Notoginsenoside Fc
(Synonyms: 三七皂苷 FC) 目录号 : GC39023
Notoginsenoside Fc 是从三七叶中分离得到的一种原卟啉二醇 (PPD-) 型皂苷，可有效抵消血小板聚集。Notoginsenoside Fc 可以通过促进自噬促进糖尿病大鼠血管损伤后的内皮细胞再生。
Cas No.:88122-52-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Notoginsenoside Fc, a protopanaxadiol- (PPD-) type saponin isolated from the leaves of Panax notoginseng, effectively counteracts platelet aggregation. Notoginsenoside Fc can accelerate reendothelialization following vascular injury in diabetic rats by promoting autophagy[1].
[1]. Liu J, et al. Notoginsenoside Fc Accelerates Reendothelialization following Vascular Injury in Diabetic Rats by Promoting Endothelial Cell Autophagy. J Diabetes Res. 2019 Sep 3;2019:9696521.
| Cas No. | 88122-52-5 | SDF | |
| 别名 | 三七皂苷 FC | ||
| 分子式 | C58H98O26 | 分子量 | 1211.38 |
| 溶解度 | DMSO : 100 mg/mL (82.55 mM; Need ultrasonic) | 储存条件 | Store at 2-8°C,protect from light |
| General tips | 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 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.8255 mL | 4.1275 mL | 8.255 mL |
| 5 mM | 0.1651 mL | 0.8255 mL | 1.651 mL |
| 10 mM | 0.0826 mL | 0.4128 mL | 0.8255 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Notoginsenoside Fc ameliorates renal tubular injury and mitochondrial damage in acetaminophen-induced acute kidney injury partly by regulating SIRT3/SOD2 pathway
Front Med (Lausanne) 2023 Jan 6;9:1055252.PMID:36714147DOI:10.3389/fmed.2022.1055252.
Introduction: Mitochondria dysfunction is one of the primary causes of tubular injury in acute kidney injury (AKI). Notoginsenoside Fc (Fc), a new saponin isolated from Panax notoginseng, exhibited numerous pharmacological actions. However, the beneficial effects of Fc on renal tubular impairment and mitochondrial dysfunction in AKI have not been fully studied. Methods: In this study, we established acetaminophen (APAP)-induced AKI model in mice to examine the therapeutic impacts of Fc on AKI. Results: Our results showed that Fc could decrease the levels of the serum creatinine (Scr), blood urea nitrogen (BUN) and Cystatin C in mice with AKI. Fc also ameliorated renal histopathology, renal tubular cells apoptosis and restored expression of apoptosis-related proteins such as Bax, Bcl-2 and caspase3 (C-caspase3). Additionally, Fc increased the protein expression of SIRT3 and SOD2 in kidneys from mice with AKI. In vitro studies further showed Fc reduced the apoptosis of HK-2 cells exposure to APAP, attenuated the loss of mitochondrial membrane potential and decreased the formation of mitochondrial superoxide. Fc also partly restored the protein expression of Bax, Bcl-2, C-Caspase3, SIRT3, and SOD2 in HK-2 cells exposure to APAP. Conclusion: In summary, Fc might reduce renal tubular injury and mitochondrial dysfunction in AKI partly through the regulation of SIRT3/SOD2 pathway.
Notoginsenoside Fc Accelerates Reendothelialization following Vascular Injury in Diabetic Rats by Promoting Endothelial Cell Autophagy
J Diabetes Res 2019 Sep 3;2019:9696521.PMID:31565658DOI:10.1155/2019/9696521.
Interventional therapies, such as percutaneous transluminal angioplasty and endovascular stent implantation, are used widely for the treatment of diabetic peripheral vascular complications. Reendothelialization is an essential process in vascular injury following interventional therapy, and hyperglycemia in diabetes mellitus (DM) plays an important role in damaging endothelial layer integrity, leading to the retardance of reendothelialization and excessive neointimal formation. Notoginsenoside Fc (Fc), a novel saponin isolated from Panax notoginseng, effectively counteracts platelet aggregation. Nevertheless, the potential effects and molecular mechanisms of Fc on reendothelialization have yet to be explored. In this study, we present novel findings that show the benefit of Fc in accelerating reendothelialization and alleviating excessive neointimal formation following carotid artery injury in diabetic Sprague-Dawley rats in vivo. Simultaneously, the decreased autophagy of the injured carotid artery in diabetic rats was restored by Fc treatment. Our in vitro results also demonstrated that Fc promoted endothelial cell proliferation and migration under high-glucose treatment by increasing autophagy. In summary, this study supported the notion that Fc could accelerate reendothelialization following vascular injury in diabetic rats by promoting autophagy, suggesting that Fc may exert therapeutic benefits for early endothelial injury and restenosis following intervention in diabetes-associated vascular diseases.
Notoginsenoside Fc attenuates high glucose-induced vascular endothelial cell injury via upregulation of PPAR-γ in diabetic Sprague-Dawley rats
Vascul Pharmacol 2018 Oct;109:27-35.PMID:29857059DOI:10.1016/j.vph.2018.05.009.
