Ginsenoside Rg2(Synonyms: 人参皂苷 Rg2; Chikusetsusaponin I; Panaxoside Rg2; Prosapogenin C2)

天然产物 糖类和糖苷 Saccharides and Glycosides

Ginsenoside Rg2;(Synonyms: 人参皂苷 Rg2; Chikusetsusaponin I; Panaxoside Rg2; Prosapogenin C2) 纯度: ge;98.0%

Ginsenoside Rg2 是人参的主要活性成分之一。Ginsenoside Rg2抑制脂多糖介导的 VCAM-1ICAM-1 表达的增加。 Ginsenoside Rg2 还降低 1-42 积聚。

Ginsenoside Rg2(Synonyms: 人参皂苷 Rg2; Chikusetsusaponin I;  Panaxoside Rg2;  Prosapogenin C2)

Ginsenoside Rg2 Chemical Structure

CAS No. : 52286-74-5

规格 价格 是否有货 数量
10;mM;*;1 mL in DMSO ¥1036 In-stock
5 mg ¥700 In-stock
10 mg ¥1200 In-stock
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100 mg ; 询价 ;

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生物活性

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 1-42 accumulation.

IC50 Target[1][2]

NF-κB

;

1-42

;

体外研究
(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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

体内研究
(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 Aβ1-42 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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

分子量

785.01

Formula

C42H72O13

CAS 号

52286-74-5

中文名称

人参皂苷 Rg2;人参皂苷 Rg2

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式
Powder -20deg;C 3 years
4deg;C 2 years
In solvent -80deg;C 6 months
-20deg;C 1 month
溶解性数据
In Vitro:;

DMSO : 100 mg/mL (127.39 mM; ultrasonic and warming and heat to 60°C)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.2739 mL 6.3693 mL 12.7387 mL
5 mM 0.2548 mL 1.2739 mL 2.5477 mL
10 mM 0.1274 mL 0.6369 mL 1.2739 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month。-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂:

——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂:;10% DMSO ;; 40% PEG300 ;; 5% Tween-80 ;; 45% saline

    Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (3.18 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀;向上述体系中加入50 μL Tween-80,混合均匀;然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠,完全溶解于 100 mL ddH₂O 中,得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂:;10% DMSO ;; 90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (3.18 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中,混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
  • 3.

    请依序添加每种溶剂:;10% DMSO ;; 90% corn oil

    Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (3.18 mM,饱和度未知) 的澄清溶液,此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献
  • [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.

    [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.

    [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.

Cell Assay

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[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.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

参考文献
  • [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.

    [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.

    [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.