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  • 牛蒡子苷元

    Arctigenin

    牛蒡子苷元
    产品编号 CFN99534
    CAS编号 7770-78-7
    分子式 = 分子量 C21H24O6 = 372.41
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Lignans
    植物来源 The roots of Arctium lappa L.
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
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    牛蒡子苷元 CFN99534 7770-78-7 10mg QQ客服:215959384
    牛蒡子苷元 CFN99534 7770-78-7 20mg QQ客服:215959384
    牛蒡子苷元 CFN99534 7770-78-7 50mg QQ客服:215959384
    牛蒡子苷元 CFN99534 7770-78-7 100mg QQ客服:215959384
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • Universidade da Beira Interior (Germany)
  • Copenhagen University (Denmark)
  • Periyar University (India)
  • Universidade Federal de Pernambuco (UFPE) (Brazil)
  • National Cancer Center Research Institute (Japan)
  • Sapienza University of Rome (Italy)
  • Universidade Federal de Santa Catarina (Brazil)
  • MTT Agrifood Research Finland (Finland)
  • Tohoku University (Japan)
  • Korea Intitute of Science and Technology (KIST) (Korea)
  • Sanford Burnham Prebys Medical Discovery Institute (USA)
  • Kyushu University (Japan)
  • University of Madras (India)
  • Universidad Industrial de Santander (Colombia)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Korean j.of Pharm.2017, 70-76
  • J Sep Sci.2018, 41(9):1938-1946
  • Pharmaceuticals.2022, 15(4), 402.
  • United States Patent Application2020, 20200038363
  • Ecol Evol.2022, 12(11):e9459.
  • Int. Conference on Med. Sci. and Bio.2017, 17973
  • Int J Mol Sci.2019, 20(11):E2734
  • Front Pharmacol.2021, 12:635510.
  • Curr Res Virol Sci.2022, 3:100019.
  • J Pharm Biomed Anal.2022, 207:114398.
  • Acta Agriculturae Scandinavica2015, 381-383
  • Molecules.2020, 25(9):2111.
  • Korean J. Medicinal Crop Sci.2022, 30(2):117-123.
  • Plants (Basel).2021, 10(4):702.
  • J of Applied Biological Chem.2020, 63(2):147-152
  • Journal of Molecular Liquids2021, 334:116014.
  • Environ Toxicol.2020, doi: 10.1002
  • Molecules.2019, 24(19):E3417
  • Foods.2023, 12(12):2412.
  • Applied Biological Chemistry 2022, 65,5(2022).
  • Food Science and Biotechnology2022, 10.1007.
  • Antioxidants (Basel).2020, 9(6):544.
  • J Cell Mol Med.2021, 25(5):2645-2654.
  • ...
  • 生物活性
    Description: Arctigenin has anti-tumor, anti-inflammation, antioxidative , neuroprotection, and endurance enhancement effects; it efficiently enhances rat swimming endurance by elevation of the antioxidant capacity of the skeletal muscles, which has thereby highlighted the potential of this natural product as an antioxidant in the treatment of fatigue and related diseases. Arctigenin as a potent indirect activator of AMPK via inhibition of respiratory complex I, with beneficial effects on metabolic disorders in ob/ob mice, this highlights the potential value of arctigenin as a possible treatment of type 2 diabetes.
    Targets: AMPK | PPAR | p53 | Nrf2 | PI3K | Akt | Caspase | mTOR | MAPK | HO-1 | NOS | TNF-α | IL Receptor | IkB | p65 | NF-kB | IKK
    In vitro:
    Cancer Res. 2006 Feb 1;66(3):1751-7.
    Identification of arctigenin as an antitumor agent having the ability to eliminate the tolerance of cancer cells to nutrient starvation.[Pubmed: 16452235]
    Tumor cells generally proliferate rapidly and the demand for essential nutrients as well as oxygen always exceeds the supply due to the unregulated growth and the insufficient and inappropriate vascular supply. However, cancer cells show an inherent ability to tolerate extreme conditions, such as that characterized by low nutrient and oxygen supply, by modulating their energy metabolism.
    METHODS AND RESULTS:
    Thus, targeting nutrient-deprived cancer cells may be a novel strategy in anticancer drug development. Based on that, we established a novel screening method to discover anticancer agents that preferentially inhibit cancer cell viability under the nutrient-deprived condition. After screening 500 medicinal plant extracts used in Japanese Kampo medicine, we found that a CH(2)Cl(2)-soluble extract of Arctium lappa exhibited 100% preferential cytotoxicity under the nutrient-deprived condition at a concentration of 50 microg/mL with virtually no cytotoxicity under nutrient-rich condition. Further bioassay-guided fractionation and isolation led to the isolation of arctigenin as the primary compound responsible for such preferential cytotoxicity; the compound exhibited 100% preferential cytotoxicity against nutrient-deprived cells at a concentration of 0.01 microg/mL. Furthermore, arctigenin was also found to strongly suppress the PANC-1 tumor growth in nude mice, as well as the growth of several of the tested pancreatic cancer cell lines, suggesting the feasibility of this novel antiausterity approach in cancer therapy.
