Ginsenoside Rb1, a main constituent of the root of Panax ginseng, inhibits Na⁺, K⁺-ATPase activity with an IC₅₀ of 6.3±1.0 μM. Ginsenoside also inhibits IRAK-1 activation and phosphorylation of NF-κB p65 .

Rat brain microsomal Na⁺, K⁺-ATPase activity is inhibited significantly and rapidly by Ginsenoside Rb1. The IC₅₀ of Ginsenoside Rb1 for Na⁺,K⁺-ATPase is 6.3±1.0 μM. The inhibition is enhanced with increasing the concentration of Ginsenoside Rb1 or decreasing that of Na⁺ and K⁺. Kinetic analysis reveals that Ginsenoside is an uncompetitive inhibitor with respect to ATP^[1]. Ginsenoside Rb1 significantly inhibits the activation of interleukin-1 receptor-associated kinase-1 (IRAK-1), IKK-β, NF-κB, and MAP kinases (ERK, JNK, and p-38); however, interaction between LPS and Toll-like receptor-4, IRAK-4 activation and IRAK-2 activation are unaffected^[2]. Ginsenoside Rb1 is an ingredient of a Chinese medicine Panax ginseng. Ginsenoside Rb1 is a major bioactive compound in the regulating pregnane X receptor (PXR)/NF-κB signaling. Ginsenoside Rb1 is the compound with potent anti-inflammatory activity in ginseng saponin extract (GSE). The concentration for Ginsenoside Rb1 (10 μM) is optimized from a preliminary study to ensure sufficient anti-inflammatory activity and without apparent cytotoxicity. Ginsenoside Rb1 significantly reduces TNF-α-induced upregulation of IL-1β and iNOS mRNA levels, and restores the mRNA levels of PXR and CYP3A4 in LS174T cells. TNF-α causes a significant reduction in PXR protein levels and increase in the ratio of phosphorylated to total NF-κB p65, both of which are significantly abrogated by Ginsenoside Rb1^[3].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Ginsenoside Rb1 at the both doses of 30 mg/kg and 60 mg/kg significantly attenuates the histological lung injury. Ginsenoside Rb1 at the dose of 30 mg/kg and 60 mg/kg both significantly attenuates the histological intestine injury^[4]. Ginsenoside Rb1 (Rb1), an ingredient of a Chinese medicine Panax ginseng, has beneficial effects on mesentery microvascular hyperpermeability induced by Lipopolysaccharide (LPS) and the underlying mechanisms. In some rats, Ginsenoside Rb1 (5 mg/kg per hour) is administrated through the left jugular vein 30 min after LPS infusion. Ginsenoside Rb1 decreases caveolae number in endothelial cells of microvessels. Ginsenoside Rb1 ameliorates microvascular hyperpermeability after the onset of endotoxemia and improves intestinal edema through inhibiting caveolae formation and junction disruption, which is correlated to suppression of NF-κB and Src activation^[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

1109.29

C₅₄H₉₂O₂₃

41753-43-9

人参皂苷 Rb1

Room temperature in continental US; may vary elsewhere.

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

In Vitro: 

DMSO : 100 mg/mL (90.15 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。

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 (2.25 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.25 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 (2.25 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.25 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 (2.25 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (2.25 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]. Cao J, et al. Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na⁺,K⁺-ATPase activity. Zhongguo Yao Li Xue Bao. 1990 Jan;11(1):10-4.

  [2]. Zhang J, et al. Ginsenosides Regulate PXR/NF-κB Signaling and Attenuate Dextran Sulfate Sodium-Induced Colitis. Drug Metab Dispos. 2015 Aug;43(8):1181-9.

  [3]. Joh EH, et al. Ginsenoside Rb1 and its metabolite compound K inhibit IRAK-1 activation–the key step of inflammation. Biochem Pharmacol. 2011 Aug 1;82(3):278-86.

  [4]. Jiang Y, et al. Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice. Oxid Med Cell Longev. 2015;2015:843721.

  [5]. Zhang Y, et al. Ginsenoside Rb1 ameliorates lipopolysaccharide-induced albumin leakage from rat mesenteric venules by intervening in both trans- and paracellular pathway. Am J Physiol Gastrointest Liver Physiol. 2014 Feb 15;306(4):G289-300.

