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  • 金丝桃苷

    Hyperoside

    金丝桃苷
    产品编号 CFN98754
    CAS编号 482-36-0
    分子式 = 分子量 C21H20O12 = 464.4
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The herbs of Hypericum perforatum 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
    金丝桃苷 CFN98754 482-36-0 10mg QQ客服:2056216494
    金丝桃苷 CFN98754 482-36-0 20mg QQ客服:2056216494
    金丝桃苷 CFN98754 482-36-0 50mg QQ客服:2056216494
    金丝桃苷 CFN98754 482-36-0 100mg QQ客服:2056216494
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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
  • Universita' Degli Studi Di Cagliari (Italy)
  • University of Medicine and Pharmacy (Romania)
  • Centrum Menselijke Erfelijkheid (Belgium)
  • University of Amsterdam (Netherlands)
  • The Australian National University (Australia)
  • Universidade Federal de Goias (UFG) (Brazil)
  • University of Bordeaux (France)
  • University of Auckland (New Zealand)
  • Ain Shams University (Egypt)
  • University of Stirling (United Kingdom)
  • University of Maryland School of Medicine (USA)
  • Kyoto University (Japan)
  • University Medical Center Mainz (Germany)
  • Korea Food Research Institute(KFRI) (Korea)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Faculty of Chem. & Nat. Resource Eng.2014, 62
  • Indian J Pharm Sci.2022, 84(3):144-151
  • Pharmaceuticals (Basel).2021, 14(7):633.
  • Srinagarind Medical Journal2017, 32(1)
  • Sci Rep.2018, 8(1)
  • J Mol Histol.2019, 50(4):343-354
  • Int J Mol Sci.2022, 23(11):6172.
  • Pharmaceuticals (Basel).2021, 14(8):742.
  • Antioxidants (Basel).2020, 9(2): E119
  • Polytechnic University of Catalonia2017, 105826
  • Key Engineering Materials2022, 931(47-53).
  • Front Immunol.2023, 14:1240800.
  • Sci Adv.2018, 4(10)
  • Exp Parasitol.2015, 153:160-4
  • J Ethnopharmacol.2017, 197:157-164
  • Sci Rep.2018, 8:9267
  • Int J Mol Sci.2022, 23(21):12816.
  • J AOAC Int.2023, 106(1):56-64.
  • International J of Green Pharmacy2019, 13(3)
  • Molecules.2020, 25(11):2599.
  • Am J Chin Med.2016, 44(6):1255-1271
  • Preprints2017, 2017120176
  • Pharmaceuticals (Basel).2022, 15(8):982.
  • ...
  • 生物活性
    Description: Hyperoside, a naturally occuring flavonoid compound, exerts multiple bioactivities, including myocardial protection, anti-redox, neuroprotective, antifungal, hepatoprotective, anti-inflammatory and antioxidative effects. Hyperoside is a potent natural activator of Nur77 receptor, and a potent selective CYP2D6 inhibitor; it inhibited the HMGB1 signaling pathway, and inhibited the PI3K/Akt/Bad/Bcl XL -regulated mitochondrial apoptotic pathway. Hyperoside is a strong inhibitor of HBsAg and HBeAgsecretion in 2.2.15 cells and DHBV-DNA levels in the HBV-infected duck model.
    Targets: ERK | cAMP | NF-kB | TNF-α | Akt | IL Receptor | JNK | P450 (e.g. CYP17) | HBV | Bcl-2/Bax | PI3K | Beta Amyloid | PARP | TNF-α | NOS | COX | HO-1 | Nrf2
    In vitro:
    Int J Mol Sci. 2013 Nov 18;14(11):22697-707.
    Hyperoside downregulates the receptor for advanced glycation end products (RAGE) and promotes proliferation in ECV304 cells via the c-Jun N-terminal kinases (JNK) pathway following stimulation by advanced glycation end-products in vitro.[Pubmed: 24252909]
    Hyperoside is a major active constituent in many medicinal plants which are traditionally used in Chinese medicines for their neuroprotective, anti-inflammatory and antioxidative effects. The molecular mechanisms underlying these effects are unknown.