    CONCLUSIONS:
    Further investigation of the mechanism of action of arctigenin revealed that the compound blocked the activation of Akt induced by glucose starvation, which is a key process in the tolerance exhibited by cancer cells to glucose starvation.
    In vivo:
    Acta Pharmacol Sin. 2014 Oct;35(10):1274-84.
    Arctigenin enhances swimming endurance of sedentary rats partially by regulation of antioxidant pathways.[Pubmed: 25152028]
    Arctigenin, a phenylpropanoid dibenzylbutyrolactone lignan found in traditional Chinese herbs, has been determined to exhibit a variety of pharmacological activities, including anti-tumor, anti-inflammation, neuroprotection, and endurance enhancement. In the present study, we investigated the antioxidation and anti-fatigue effects of arctigenin in rats.
    METHODS AND RESULTS:
    Rat L6 skeletal muscle cell line was exposed to H2O2 (700 μmol/L), and ROS level was assayed using DCFH-DA as a probe. Male SD rats were injected with arctigenin (15 mg·kg(-1)·d(-1), ip) for 6 weeks, and then the weight-loaded forced swimming test (WFST) was performed to evaluate their endurance. The levels of antioxidant-related genes in L6 cells and the skeletal muscles of rats were analyzed using real-time RT-PCR and Western blotting. Incubation of L6 cells with arctigenin (1, 5, 20 μmol/L) dose-dependently decreased the H2O2-induced ROS production. WFST results demonstrated that chronic administration of arctigenin significantly enhanced the endurance of rats. Furthermore, molecular biology studies on L6 cells and skeletal muscles of the rats showed that arctigenin effectively increased the expression of the antioxidant-related genes, including superoxide dismutase (SOD), glutathione reductase (Gsr), glutathione peroxidase (GPX1), thioredoxin (Txn) and uncoupling protein 2 (UCP2), through regulation of two potential antioxidant pathways: AMPK/PGC-1α/PPARα in mitochondria and AMPK/p53/Nrf2 in the cell nucleus.
    CONCLUSIONS:
    Arctigenin efficiently enhances rat swimming endurance by elevation of the antioxidant capacity of the skeletal muscles, which has thereby highlighted the potential of this natural product as an antioxidant in the treatment of fatigue and related diseases.
    Int Immunopharmacol. 2014 Dec;23(2):505-15.
    Arctigenin but not arctiin acts as the major effective constituent of Arctium lappa L. fruit for attenuating colonic inflammatory response induced by dextran sulfate sodium in mice.[Pubmed: 25284342]
    The crude powder of the fruit of Arctium lappa L. (ALF) has previously been reported to attenuate experimental colitis in mice. But, its main effective ingredient and underlying mechanisms remain to be identified.
    METHODS AND RESULTS:
    In this study, ALF was extracted with ethanol, and then successively fractionated into petroleum ether, ethyl acetate, n-butanol and water fraction. Experimental colitis was induced by dextran sulfate sodium (DSS) in mice. Among the four fractions of ALF, the ethyl acetate fraction showed the most significant inhibition of DSS-induced colitis in mice. The comparative studies of arctigenin and arctiin (the two main ingredients of ethyl acetate fraction) indicated that arctigenin rather than arctiin could reduce the loss of body weight, disease activity index and histological damage in the colon. Arctigenin markedly recovered the loss of intestinal epithelial cells (E-cadherin-positive cells) and decreased the infiltration of neutrophils (MPO-positive cells) and macrophages (CD68-positive cells). Arctigenin could down-regulate the expressions of TNF-α, IL-6, MIP-2, MCP-1, MAdCAM-1, ICAM-1 and VCAM-1 at both protein and mRNA levels in colonic tissues. Also, it markedly decreased the MDA level, but increased SOD activity and the GSH level. Of note, the efficacy of arctigenin was comparable or even superior to that of the positive control mesalazine. Moreover, it significantly suppressed the phosphorylation of MAPKs and the activation of NF-κB, including phosphorylation of IκBα and p65, p65 translocation and DNA binding activity.
    CONCLUSIONS:
    In conclusion, arctigenin but not arctiin is the main active ingredient of ALF for attenuating colitis via down-regulating the activation of MAPK and NF-κB pathways.
    Diabetologia. 2012 May;55(5):1469-81.
    Arctigenin, a natural compound, activates AMP-activated protein kinase via inhibition of mitochondria complex I and ameliorates metabolic disorders in ob/ob mice.[Pubmed: 22095235 ]
    Arctigenin is a natural compound that had never been previously demonstrated to have a glucose-lowering effect. Here it was found to activate AMP-activated protein kinase (AMPK), and the mechanism by which this occurred, as well as the effects on glucose and lipid metabolism were investigated.
