1. PI3K/Akt/mTOR Apoptosis MAPK/ERK Pathway Stem Cell/Wnt Immunology/Inflammation Metabolic Enzyme/Protease Vitamin D Related/Nuclear Receptor Neuronal Signaling Membrane Transporter/Ion Channel GPCR/G Protein
  2. PI3K mTOR Akt Apoptosis p38 MAPK ERK Transmembrane Glycoprotein Glutathione Reductase (GR) Estrogen Receptor/ERR Calcium Channel Ferroptosis G protein-coupled Bile Acid Receptor 1 FXR
  3. Notoginsenoside Ft1

Notoginsenoside Ft1  (Synonyms: 三七皂苷FT1)

目录号: HY-N0910 纯度: ≥98.0%
COA 产品使用指南 技术支持

Notoginsenoside Ft1 是从一种可从三七 (Panax notoginseng) 中分离得到的一种生物活性皂苷。Notoginsenoside Ft1 通过抑制 PI3K/AKT/mTOR 信号通路,激活 p38 MAPKERK1/2 信号通路,增加 CD8+ T 细胞比例,可诱导多种癌细胞凋亡 (apoptosis) 和溶酶体细胞死亡,并可促进血管生成。Notoginsenoside Ft1 通过激活内皮细胞中的糖皮质激素受体 (GR) 和雌激素受体 β (ERβ) 引起血管舒张。Notoginsenoside Ft1 通过激活一个由 P2Y12 受体介导的信号网络,增加细胞内 Ca2+ 积累,降低 cAMP 水平,促进血小板聚集,发挥促凝血作用。Notoginsenoside Ft1 通过激活 TGR5 受体,抑制肾小管上皮细胞铁死亡 (ferroptosis),从而显示出肾脏保护作用。Notoginsenoside Ft1 可作为 TGR5 激动剂和 FXR 拮抗剂抵抗肥胖和胰岛素抵抗。

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Notoginsenoside Ft1

Notoginsenoside Ft1 Chemical Structure

CAS No. : 155683-00-4

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MCE 顾客使用本产品发表的 1 篇科研文献

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

NotoginsenosideFt1 is a saponin found in Panax notoginseng. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8+ T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance[1][2][3][4][5][6][7][8].

体外研究
(In Vitro)

Notoginsenoside Ft1 (0-10 μM,0-48 小时) 显著促进 HUVEC 增殖和迁移,促进细胞周期由 G1 期向 S 期转变,显著促进 HUVEC 管状结构的形成,并通过抑制 PI3K/AKT/mTOR 通路和 Raf/MEK/ERK 通路促进 VEGF 的表达和分泌[1]
Notoginsenoside Ft1 (0-250 μM) 在中以剂量依赖性方式促进大鼠血小板聚集 (EC50 = 56.42 μM) ,并在人血浆 (240 μg/mL,5 分钟) 和大鼠血浆 (80 μg/mL,5 分钟) 中均表现出全面的促凝作用,影响外源性及自身凝血途径[2]
Notoginsenoside Ft1 (56.4 μM) 可诱导血小板和 P2Y12-HEK293 细胞内 Ca²⁺ 升高,显著抑制 cAMP 的产生,并诱导 PI3KAkt 的磷酸化[2]
Notoginsenoside Ft1 (1 nM-10 mM,30 分钟) 可刺激大鼠肠系膜动脉内皮细胞 GR 和 ERb,随后激活 PI3K/Akt 和 ERK1/2 通路,导致 eNOS 磷酸化和 NO 释放,进而激活血管平滑肌细胞中的可溶性鸟苷酸环化酶,导致血管扩张[3]
Notoginsenoside Ft1 (0.1-100 μM,24 小时) 可抑制 SH-SY5Y 细胞 (IC50 = 45 μM),导致细胞周期停滞并诱导细胞凋亡,涉及调节 p38 MAPK 和 ERK1/2 通路[4]
Notoginsenoside Ft1 (0.1-10 μM,0.5-24 小时) 显著激活 TGR5 的荧光素酶活性,增加 Tgr5-HEK293 细胞中的 cAMP 水平,并促进 NCI-H716 细胞中 GLP-1 的分泌[5]
Notoginsenoside Ft1 (10 μM,24 小时) 显著抑制 Caco-2 细胞中的 FXR 靶基因,并抑制 GW4064 (HY-50108) 诱导的 HEK293T 细胞中的 FXR 活性细胞[5]
Notoginsenoside Ft1 (10 μM,24 小时) 对 HepG2 (IC50 = 46.3 μM)、Huh7 (IC50 = 35.2 μM) 和 PLC/PRF/5 (IC50 = 58.9 μM) 细胞有抑制作用,但对 THLE-2 (IC50 = 82.2 μM) 细胞无抑制作用[6]
Notoginsenoside Ft1 (12.5-50 μM,12-24 小时) 通过抑制 PI3K/AKT/mTOR 通路诱导细胞凋亡,并通过激活 HepG2 细胞中的 TFEB 促进溶酶体细胞死亡[6]
Notoginsenoside Ft1 (0-100 μM,24 小时-14 天) 可抑制 MC38、CT26、HT29 细胞的生长,IC50 分别为 32.87、30.75 和 27.59 μM,抑制 MC38 细胞的克隆形成,显著抑制 MC38 和 CT26 细胞的迁移能力,抑制集落形成数量[7]
Notoginsenoside Ft1 (5 μM,24 小时) 成功抑制了 HK2 细胞中的铁死亡模型,表现为细胞活力增加、抑制 ROS 积累、线粒体功能障碍改善以及铁死亡标志蛋白的表达改变[8]

