52286-74-5
基本信息
人参皂苷-RG2
(R型)人参皂苷
人参皂苷RG2(S)
(S型)人参皂苷RG2
人参皂苷RG2(标准品)
人参皂苷20(S)-RG2
S-人参皂苷RG2,人参皂甙RG2
人参皂苷RG2/20(S)-人参皂苷RG2
GINSENOSIDE RG2 人参皂苷RG2
GinsesideRg2
Panaxoside Rg2
product/154570
Ginsenosdie Rg2
PROSAPOGENIN C2
GINSENOSIDE RG2
mannopyranosyl)-
iGInsenoside Rg2
GINSENOSIDE Rg2(SH)
物理化学性质
| 外观性状 | 白色结晶粉末，可溶于甲醇、乙醇、DMSO等有机溶剂，来源于人参、西洋参。 |
| 熔点 | 187～189℃ |
| 沸点 | 881.0±65.0 °C(Predicted) |
| 密度 | 1.30±0.1 g/cm3(Predicted) |
| 储存条件 | 2-8°C |
| 溶解度 | 甲醇（微溶、加热、超声处理）、吡啶（微溶、超声处理） |
| 酸度系数(pKa) | 12.85±0.70(Predicted) |
| 形态 | 固体 |
| 颜色 | 白色至灰白色 |
| 稳定性 | 吸湿性 |
| InChIKey | AGBCLJAHARWNLA-DJZXLMSJSA-N |
| LogP | 6.830 (est) |
安全数据
| 危险性符号(GHS) |  GHS07 |
| 警示词 | 警告 |
| 危险性描述 | H302 |
| 防范说明 | P301+P312+P330 |
| 危险品标志 | Xn |
| 危险类别码 | 22 |
| 安全说明 | 24/25 |
| WGK Germany | 3 |
| RTECS号 | LZ6430000 |
| 海关编码 | 29389090 |
| 毒性 | mouse,LD50,intraperitoneal,1340mg/kg (1340mg/kg),Arzneimittel-Forschung. Drug Research. Vol. 25, Pg. 343, 1975. |
常见问题列表
人参皂苷 Rg2 是人参的主要活性成分之一。人参皂苷 Rg2 是一种 NF-κB 抑制剂。 人参皂苷 Rg2还降低 Aβ1-42 积聚。
人参皂苷Rg2对急性心源性休克有保护作用，具有抗休克、抗心衰、抗凝血、抗血栓作用。主要表现在强壮心肌，增强心肌收缩力，减慢心率，扩张血管，增加心输出量和提高冠脉流量，能快速改善心肌缺血和缺氧，具有明显的增强心功能作用。
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NF-κB
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Aβ 1-42
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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.
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.