    METHODS AND RESULTS:
    2-Deoxyglucose uptake and AMPK phosphorylation were examined in L6 myotubes and isolated skeletal muscle. Gluconeogenesis and lipid synthesis were evaluated in rat primary hepatocytes. The acute and chronic effects of arctigenin on metabolic abnormalities were observed in C57BL/6J and ob/ob mice. Changes in mitochondrial membrane potential were measured using the J-aggregate-forming dye, JC-1. Analysis of respiration of L6 myotubes or isolated mitochondria was conducted in a channel oxygen system. Arctigenin increased AMPK phosphorylation and stimulated glucose uptake in L6 myotubes and isolated skeletal muscles. In primary hepatocytes, it decreased gluconeogenesis and lipid synthesis. The enhancement of glucose uptake and suppression of hepatic gluconeogenesis and lipid synthesis by arctigenin were prevented by blockade of AMPK activation. The respiration of L6 myotubes or isolated mitochondria was inhibited by arctigenin with a specific effect on respiratory complex I. A single oral dose of arctigenin reduced gluconeogenesis in C57BL/6J mice. Chronic oral administration of arctigenin lowered blood glucose and improved lipid metabolism in ob/ob mice.
    CONCLUSIONS:
    This study demonstrates a new role for arctigenin as a potent indirect activator of AMPK via inhibition of respiratory complex I, with beneficial effects on metabolic disorders in ob/ob mice. This highlights the potential value of arctigenin as a possible treatment of type 2 diabetes.
    Front Immunol . 2021 Jul 19;12:691590.
    Arctigenin Exerts Neuroprotective Effect by Ameliorating Cortical Activities in Experimental Autoimmune Encephalomyelitis In Vivo[Pubmed: 34349758]
    Abstract Multiple sclerosis (MS) is a chronic disease in the central nervous system (CNS), characterized by inflammatory cells that invade into the brain and the spinal cord. Among a bulk of different MS models, the most widely used and best understood rodent model is experimental autoimmune encephalomyelitis (EAE). Arctigenin, a botanical extract from Arctium lappa, is reported to exhibit pharmacological properties, including anti-inflammation and neuroprotection. However, the effects of arctigenin on neural activity attacked by inflammation in MS are still unclear. Here, we use two-photon calcium imaging to observe the activity of somatosensory cortex neurons in awake EAE mice in vivo and found added hyperactive cells, calcium influx, network connectivity, and synchronization, mainly at preclinical stage of EAE model. Besides, more silent cells and decreased calcium influx and reduced network synchronization accompanied by a compensatory rise in functional connectivity are found at the remission stage. Arctigenin treatment not only restricts inordinate individually neural spiking, calcium influx, and network activity at preclinical stage but also restores neuronal activity and communication at remission stage. In addition, we confirm that the frequency of AMPA receptor-mediated spontaneous excitatory postsynaptic current (sEPSC) is also increased at preclinical stage and can be blunted by arctigenin. These findings suggest that excitotoxicity characterized by calcium influx is involved in EAE at preclinical stage. What is more, arctigenin exerts neuroprotective effect by limiting hyperactivity at preclinical stage and ameliorates EAE symptoms, indicating that arctigenin could be a potential therapeutic drug for neuroprotection in MS-related neuropsychological disorders.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.6852 mL 13.4261 mL 26.8521 mL 53.7043 mL 67.1303 mL
    5 mM 0.537 mL 2.6852 mL 5.3704 mL 10.7409 mL 13.4261 mL
    10 mM 0.2685 mL 1.3426 mL 2.6852 mL 5.3704 mL 6.713 mL
    50 mM 0.0537 mL 0.2685 mL 0.537 mL 1.0741 mL 1.3426 mL
    100 mM 0.0269 mL 0.1343 mL 0.2685 mL 0.537 mL 0.6713 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    表去甲络石甙元; Epinortrachelogenin CFN92816 125072-69-7 C20H22O7 = 374.4 5mg QQ客服:2159513211
    牛蒡子苷元; Arctigenin CFN99534 7770-78-7 C21H24O6 = 372.41 20mg QQ客服:1457312923
    牛蒡子苷; Arctiin CFN99991 20362-31-6 C27H34O11 = 534.55 20mg QQ客服:2056216494
    牛蒡子苷元-4'-O-β-龙胆二糖苷; Arctigenin 4'-O-beta-gentiobioside CFN90714 41682-24-0 C33H44O16 = 696.69 5mg QQ客服:3257982914
    罗汉松脂苷; Matairesinoside CFN89301 23202-85-9 C26H32O11 = 520.53 10mg QQ客服:1413575084
    罗汉松树脂酚-4'-O-β-龙胆二糖苷; Matairesinol 4'-O-beta-gentiobioside CFN90715 106647-14-7 C32H42O16 = 682.25 10mg QQ客服:215959384
    (-)-Haplomyrfolin; (-)-Haplomyrfolin CFN92253 85404-48-4 C20H20O6 = 356.4 5mg QQ客服:1413575084
    Kusunokinin; Kusunokinin CFN92254 58311-20-9 C21H22O6 = 370.4 5mg QQ客服:2056216494
    裂榄脂素; Bursehernin CFN92058 40456-51-7 C21H22O6 = 370.4 5mg QQ客服:1457312923
    (-)-扁柏脂素,荜澄茄内脂; (-)-Hinokinin CFN92255 26543-89-5 C20H18O6 = 354.4 5mg QQ客服:3257982914

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