LS174T cells are seeded in cell imaging dish. After overnight incubation, cells are treated with GSE (100 μg/mL), Ginsenoside Rb1 (10 μM), or CK (10 μM) for 3 hours, followed by an additional incubation with or without TNF-α (20 ng/ml) for 6 hours. At the end of the incubation, cells are harvested and fixed with 4% paraformaldehyde solution at 20°C for 20 minutes. After washing in PBS, cells are permeabilized with 0.2% Triton X-100 in PBS at room temperature for 5 minutes. After incubation in blocking buffer containing 0.1% Triton X-100 and 5% bovine serum albumin, cells are incubated with rabbit NF-κB p65 antibody at 4°C overnight and then with Alexa Fluor 488-conjugated anti-rabbit IgG antibody at room temperature for 30 minutes in 1% bovine serum albumin in PBS. Fluorescence photographs are obtained using a Zeiss 710 confocal microscope^[3].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Mice^[4]
Male C57BL/6 mice (9-12 weeks old; 17-22 g) are randomly allocated into eight groups (n=8 in each group): (1) Sham surgical preparation including isolation of the superior mesenteric artery (SMA) without occlusion is performed (Sham); (2) mice are subjected to II/R without treatment (II/R); (3) mice are subjected to II/R with treatment of normal saline 10 minutes before reperfusion (II/R+NS); (4), (5) mice are treated with 30 mg/kg (II/R+Rb1-30) or 60 mg/kg (II/R+Rb1-60) Ginsenoside Rb1, in which surgery is performed as in the II/R group with administration of the Ginsenoside Rb1 intraperitoneally 10 minutes before reperfusion; (6) mice are subjected to Sham surgery and treated with ATRA (ATRA+Sham), which is the inhibitor of Nrf2/ARE signaling pathway; (7) mice are subjected to II/R and treated with ATRA (ATRA+II/R); (8) mice are subjected to II/R and treated with ATRA and 60 mg/kg Ginsenoside Rb1 as group 5 (ATRA+II/R+Rb1-60). During the last two weeks before the operation, the mice in the group 6, 7, 8 receive ATRA i.p. daily at 10 mg/kg and fed on a vitamin A-deficient diet, and the mice in the other groups receive the equivalent volume of corn oil and fed on a control normal diet.
Rats^[5]
Male Wistar rats weighing 200-250 g are used. The rats are randomly divided into four groups, 26 animals in each. After being anesthetized with urethane (2 g/kg body wt im), the left femoral vein and left jugular vein of the rat are cannulated. In the LPS group, LPS solution in saline is infused (5 mg/kg per hour) for 90 min via the left femoral vein. The vehicle, instead of LPS solution, is administrated in Sham and Ginsenoside Rb1 alone (Rb1, 5 mg/kg) groups. In the Rb1 posttreatment (LPS+Rb1) group, Ginsenoside Rb1 solution is infused continuously through the left jugular vein 30 min after LPS administration at the dose of 5 mg/kg. Ginsenoside Rb1 solution and the same volume of saline are infused in Ginsenoside Rb1 and Sham groups, respectively, without subsequent LPS administration. In a separate set of experiments, the rats are anesthetized with 2% penobarbital sodium (60 mg/kg body wt ip), and saline, LPS, and Ginsenoside Rb1. After recovery from anesthesia, the animals are allowed access to water and rodent chow, and survival rate is recorded over time until 4 days after LPS stimulation.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Cao J, et al. Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na⁺,K⁺-ATPase activity. Zhongguo Yao Li Xue Bao. 1990 Jan;11(1):10-4.

  [2]. Zhang J, et al. Ginsenosides Regulate PXR/NF-κB Signaling and Attenuate Dextran Sulfate Sodium-Induced Colitis. Drug Metab Dispos. 2015 Aug;43(8):1181-9.

  [3]. Joh EH, et al. Ginsenoside Rb1 and its metabolite compound K inhibit IRAK-1 activation–the key step of inflammation. Biochem Pharmacol. 2011 Aug 1;82(3):278-86.

  [4]. Jiang Y, et al. Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice. Oxid Med Cell Longev. 2015;2015:843721.

  [5]. Zhang Y, et al. Ginsenoside Rb1 ameliorates lipopolysaccharide-induced albumin leakage from rat mesenteric venules by intervening in both trans- and paracellular pathway. Am J Physiol Gastrointest Liver Physiol. 2014 Feb 15;306(4):G289-300.