside Rg1,22427-39-0,Panaxoside A; Panaxoside Rg1,Natural Products, buy Ginsenoside Rg1 , Ginsenoside Rg1 supplier , purchase Ginsenoside Rg1 , Ginsenoside Rg1 cost , Ginsenoside Rg1 manufacturer , order Ginsenoside Rg1 , high purity Ginsenoside Rg1