Ginsenoside Rg1 is one of the major active components ofPanax ginseng. Ginsenoside Rg1 ameliorates the impaired cognitive function, displays promising effects by reducing cerebralAβlevels. Ginsenoside Rg1 also reducesNF-κBnuclear translocation.

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 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_1-42accumulation 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].

801.01

Solid

C₄₂H₇₂O₁₄

22427-39-0

人参皂苷 Rg1

• Terpenoids
• Triterpenes

• Plants
• Araliaceae
• Panax ginsengC. A. Meyer

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 100 mg/mL(124.84 mM)

H₂O : 10 mg/mL(12.48 mM;Need ultrasonic)

*"≥" means soluble, but saturation unknown.

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℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

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： Saline

  Solubility: 10 mg/mL (12.48 mM); Clear solution; Need ultrasonic
• 2.

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

  Solubility: ≥ 2.5 mg/mL (3.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.12 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
• 3.

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

  Solubility: ≥ 2.5 mg/mL (3.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.12 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 μL20% 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
• 4.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.5 mg/mL (3.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.12 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。