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  • 山奈酚

    Kaempferol

    山奈酚
    产品编号 CFN98838
    CAS编号 520-18-3
    分子式 = 分子量 C15H10O6 = 286.2
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The roots of Kaempferia galangal 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
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    山奈酚 CFN98838 520-18-3 10mg QQ客服:2159513211
    山奈酚 CFN98838 520-18-3 20mg QQ客服:2159513211
    山奈酚 CFN98838 520-18-3 50mg QQ客服:2159513211
    山奈酚 CFN98838 520-18-3 100mg QQ客服:2159513211
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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
  • Florida International University (USA)
  • Texas A&M University (USA)
  • Tokyo Woman's Christian University (Japan)
  • University of Wuerzburg (Germany)
  • Tohoku University (Japan)
  • Northeast Normal University Changchun (China)
  • CSIRO - Agriculture Flagship (Australia)
  • University of Brasilia (Brazil)
  • University of British Columbia (Canada)
  • University of Sao Paulo (Brazil)
  • Institute of Bioorganic Chemistry Polish Academy of Sciences (Poland)
  • Sanford Burnham Prebys Medical Discovery Institute (USA)
  • University of Melbourne (Australia)
  • Universidade Federal de Santa Catarina (Brazil)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Mediators Inflamm.2016, 2016:7216912
  • J Pharm Anal.2016, 6(6):363-373
  • Acta Pharmaceutica Hungarica2016, 86:35-40
  • Int J Mol Sci.2017, 18(12)
  • Cell Physiol Biochem.2017, 44(4):1381-1395
  • Korean J of Food Science&Technology 2017, 49(2):146-150
  • Korean J. of Horticultural Sci. & Tech. 2017, 793-804
  • J Hematol Oncol.2018, 11(1):112
  • Int J Mol Sci.2018, 19(9):E2681
  • Korean J of Medicinal Crop Science2018, 220-226
  • Sci Adv.2018, 4(10)
  • J of Health Science and Alternative Medicine2019, 1(1)
  • Nutrients.2019, 11(11):E2694
  • Enzyme Microb Technol.2019, 122:64-73
  • Exp Ther Med.2019, 18(6):4388-4396
  • Molecules.2019, 24(24):E4536
  • Chinese Pharmacological Bulletin2019, 35(8):1120-1125
  • J Food Biochem.2019, 43(9):e12970
  • Korean Journal of Pharmacognosy2019, 50(4):285-290
  • Int J Oncol.2019, 55(1):320-330
  • Antioxidants (Basel).2019, 8(8):E307
  • Planta Med.2019, 85(4):347-355
  • Sci Rep.2019, 9:12132
  • ...
  • 生物活性
    Description: 1. Kaempferol activates LXR-β and suppresses SREBP-1 to enhance symptoms in metabolic syndrome.
    2. Kaempferol exerts a potent inhibitory effect on in vitro bone resorption.
    3. Kaempferol has anti-inflammatory action, can prevent and treat inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis.
    4. Kaempferol has therapeutic potential for the prevention and treatment of thrombovascular diseases, can enhance relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization.
    5. Kaempferol can inhibit cancer cell invasion through blocking the PKCδ/MAPK/AP-1 cascade and subsequent MMP-9 expression and its activity, may act as a therapeutic potential candidate for cancer metastasis.
    6. Kaempferol is an autophagic enhancer, has a more general protection in Parkinson's disease, can mediate antiapoptotic and antioxidant effects is the enhancement of mitochondrial turnover by autophagy.
    Targets: ROS | AP-1 | MMP(e.g.TIMP) | PKC | NO | Autophagy
    In vitro:
    Free Radic Biol Med. 2015 Jun;83:41-53.
    Kaempferol suppresses collagen-induced platelet activation by inhibiting NADPH oxidase and protecting SHP-2 from oxidative inactivation.[Pubmed: 25645952]
    Reactive oxygen species (ROS) generated upon collagen stimulation act as second messengers to propagate various platelet-activating events. Among the ROS-generating enzymes, NADPH oxidase (NOX) plays a prominent role in platelet activation. Thus, NOX has been suggested as a novel target for anti-platelet drug development. Although kaempferol has been identified as a NOX inhibitor, the influence of kaempferol on the activation of platelets and the underlying mechanism have never been investigated. Here, we studied the effects of kaempferol on NOX activation, ROS-dependent signaling pathways, and functional responses in collagen-stimulated platelets.
