tcsc3833 Ginsenoside Rg2

Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 acts as a NF-κB inhibitor. Ginsenoside Rg2 also reduces Aβ_1-42 accumulation.

IC50 & Target: NF-κB ^[1]


Aβ_1-42^[2]

In Vitro: Ginsenoside Rg2 prevents the decrease of IκB expression stimulated with lipopolysaccharide (LPS). IκB dissociation from RelA-p50 complex is crucial for NF-κB activity. Ginsenoside Rg2, protopanaxatriol, inhibits vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression stimulated with LPS from human umbilical vein endothelial cell (HUVEC). The inhibition of VCAM-1 and ICAM-1 expression by Ginsenoside Rg2 is in a concentration-dependent manner, significantly. Treatment of endothelial cells with LPS (1µg/mL) decreases IκBα expression. By 1 hr after LPS treatment, significant decrease of IκBα is attained. To determine whether LPS-stimulated IκBα expression is affected by Ginsenoside Rg2, endothelial cells are treated for 1 hr with Ginsenoside Rg2 (1~50 µM) prior to LPS (1 µg/mL) stimulation for 1 hr. Ginsenoside Rg2 reverses the decrease of LPS-induced IκBα expression in a concentration-dependent manner, significantly. The adhesion of THP-1 cells to endothelial cells is measured using quantitative monolayer adhesion assay. The adhesion of THP-1 cells onto endothelial cells are increased to five folds by LPS (1 µg/mL) stimulation for 8 hrs. Ginsenoside Rg2 (1~50 µM) inhibits the adhesion of THP-1 cells to endothelial cells stimulated with LPS, in a concentration-dependent manner^[1].

In Vivo: 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 G-Rg1 and Ginsenoside Rg2 (G-Rg1, p<0.01; Ginsenoside Rg2, p<0.05). Treatment with G-Rg1 and Ginsenoside Rg2 effectively improve cognitive function of the mice that have declined due to AD. G-Rg1 and Ginsenoside Rg2 reduce Aβ_1-42 accumulation in APP/PS1 mice. In the G-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^[2].