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

Cell Cycle Analysis[1]

Cell Line: HUVECs
Concentration: 10 μM
Incubation Time: 0, 3, 6, 12, 16, 24 h
Result: Increased the proportion of cells in the S phase and decreased the proportion of cells in the G1 phase.

Cell Migration Assay [1]

Cell Line: HUVECs
Concentration: 0, 0.5, 1, 2.5, 5 and 10 μM
Incubation Time: 24 h
Result: Promoted HUVECs migration in a dose-dependent manner.

Western Blot Analysis[1]

Cell Line: HUVECs
Concentration: 10 μM
Incubation Time: 0, 15, 30 min, 1, 2, 4, 8, 12 and 24 h
Result: Promoted PI3K, AKT, mTOR, c-Raf, MEK1/2 and ERK1/2 phosphorylation.
Promoted HIF-1α translocation from the cytoplasm to the nucleus in a time-dependent manner.

Western Blot Analysis[3]

Cell Line: Rat mesenteric arteries
Concentration: 100 μM
Incubation Time: 30 min
Result: Significantly increased p-eNOS, but no significant change in total eNOS expression; eNOS expression was almost undetectable in the endothelial removal group.
Increased Akt phosphorylation and ERK1/2 phosphorylation.
Increased the levels of p-GR (Ser211) and p-ERβ (Ser87) in the endothelial layer.

Cell Cycle Analysis[4]

Cell Line: SH-SY5Y cells
Concentration: 22.5, 45 and 67.5 μM
Incubation Time: 24 h
Result: Caused arrest at the S phase and G2/M phase22.5-45 μM.
Only causes G2/M phase arrest at 67.5 μM.

Apoptosis Analysis[4]

Cell Line: SH-SY5Y cells
Concentration: 45 and 67.5 μM
Incubation Time: 24 h
Result: Showed nuclear enrichment and fragmentation.
showed that the rate of early apoptosis increased from 13.6% to 48.9%.

Western Blot Analysis[4]

Cell Line: SH-SY5Y cells
Concentration: 22.5, 45 and 67.5 μM
Incubation Time: 24 h
Result: Increased cleaved caspase-3 and decreased Bcl-2.
Increased p-p53, p21 and cyclin B1.
Increased p-ERK1/2, p-JNK and p-p38, decreased p-Jak2 and p-PI3K.