    METHODS AND RESULTS:
    In this study, quiescent ECV304 cells were treated in vitro with advanced glycation end products (AGEs) in the presence or absence of hyperoside. The results demonstrated that AGEs induced c-Jun N-terminal kinases (JNK) activation and apoptosis in ECV304 cells. Hyperoside inhibited these effects and promoted ECV304 cell proliferation. Furthermore, hyperoside significantly inhibited RAGE expression in AGE-stimulated ECV304 cells, whereas knockdown of RAGE inhibited AGE-induced JNK activation. These results suggested that AGEs may promote JNK activation, leading to viability inhibition of ECV304 cells via the RAGE signaling pathway. These effects could be inhibited by hyperoside.
    CONCLUSIONS:
    Our findings suggest a novel role for hyperoside in the treatment and prevention of diabetes.
    J Agric Food Chem. 2005 Jan 12;53(1):32-7.
    Antifungal activity of camptothecin, trifolin, and hyperoside isolated from Camptotheca acuminata.[Pubmed: 15631505]
    Leaf spots and root rots are major fungal diseases in Camptotheca acuminata that limit cultivation of the plant for camptothecin (CPT), a promising anticancer and antiviral alkaloid.
    METHODS AND RESULTS:
    Bioassays showed that pure CPT and flavonoids (trifolin and hyperoside) isolated from Camptotheca effectively control fungal pathogens in vitro, including Alternaria alternata, Epicoccum nigrum, Pestalotia guepinii, Drechslera sp., and Fusarium avenaceum, although antifungal activity of these compounds in the plant is limited. CPT inhibited mycelial growth by approximately 50% (EC50) at 10-30 microg/mL and fully inhibited growth at 75-125 microg/mL. The flavonoids were less effective than CPT at 50 microg/mL, particularly within 20 days after treatment, but more effective at 100 or 150 microg/mL.
    CONCLUSIONS:
    CPT, trifolin, and hyperoside may serve as leads for the development of fungicides.
    Eur J Pharmacol. 2011 Dec 15;672(1-3):45-55.
    Hyperoside protects primary rat cortical neurons from neurotoxicity induced by amyloid β-protein via the PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway.[Pubmed: 21978835 ]
    Amyloid β-protein (Aβ), which is deposited in neurons as neurofibrillary tangles, is known to exert cytotoxic effects by inducing mitochondrial dysfunction. Additionally, the PI3K/Akt-mediated interaction between Bad and Bcl(XL) plays an important role in maintaining mitochondrial integrity. However, the application of therapeutic drugs, especially natural products in Alzheimer's disease therapy via PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway has not aroused extensive attention.
    METHODS AND RESULTS:
    In the present study, we investigated the neuroprotective effects of Hyperoside, a bioactive flavonoid compound from Hypericum perforatum, on Aβ(25-35)-induced primary cultured cortical neurons, and also examined the potential cellular signaling mechanism for Aβ detoxication. Our results showed that treatment with Hyperoside significantly inhibited Aβ(25-35)-induced cytotoxicity and apoptosis by reversing Aβ-induced mitochondrial dysfunction, including mitochondrial membrane potential decrease, reactive oxygen species production, and mitochondrial release of cytochrome c. Further study indicated that Hyperoside can activate the PI3K/Akt signaling pathway, resulting in inhibition of the interaction between Bad and Bcl(XL), without effects on the interaction between Bad and Bcl-2. Furthermore, Hyperoside inhibited mitochondria-dependent downstream caspase-mediated apoptotic pathway, such as that involving caspase-9, caspase-3, and poly ADP-ribose polymerase (PARP).
    CONCLUSIONS:
    These results demonstrate that Hyperoside can protect Aβ-induced primary cultured cortical neurons via PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway, and they raise the possibility that Hyperoside could be developed into a clinically valuable treatment for Alzheimer's disease and other neuronal degenerative diseases associated with mitochondrial dysfunction.
