Info: Read More
  • 中药标准品生产商,产品定制服务
  • 宝藿苷I

    Baohuoside I

    宝藿苷I
    产品编号 CFN98525
    CAS编号 113558-15-9
    分子式 = 分子量 C27H30O10 = 514.52
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The roots of Epimedium brevicornu Maxim
    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
    宝藿苷I CFN98525 113558-15-9 10mg QQ客服:3257982914
    宝藿苷I CFN98525 113558-15-9 20mg QQ客服:3257982914
    宝藿苷I CFN98525 113558-15-9 50mg QQ客服:3257982914
    宝藿苷I CFN98525 113558-15-9 100mg QQ客服:3257982914
    存储与注意事项
    1. 在您收到产品后请检查产品。如无问题,请将产品存入冰霜并且样品瓶保持密封,产品可以存放长达24个月(2-8摄氏度)。

    2. 只要有可能,产品溶解后,您应该在同一天应用于您的实验。 但是,如果您需要提前做预实验,或者需要全部溶解,我们建议您将溶液以等分试样的形式存放在-20℃的密封小瓶中。 通常,这些可用于长达两周。 使用前,打开样品瓶前,我们建议您将产品平衡至室温至少1小时。

    3. 需要更多关于溶解度,使用和处理的建议? 请发送电子邮件至:service@chemfaces.com
    订购流程
  • 1. 在线订购
  • 请联系我们QQ客服

  • 2. 电话订购
  • 请拨打电话:
    027-84237683 或 027-84237783

  • 3. 邮件或传真订购
  • 发送电子邮件到: manager@chemfaces.com 或
    发送传真到:027-84254680

  • 提供订购信息
  • 为了方便客户的订购,请需要订购ChemFaces产品的客户,在下单的时候请提供下列信息,以供我们快速为您建立发货信息。
  •  
  • 1. 产品编号(CAS No.或产品名称)
  • 2. 发货地址
  • 3. 联系方法 (联系人,电话)
  • 4. 开票抬头 (如果需要发票的客户)
  • 5. 发票地址(发货地址与发票地址不同)
  • 发货时间
    1. 付款方式为100%预付款客户,我们将在确认收到货款后当天或1-3个工作日发货。