Apoptosis Analysis[6]

Cell Line: HepG2 and Huh7 cells
Concentration: 12.5, 25 and 50 μM
Incubation Time: 24 h
Result: Increased significantly the proportion of early and late apoptotic cells.
Increased expression of cleaved PARP, caspase-9, caspase-8, and caspase-3.
体内研究
(In Vivo)

Notoginsenoside Ft1 (1-25 μM 用于 Matrigel 栓塞试验,0.25-25 mg/kg 用于耳部伤口愈合试验,腹腔注射,单次给药和隔日给药,共 28 天) 可促进小鼠 Matrigel 栓塞中血管的形成和伤口愈合[1]
Notoginsenoside Ft1 (1.25 mg/kg,静脉注射,单次给药) 可显著增加 Wistar 大鼠的血栓形成并缩短出血时间[2]
Notoginsenoside Ft1 (50-100 mg/100 g 饮食,口服,共 6 周) 可改善肥胖症,通过激活 Tgr5 改善高脂饮食 (HFD) 小鼠的血糖紊乱,并通过拮抗 FXR 增强肝脏胆汁酸 (BA) 的合成[5]
Notoginsenoside Ft1 (25-50 mg/kg,口服,每日一次,连续 3 周) 在 HepG2 异种移植瘤小鼠模型中显示出抗癌作用[6]
Notoginsenoside Ft1 (10-30 mg/kg,腹腔注射,每日一次,连续 24 天) 显著抑制结直肠癌 (CRC) 皮下肿瘤形成,并提高荷瘤小鼠 CD8+ T 细胞比例,从而抑制肿瘤生长[7]
Notoginsenoside Ft1 可通过激活 JUN 信号通路控制小鼠血糖,减少肾小管损伤,并干预肾脏铁死亡的发生[8]

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

Animal Model: Matrigel plug assay established in Balb/c nude mice (8 weeks old)[1]
Dosage: 1, 5 and 25 μM with Heparin (HY-17567) in Matrigel
Administration: Intraperitoneal injection (i.p.), single dose
Result: Formed of a functional vasculature inside the Matrigel.
Increased the hemoglobin content in a dose-dependent manner.
Revealed a dose-dependent increase in staining with the blood vessel endothelial cell marker CD-31 Matrigels with more enlarged and more blood vessels.
Animal Model: Ear wound healing assay established in Balb/c nude mice (8 weeks old)[1]
Dosage: 0.25 mg/kg, 2.5 mg/kg or 25 mg/kg
Administration: Intraperitoneal injection (i.p.), every other day for 28 days
Result: Significantly reduced the diameter of the wound, and more new blood vessels could be observed at the wound edge.
Significantly upregulated the expression of VEGF mRNA.
No significant difference in the weight changes of the mice in each group.
Animal Model: Diet-induced obesity model established in Tgr5 -/- mice, Cyp27a1-/- mice and wild-type mice[5]
Dosage: 50 and 100 mg/100 g diet
Administration: Oral administration (p.o.) with diet, for 6 weeks
Result: Reduced the weight gain of mice, significantly decreased the diameter of fat cells, and reduced the deposition of lipid droplets in the liver.
Reduced fasting metabolic parameters, lowered blood sugar, improved insulin resistance index (HOMA-IR) and enhanced insulin sensitivity.
Increased energy digestion and improved cold tolerance.
Upregulated Cyp7a1 and Cyp27a1 mRNA in the liver and downregulated Fgf15 mRNA in the ileum.
Increased Ucp1 expression in BAT and iWAT, and upregulated genes such as Pgc1a and Prdm16.
Increased PKA substrate phosphorylation, HSL phosphorylation, and serum glycerol levels.
Animal Model: HepG2 xenograft tumor model established in adult male mice[6]
Dosage: 25 and 50 mg/kg
Administration: Oral administration (p.o.), once daily for 3 weeks
Result: Significantly reduced tumor volume and weight.
No significant weight loss caused, and no obvious pathological changes found in major organs.
Reduced KRAS, ERK1/2, c-Fos, and JUND proteins levels.
Animal Model: MC38 or CT26 -induced CRC model established in C57BL/6J and Balb/c mice, male, SPF grade, aged 6-8 weeks, and weighing 18 g[7]
Dosage: 10 and 30 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 24 days
Result: Significantly inhibited tumor growth at 30 mg/kg.
No obvious weight loss, no obvious pathological changes in major organs such as liver and kidney.
Significantly increased the proportion of CD8+ T cells in tumors.
分子量