    METHODS AND RESULTS:
    Superoxide anion generation stimulated by collagen was significantly inhibited by kaempferol in a concentration-dependent manner. More importantly, kaempferol directly bound p47(phox), a major regulatory subunit of NOX, and significantly inhibited collagen-induced phosphorylation of p47(phox) and NOX activation. In accordance with the inhibition of NOX, ROS-dependent inactivation of SH2 domain-containing protein tyrosine phosphatase-2 (SHP-2) was potently protected by kaempferol. Subsequently, the specific tyrosine phosphorylation of key components (Syk, Vav1, Btk, and PLCγ2) of collagen receptor signaling pathways was suppressed by kaempferol. Kaempferol also attenuated downstream responses, including cytosolic calcium elevation, P-selectin surface exposure, and integrin-αIIbβ3 activation. Ultimately, kaempferol inhibited platelet aggregation and adhesion in response to collagen in vitro and prolonged in vivo thrombotic response in carotid arteries of mice.
    CONCLUSIONS:
    This study shows that kaempferol impairs collagen-induced platelet activation through inhibition of NOX-derived ROS production and subsequent oxidative inactivation of SHP-2. This effect suggests that kaempferol has therapeutic potential for the prevention and treatment of thrombovascular diseases.
    Int Immunopharmacol. 2015 Apr 11.
    Kaempferol enhances the suppressive function of Treg cells by inhibiting FOXP3 phosphorylation.[Pubmed: 25870037]
    Kaempferol is a natural flavonoid found in many vegetables and fruits. Epidemiologic studies have described that Kaempferol intake could reduce risk of cancer, especially lung, gastric, pancreatic and ovarian cancers. Recent studies have shown that Kaempferol could also be beneficial to the body to defend against inflammation, and infection by bacteria and viruses; however, the molecular mechanism of its immunoregulatory function remains largely unknown.
    METHODS AND RESULTS:
    Through screening a small molecule library of traditional Chinese medicine (TCM), we identified that Kaempferol could enhance the suppressive function of regulatory T cells (Tregs). Kaempferol was found to increase FOXP3 expression level in Treg cells and prevent pathological symptoms of collagen-induced arthritis in a rat animal model. Kaempferol could also reduce PIM1-mediated FOXP3 phosphorylation at S422.
    CONCLUSIONS:
    Our study reveals a molecular mechanism that underlies the anti-inflammatory action of Kaempferol for the prevention and treatment of inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis.
    Br J Pharmacol. 2015 Jun;172(12):3003-14.
    Kaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca(2+) -activated K(+) channels.[Pubmed: 25652142]
    BACKGROUND AND PURPOSE: Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone.EXPERIMENTAL APPROACH: The effect of kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone. The present study aimed to elucidate the signalling pathway through which this flavonoid enhanced relaxation of vascular smooth muscle.
    METHODS AND RESULTS:
    The effect of kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) relaxing agents was studied in an in vitro organ chamber setup. The whole-cell patch-clamp technique was used to determine the effect of kaempferol on potassium channels in porcine coronary artery smooth muscle cells (PCASMCs). At a concentration without direct effect on vascular tone, kaempferol (3 × 10(-6) M) enhanced relaxations produced by bradykinin and sodium nitroprusside. The potentiation by kaempferol of the bradykinin-induced relaxation was not affected by N(ω)-nitro-L-arginine methyl ester, an inhibitor of NO synthase (10(-4) M) or TRAM-34 plus UCL 1684, inhibitors of intermediate- and small-conductance calcium-activated potassium channels, respectively (10(-6) M each), but was abolished by tetraethylammonium chloride, a non-selective inhibitor of calcium-activated potassium channels (10(-3) M), and iberiotoxin, a selective inhibitor of large-conductance calcium-activated potassium channel (KCa 1.1; 10(-7) M). Iberiotoxin also inhibited the potentiation by kaempferol of sodium nitroprusside-induced relaxations. Kaempferol stimulated an outward-rectifying current in PCASMCs, which was abolished by iberiotoxin.