    In vivo:
    Inflammation. 2015 Apr;38(2):784-99.
    Anti-inflammatory effects of hyperoside in human endothelial cells and in mice.[Pubmed: 25097077]
    High-mobility group box 1 (HMGB1) was recently shown to be an important extracellular mediator of systemic inflammation, and endothelial cell protein C receptor (EPCR) has been shown to be involved in vascular inflammation. Hyperoside is an active compound isolated from Rhododendron brachycarpum G. Don (Ericaceae) that was reported to have anti-oxidant, anti-hyperglycemic, anti-cancer, and anti-coagulant activities.
    METHODS AND RESULTS:
    Here, we show, for the first time, the anti-septic effects of hyperoside in HMGB1-mediated inflammatory responses and on the shedding of EPCR in vitro and in vivo. The data showed that hyperoside posttreatment suppressed lipopolysaccharide (LPS)-mediated release of HMGB1 and HMGB1-mediated cytoskeletal rearrangement. Hyperoside also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in septic mice and phorbol-12-myristate 13-acetate (PMA) of cecal ligation and puncture (CLP)-induced EPCR shedding. In addition, hyperoside inhibited the production of tumor necrosis factor-α (TNF-α) and the HMGB1-mediated activation of Akt, nuclear factor-κB (NF-κB), and extracellular regulated kinase (ERK) 1/2 in HUVECs. Hyperoside also reduced the CLP-induced release of HMGB1, the production of interleukin (IL)-1β, and septic mortality.
    CONCLUSIONS:
    Collectively, these results suggest hyperoside as a candidate therapeutic agent for the treatment of vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1533 mL 10.7666 mL 21.5332 mL 43.0663 mL 53.8329 mL
    5 mM 0.4307 mL 2.1533 mL 4.3066 mL 8.6133 mL 10.7666 mL
    10 mM 0.2153 mL 1.0767 mL 2.1533 mL 4.3066 mL 5.3833 mL
    50 mM 0.0431 mL 0.2153 mL 0.4307 mL 0.8613 mL 1.0767 mL
    100 mM 0.0215 mL 0.1077 mL 0.2153 mL 0.4307 mL 0.5383 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
    槲皮素-3-芸香糖苷-7-葡萄糖苷; Quercetin 3-rutinoside 7-glucoside (Morkotin A) CFN70335 30311-61-6 C33H40O21 = 772.7 10mg QQ客服:2056216494
    槲皮素3-O-刺槐糖苷-7-O-葡萄糖苷; Quercetin 3-O-robinoside-7-O-glucoside CFN91650 115794-37-1 C33H40O21 = 772.66 5mg QQ客服:2056216494
    槲皮素-3,7-二-O-β-D-龙胆双糖苷; Quercetin-3,7-di-O-beta-D-gentiobioside CFN91831 N/A C39H50O27 = 950.8 5mg QQ客服:1457312923
    槲皮素-3'-葡萄糖苷; Quercetin-3'-glucoside CFN95271 19254-30-9 C21H20O12 = 464.4 10mg QQ客服:2159513211
    绣线菊苷; Spiraeoside CFN70300 20229-56-5 C21H20O12 = 464.4 5mg QQ客服:215959384
    槲皮素3,4'-二葡萄糖苷; Quercetin 3,4'-diglucoside CFN70333 29125-80-2 C27H30O17 = 626.5 5mg QQ客服:1413575084
    槲皮素 3,5-双葡萄糖苷; Quercetin 3,5-O-diglucoside CFN95486 206257-35-4 C27H30O17 = 626.5 5mg QQ客服:1457312923
    番石榴苷; Guaijaverin CFN98211 22255-13-6 C20H18O11 = 434.4 20mg QQ客服:215959384
    槲皮素-3-O-β-D-木糖甙; Quercetin 3-O-beta-D-xylopyranoside CFN90718 549-32-6 C20H18O11 = 434.08 10mg QQ客服:2056216494
    槲皮苷; Quercitrin CFN98850 522-12-3 C21H20O11 = 448.4 20mg QQ客服:2159513211

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