917.13

Formula

C47H80O17

CAS 号
性状

固体

颜色

White to off-white

中文名称

三七皂甙 Ft1

结构分类
初始来源
运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

4°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

溶解性数据
细胞实验: 

DMSO 中的溶解度 : 100 mg/mL (109.04 mM; 超声助溶; 吸湿的 DMSO 对产品的溶解度有显著影响,请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.0904 mL 5.4518 mL 10.9036 mL
5 mM 0.2181 mL 1.0904 mL 2.1807 mL
查看完整储备液配制表

* 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 (stored under nitrogen)。-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。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
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浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物实验:

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

  • 方案 一

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

    Solubility: ≥ 2.5 mg/mL (2.73 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液。

    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;再向上述体系中加入 50 μL Tween-80,混合均匀;然后再继续加入 450 μL 生理盐水 定容至 1 mL

    生理盐水的配制:将 0.9 g 氯化钠,溶解于 ddH₂O 并定容至 100 mL,可以得到澄清透明的生理盐水溶液。
  • 方案 二

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

    Solubility: ≥ 2.5 mg/mL (2.73 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液。

    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。

    2 g SBE-β-CD(磺丁基醚 β-环糊精)粉末定容于 10 mL 的生理盐水中,完全溶解至澄清透明。
动物溶解方案计算器
请输入动物实验的基本信息:

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

由于实验过程有损耗,建议您多配一只动物的量
请输入您的动物体内配方组成:
%
DMSO +
+
%
Tween-80 +
%
Saline
如果您的动物是免疫缺陷鼠或者体弱鼠,建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。
方案所需 助溶剂 包括:DMSO ,均可在 MCE 网站选购。 Tween 80,均可在 MCE 网站选购。
计算结果
工作液所需浓度 : mg/mL
储备液配制方法 : mg 药物溶于 μL  DMSO(母液浓度为 mg/mL)。

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

您所需的储备液浓度超过该产品的实测溶解度,以下方案仅供参考,如有需要,请与 MCE 中国技术支持联系。
动物实验体内工作液的配制方法 : 取 μL DMSO 储备液,加入 μL  μL ,混合均匀至澄清,再加 μL Tween 80,混合均匀至澄清,再加 μL 生理盐水
连续给药周期超过半月以上,请谨慎选择该方案。
请确保第一步储备液溶解至澄清状态,从左到右依次添加助溶剂。您可采用超声加热 (超声清洗仪,建议频次 20-40 kHz),涡旋吹打等方式辅助溶解。
纯度 & 产品资料

纯度: ≥98.0%

参考文献

完整储备液配制表

* 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 (stored under nitrogen)。-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。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.0904 mL 5.4518 mL 10.9036 mL 27.2589 mL
5 mM 0.2181 mL 1.0904 mL 2.1807 mL 5.4518 mL
10 mM 0.1090 mL 0.5452 mL 1.0904 mL 2.7259 mL
15 mM 0.0727 mL 0.3635 mL 0.7269 mL 1.8173 mL
20 mM 0.0545 mL 0.2726 mL 0.5452 mL 1.3629 mL
25 mM 0.0436 mL 0.2181 mL 0.4361 mL 1.0904 mL
30 mM 0.0363 mL 0.1817 mL 0.3635 mL 0.9086 mL
40 mM 0.0273 mL 0.1363 mL 0.2726 mL 0.6815 mL
50 mM 0.0218 mL 0.1090 mL 0.2181 mL 0.5452 mL
60 mM 0.0182 mL 0.0909 mL 0.1817 mL 0.4543 mL
80 mM 0.0136 mL 0.0681 mL 0.1363 mL 0.3407 mL
100 mM 0.0109 mL 0.0545 mL 0.1090 mL 0.2726 mL
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Notoginsenoside Ft1
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