Ginsenoside Rd inhibits TNFα-induced NF-κB transcriptional activity with an IC₅₀ of 12.05±0.82 μM in HepG2 cells. Ginsenoside Rd inhibits expression of COX-2 and iNOS mRNA. Ginsenoside Rd also inhibits Ca²⁺ influx. Ginsenoside Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9, with IC₅₀s of 58.0±4.5 μM, 78.4±5.3 μM, 81.7±2.6 μM, and 85.1±9.1 μM, respectively.

Ginsenoside Rd is one of the most abundant ingredients of Panax ginseng. Ginsenoside Rd significantly inhibits TNF-α-induced NF-κB transcriptional activity with an IC₅₀ of 12.05±0.82 in HepG2 cells. Ginsenoside Rd also inhibits expression of COX-2 and iNOS mRNA and iNOS promoter activity in a dose-dependent manner. To determine nontoxic concentrations, HepG2 cells are treated with various concentrations (0.1, 1, and 10 μM) of compounds (e.g., Ginsenoside Rd) and cell viability is measured using an MTS assay. No compounds are significantly cytotoxic at up to 10 μM, indicating that NF-κB inhibition is not due to cell toxicity^[1]. Ginsenoside Rd is one of the most abundant ingredients of Panax ginseng, protects the heart via multiple mechanisms including the inhibition of Ca²⁺ influx. Ginsenoside Rd reduces I_Ca,L peak amplitude in a concentration-dependent manner (IC₅₀=32.4±7.1 μM)^[2]. Ginsenoside Rd exhibits an inhibition against the activity of CYP2D6 in human liver microsomes with an IC₅₀ of 58.0±4.5 μM, a weak inhibition against the activity of CYP1A2, CYP3A4, and CYP2C9 in human liver microsomes with IC₅₀s of 78.4±5.3, 81.7±2.6, and 85.1±9.1, respectively, and an even weaker inhibition against the activity of CYP2A6 in human liver microsomes with an IC₅₀ value of more than 100 μM^[4].

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

Ginsenosides Rd is a major compound isolated from Gynostemma pentaphyllum that holistically improves gut microenvironment and induces anti-polyposis in Apc^Min/+ mice. Six-weeks-old mice are subjected to Ginsenoside Rd treatment, before the appearance of the intestinal polyps. All the mice are monitored for food intake, water consumption, and weight changes. Throughout the experiment, no Rb3/ Ginsenoside Rd-associated weight loss in mice is observed. In addition, none of the treated mice show variations in food and water consumption. Whereas, the number and size of the polyps are effectively reduced by Ginsenoside Rd treatments^[3].

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

947.15

C₄₈H₈₂O₁₈

52705-93-8

人参皂苷 Rd

Room temperature in continental US; may vary elsewhere.

DMSO : 100 mg/mL (105.58 mM; Need ultrasonic)

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。

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 (2.64 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.64 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 (2.64 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.64 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 (2.64 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.64 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。

• [1]. Song SB, et al. Inhibition of TNF-α-mediated NF-κB Transcriptional Activity in HepG2 Cells by Dammarane-type Saponins from Panax ginseng Leaves. J Ginseng Res. 2012 Apr;36(2):146-52.

  [2]. Liu Y, et al. Ginsenoside metabolites, rather than naturally occurring ginsenosides, lead to inhibition of human cytochrome P450 enzymes. Toxicol Sci. 2006 Jun;91(2):356-64.

  [3]. Lu C, et al. Inhibition of L-type Ca²⁺ current by ginsenoside Rd in rat ventricular myocytes. J Ginseng Res. 2015 Apr;39(2):169-77.

  [4]. Huang G, et al. Ginsenosides Rb3 and Rd reduce polyps formation while reinstate the dysbiotic gut microbiota and the intestinal microenvironment in Apc^Min/+ mice. Sci Rep. 2017 Oct 2;7(1):12552.

An MTS assay is used to analyze the effects of the compounds on cell viability. HepG2 cells are cultured overnight in a 96-well plate (1×10⁴ cells/well). Cell viability is assessed after adding the compounds (e.g., Ginsenoside Rd; 0.1, 1, and 10 μM) for 24 h. The number of viable cells is determined by the A490nm of the dissolved formazan product, after addition of MTS for 30 min^[1].

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

Mice^[3]
Heterozygous male Apc^Min/+ (C57BL/6J-Apc^Min/+) mice are used. Total 32 male Apc^Min/+ mice (aged 6 weeks) are divided into three groups; 10 mice in the control group and 22 mice equally divided for Rb3 and Rd treatments. The mice are daily gavage with a single dose of Ginsenoside Rb3 or Ginsenoside Rd at 20 mg/kg, or solvent control. The treatments are carried out for 8 consecutive weeks.

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

• [1]. Song SB, et al. Inhibition of TNF-α-mediated NF-κB Transcriptional Activity in HepG2 Cells by Dammarane-type Saponins from Panax ginseng Leaves. J Ginseng Res. 2012 Apr;36(2):146-52.

  [2]. Liu Y, et al. Ginsenoside metabolites, rather than naturally occurring ginsenosides, lead to inhibition of human cytochrome P450 enzymes. Toxicol Sci. 2006 Jun;91(2):356-64.

  [3]. Lu C, et al. Inhibition of L-type Ca²⁺ current by ginsenoside Rd in rat ventricular myocytes. J Ginseng Res. 2015 Apr;39(2):169-77.

  [4]. Huang G, et al. Ginsenosides Rb3 and Rd reduce polyps formation while reinstate the dysbiotic gut microbiota and the intestinal microenvironment in Apc^Min/+ mice. Sci Rep. 2017 Oct 2;7(1):12552.