Endothelial injury from high glucose (HG) plays a dominant role in atherosclerosis, diabetes-induced vasculopathy, and vascular remodeling. Notoginsenoside Fc (Fc), a novel saponin isolated from P. notoginseng, has been shown to exhibit properties that counteract platelet aggregation. However, the potential roles and molecular mechanisms of Fc in preventing cardiovascular injury have yet to be explored. In this study, we present novel data that show the ability of Fc to prevent early atherosclerosis of diabetic Sprague-Dawley (SD) rats in vivo and to attenuate endothelial cell injury in vitro. Our results indicate that Fc protects rat aortic endothelial cells (RAOECs) from HG-induced injury by inhibiting apoptosis and promoting proliferation as well as by reducing endothelial cell production of pro-inflammatory cytokines: TNF-α, IL-1β, IL-6, ICAM-1. Furthermore, the downregulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) in HG-challenged endothelial cells was prevented by Fc. Inhibition of PPAR-γ abrogated the effects of Fc on HG-induced pro-inflammatory cytokine production in RAOECs. These results indicate that Fc has a preventative effect on HG-induced endothelial cell injury partly through a PPARγ-mediated pathway, suggesting that Fc might provide a potential new therapeutic option for the treatment of diabetic vascular complications.
Phospholipase Cγ2 Signaling Cascade Contribute to the Antiplatelet Effect of Notoginsenoside Fc
Front Pharmacol 2018 Nov 6;9:1293.PMID:30459626DOI:10.3389/fphar.2018.01293.
Scope: Bleeding, the main drawback of clinically used chemical anti-thrombotic drug is resulted from the unidirectional suppression of platelet activity. Therefore, dual-directional regulatory effect on platelet is the main preponderance of Panax notoginseng over these drugs. The dual-directional regulatory effect should be ascribed to the resourceful Panax notoginseng saponins (PNS). Clarifying the mechanism of main PNS in both inhibiting and promoting platelet aggregation will give a full outlook for the dual-directional regulatory effect. The present study is aimed at explaining the mechanism of Notoginsenoside Fc (Fc), a main PNS, in inhibiting platelet aggregation. Methods: In the in vitro study, after incubating platelets with Fc and m-3M3FBS, platelet aggregation was triggered by thrombin, collagen or ADP. Platelet aggregation was measured by aggregometer. Phospholipase Cγ2 (PLCγ2) and protein kinase C (PKC) activities were studied by western blotting. Diacylglycerol (DAG), thromboxane B2 (TXB2) and 1,4,5-inositol trisphosphate (IP3) concentrations were measured by corresponding ELISA kits. Calcium concentrations ([Ca2+]) were estimated through the fluorescence intensity emitted from Fluo-4. In the in vivo study, thrombus model was induced by FeCl3. The effect of Fc on thrombosis was evaluated by measurement of protein content and observation of injured blood vessel. Results: thrombin, collagen and ADP induced platelet aggregation were all suppressed by incubating platelets with Fc. Platelet PLCγ2 and subsequent DAG-PKC-TXA2 and IP3 were down-regulated by Fc as well. However, the basal [Ca2+] in platelet was not altered by Fc. Nevertheless, thrombin triggered activation of PLCγ2 and subsequent DAG-PKC-TXA2 and IP3-[Ca2+] were all abolished by Fc. Fc also attenuated platelet aggregation and PLCγ2 signaling activation induced by PLC activator, m-3M3FBS. In the in vivo study, FeCl3 induced thrombosis in rat femoral artery was significantly alleviated by administration of Fc. Conclusion: The results above suggested the antiplatelet and antithrombotic effects of Fc are carried out through oppression of PLCγ2 and subsequent DAG-PKC-TXA2 and IP3-[Ca2+]. The present study provided theoretical support for new anti-thrombotic drug exploitation by Panax notoginseng.
Identification and quantitative investigation of the effects of intestinal microflora on the metabolism and pharmacokinetics of Notoginsenoside Fc assayed by liquid chromatography with electrospray ionization tandem mass spectrometry
J Sep Sci 2019 May;42(9):1740-1749.PMID:30805999DOI:10.1002/jssc.201801237.
Notoginsenoside Fc, which is a protopanaxdiol-type saponin isolated from the leaves of Panax notoginseng, exhibits an exceptional antiplatelet aggregatory effect. To study the modulating effect of gastrointestinal contents on the metabolic profile and pharmacokinetics, pseudo germ-free rats were used to study the influence of the bacterial community structure on the metabolic profile. Glycosidase activities were measured using the spectrophotometric method. Biotransformations of Notoginsenoside Fc in normal and pseudo germ-free rat intestinal microflora were systematically investigated using ultra high performance liquid chromatography with tandem quadrupole/time-of-flight mass spectrometry. Moreover, a liquid chromatography with tandem mass spectrometry method was established for simultaneous determination of the Notoginsenoside Fc prototype and its degradation products. Through an in vivo pharmacokinetic study, the pharmacokinetic characteristics were compared between normal rats and pseudo germ-free rats. During the in vitro biotransformation, seven deglycosylated products were detected and identified after incubation in the intestinal bacteria of normal rats. In pseudo germ-free rats, glycosidase activities were significantly decreased, and no obvious degradation occurred. In an in vivo study, the systemic exposure was significantly increased 40%, as evidenced by the area under the blood concentration-time curve from time zero to infinity value and half-life value, which were prolonged more in the pseudo germ-free group than in normal rats. The results demonstrate that patients who use intestinal bacteria-metabolized herbs, such as panax notoginseng, should understand the profile of intestinal bacteria to ensure therapeutic efficacy.