Ginsenoside Rg2Ginsenoside Rg2
MedChemExpress (MCE)
HY-N0602
52286-74-5
Chikusetsusaponin I
Panaxoside Rg2
Prosapogenin C2
98.11%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 inhibits VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS). Ginsenoside Rg2 also reduces Aβ1-42 accumulation.
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].
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 (p1-42 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].
Mice[2] Male APP/PS1 mice, weighing 20±2 g, and male C57BL/6J mice, weighing 20±2 g, are used. The animals are maintained in an air-conditioned animal center at 23±2°C and a relative humidity of 50±10%, with a natural light-dark cycle. Food and water are available ad libitum. After acclimatization for 1 wk, the mice are divided into four groups (n=10 in each group): the normal control group, the AD model group, the G-Rg1 group, and the Ginsenoside Rg2 group. According to the concentration-response curves, the mice in the G-Rg1 and Ginsenoside Rg2 groups are injected intraperitoneally once daily with G-Rg1 and Ginsenoside Rg2 (30 mg/kg), respectively, dissolved in saline. The mice in the AD model group (APP/PS1 mice) and the normal control group (C57BL/6J nontransgenic littermates) are treated with isodose saline (0.9% w/v). All mice are treated for 1 mo before brain metabolite profiling.
HUVECs ares grown in EBM-2 containing 10% FBS at a density of 2.0×105 cells/well on 24-well plates. Endothelial cells at 90~95% confluence are treated with Ginsenoside Rg2 (1, 20, 50 µM) for 1 hr prior to 1 µg/mL of LPS stimulation for 8 hr. THP-1 cells are labeled with Calcein-AM (5 µM) in RPMI 1640 medium containing 10% FBS for 30 min. After extensive washing with PBS, the labeled THP-1 cells are seeded at a density of 5.0×105 cells/well onto endothelial cells which are treated with the Rg2 and/or LPS and, then, incubated for 1 hr at 37°C while gentle shaking. After incubation, non-adherent cells are removed by gentle washing two times with PBS. Photograph images are obtained at 485 nm excitation and 538 nm emission using a SPOT II digital camera-attached fluorescence microscope[1].
NF-κB Aβ1-42
| | | |
| | | | | |
[1]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013 Apr
17(2):133-7. [Content Brief]
[2]. 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. [Content Brief]
[3]. Cho YS, et al. Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell. Korean J Physiol Pharmacol. 2013
17(2):133-137. [Content Brief]
