tcsc3832 Ginsenoside Rg1

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.

IC50 & Target: Aβ^[1]


NF-κB p65^[2]

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 Aβ_1-42 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].