    CONCLUSIONS:
    The present results suggest that, in smooth muscle cells of the porcine coronary artery, kaempferol enhanced relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization. This vascular effect of kaempferol involved the activation of KCa 1.1 channels.
    In vivo:
    J Nutr Biochem. 2015 Aug;26(8):868-75.
    Kaempferol ameliorates symptoms of metabolic syndrome by regulating activities of liver X receptor-β.[Pubmed: 25959373]
    Kaempferol is a dietary flavonol previously shown to regulate cellular lipid and glucose metabolism. However, its molecular mechanisms of action and target proteins have remained elusive, probably due to the involvement of multiple proteins.
    METHODS AND RESULTS:
    This study investigated the molecular targets of kaempferol. Ligand binding of kaempferol to liver X receptors (LXRs) was quantified by time-resolved fluorescence resonance energy transfer and surface plasmon resonance analyses. Kaempferol directly binds to and induces the transactivation of LXRs, with stronger specificity for the β-subtype (EC50 = 0.33 μM). The oral administration of kaempferol in apolipoprotein-E-deficient mice (150 mg/day/kg body weight) significantly reduced plasma glucose and increased high-density lipoprotein cholesterol levels and insulin sensitivity compared with the vehicle-fed control. Kaempferol also reduced plasma triglyceride concentrations and did not cause liver steatosis, a common side effect of potent LXR activation. In immunoblotting analysis, kaempferol reduced the nuclear accumulation of sterol regulatory element-binding protein-1 (SREBP-1).
    CONCLUSIONS:
    Our results show that the suppression of SREBP-1 activity and the selectivity for LXR-β over LXR-α by kaempferol contribute to the reductions of plasma and hepatic triglyceride concentrations in mice fed kaempferol. They also suggest that kaempferol activates LXR-β and suppresses SREBP-1 to enhance symptoms in metabolic syndrome.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.4941 mL 17.4703 mL 34.9406 mL 69.8812 mL 87.3515 mL
    5 mM 0.6988 mL 3.4941 mL 6.9881 mL 13.9762 mL 17.4703 mL
    10 mM 0.3494 mL 1.747 mL 3.4941 mL 6.9881 mL 8.7352 mL
    50 mM 0.0699 mL 0.3494 mL 0.6988 mL 1.3976 mL 1.747 mL
    100 mM 0.0349 mL 0.1747 mL 0.3494 mL 0.6988 mL 0.8735 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
    Eupalitin; Eupalitin CFN70334 29536-41-2 C17H14O7 = 330.3 5mg QQ客服:215959384
    3,6-二甲氧基芹菜素; 3,6-Dimethoxyapigenin CFN97961 22697-65-0 C17H14O7 = 330.3 5mg QQ客服:1148253675
    4',5-二羟基- 3,6,7-三甲氧基黄酮; Penduletin CFN98957 569-80-2 C18H16O7 = 344.3 5mg QQ客服:2932563308
    草质素; Herbacetin CFN99778 527-95-7 C15H10O7 = 302.24 20mg QQ客服:1148253675
    8-甲氧基山奈酚; 8-甲氧基莰非醇; 8-Methoxykaempferol CFN92382 571-74-4 C16H12O7 = 316.3 5mg QQ客服:2159513211
    3,5,7-三羟基-8,4'-二甲氧基黄酮; Prudomestin CFN98453 3443-28-5 C17H14O7 = 330.3 5mg QQ客服:2932563308
    5,7-二羟基-3,4',8-三甲氧基黄酮; 5,7-Dihydroxy-3,4',8-trimethoxyflavone CFN99666 1570-09-8 C18H16O7 = 344.3 5mg QQ客服:2932563308
    5,7-二乙酰氧基-3,4',8-三甲氧基黄酮; 5,7-Diacetoxy-3,4',8-trimethoxyflavone CFN98818 5128-43-8 C22H20O9 = 428.4 5mg QQ客服:1148253675
    4',5,7-三羟基 3,6,8-三甲氧基黄酮; 4',5,7-Trihydroxy 3,6,8-trimethoxyflavone CFN70413 57393-71-2 C18H16O8 = 360.3 5mg QQ客服:1148253675
    Calycopterin; Calycopterin CFN70374 481-52-7 C19H18O8 = 374.4 5mg QQ客服:1148253675

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