    2. 付款方式为月结的客户,我们承诺在收到订单后当天或1-3个工作日内发货。

    3. 如果客户所需要的产品,需要重新生产,我们有权告知客户,交货时间需要延期。
    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
  • Chinese University of Hong Kong (China)
  • Istanbul University (Turkey)
  • Biotech R&D Institute (USA)
  • Pennsylvania State University (USA)
  • Guangzhou Institutes of Biomedicine and Health (China)
  • Universidade Católica Portuguesa (Portugal)
  • University of Zurich (Switzerland)
  • Universidad Veracuzana (Mexico)
  • Institute of Tropical Disease Universitas Airlangga (Indonesia)
  • Kyung Hee University (Korea)
  • Massachusetts General Hospital (USA)
  • Cornell University (USA)
  • University of Stirling (United Kingdom)
  • Auburn University (USA)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Mol Pharm.2017, 14(9):3164-3177
  • Pharmacognosy Magazine2017, 13(52):868-874
  • Drug Invention Today2019, 12(6):1303-1306
  • Enzyme Microb Technol.2022, 153:109941.
  • J Anal Methods Chem.2022, 2022:2229500.
  • LWT2021, 138:110630.
  • Food Sci Biotechnol.2021, 30(2):217-226.
  • Molecules.2019, 24(7):E1290
  • Plants (Basel).2020, 9(11):1422.
  • Food Chem.2018, 252:207-214
  • Rev. Chim.2020, 71(3),558-564
  • Russian J Bioorganic Chemistry 2021, 47:1411-1417.
  • Chung Shan Medical University2020, US20200323790A1
  • Int J Mol Med.2015, 35(5):1237-45
  • Enzyme Microb Technol.2019, 122:64-73
  • Biol Pharm Bull.2018, 41(11):1685-1693
  • Sci Rep.2017, 7:46299
  • Mol Med Rep.2022, 25(1):8.
  • J Food Compos Anal2017, 62:197-204
  • Applied Biological Chemistry2020, 63:37.
  • Molecules2022, 27(11):3606.
  • Biochem Pharmacol.2017, 130:10-20
  • J Agric Food Chem.2015, 63(44):9869-78
  • ...
  • 生物活性
    Description: Baohuoside I is a novel immunosuppressive molecule, exhibits antimetastatic, anti-osteoporosis, anti-inflammatory and anti-cancer activities. Baohuoside I can inhibit the proliferation of Eca-109 cells, this effect associats with down-regulation expression of β-catenin,Cyclin D1,Survivin,and their proteins,which affects on the Wnt/β-catenin signaling pathway.
    Targets: CXCR | Wnt/β-catenin | ROS | Bcl-2/Bax | Caspase | JNK | p38MAPK
    In vitro:
    Chinese Traditional & Herbal Drugs, 2011, 42(1):124-6.
    Effect of baohuoside-I on Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109.[Reference: WebLink]
    To study the effect of baohuoside-I extracted from Periplocae Cortex on proliferation and Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109.
    METHODS AND RESULTS:
    The expressions of β-catenin, Cyclin D1, and Survivin protein in Eca-109 cells were measured with flow cytometry (FCM). The expressions of β-catenin, Cyclin D1, and Survivin mRNA were detected by RT-PCR. After treatment with 25 and 50 μg/mL of baohuoside I for 48 h, the expression levels of β-catenin, Cyclin D1, Survivin mRNA, and protein were decreased significantly (P<0.01), but with 12.5 μg/ML of baohuoside I the expression level was not decreased significantly compared with the control group.
    CONCLUSIONS:
    : baohuoside I from Periplocae Cortex could inhibit the proliferation of Eca-109 cells. This effect associais with down-regulation expression of β-catenin, Cyclin D1, Survivin, and their proteins, which affects on the Wnt/β-catenin signaling pathway.
    Chem Biol Interact. 2012 Jul 30;199(1):9-17.
    Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer.[Pubmed: 22687635]
    Baohuoside I (also known as Icariside II) is a flavonoid isolated from Epimedium koreanum Nakai. Although Baohuoside I exhibits anti-inflammatory and anti-cancer activities, its molecular targets/pathways in human lung cancer cells are poorly understood. Therefore, in the present study, we investigated the usefulness of Baohuoside I as a potential apoptosis-inducing cytotoxic agent using human adenocarcinoma alveolar basal epithelial A549 cells as in vitro model.
    METHODS AND RESULTS:
    The apoptosis induced by Baohuoside I in A549 cells was confirmed by annexin V/propidium iodide double staining, cell cycle analysis and dUTP nick end labeling. Further research revealed that Baohuoside I accelerated apoptosis through the mitochondrial apoptotic pathway, involving the increment of BAX/Bcl-2 ratio, dissipation of mitochondrial membrane potential, transposition of cytochrome c, caspase 3 and caspase 9 activation, degradation of poly (ADP-ribose) polymerase and the over-production of reactive oxygen species (ROS). A pan-caspase inhibitor, Z-VAD-FMK, only partially prevented apoptosis induced by Baohuoside I, while NAC, a scavenger of ROS, diminished its effect more potently. In addition, the apoptotic effect of Baohuoside I was dependent on the activation of ROS downstream effectors, JNK and p38(MAPK), which could be almost abrogated by using inhibitors SB203580 (an inhibitor of p38(MAPK)) and SP600125 (an inhibitor of JNK).
    CONCLUSIONS:
    These findings suggested that Baohuoside I might exert its cytotoxic effect via the ROS/MAPK pathway.
    Transplantation. 2004 Sep 27;78(6):831-8.
    Baohuoside-1, a novel immunosuppressive molecule, inhibits lymphocyte activation in vitro and in vivo.[Pubmed: 15385801]
    We evaluated the in vitro and in vivo immunosuppressive effects of Baohuoside I (B1), a novel flavonoid isolated from Epimedium davidii.
    METHODS AND RESULTS:
    Proliferation assay was used to determine the antiproliferative properties on T-cell and B-cell proliferation. Flow cytometry analysis was applied to detect changes of phenotypes on activated cells. B1 inhibits the lymphocyte proliferation activated by polyclonal mitogens and mixed lymphocyte reaction with a 50% inhibitory concentration of low micromolar concentration. Also, B1 suppressed T-cell activation in T cell receptor/CD3-mediated signaling pathways in a dose- and time-dependent manner. The suppression of B1 was not simply a result of a toxic effect and was recovered by withdrawing the drug. B1 down-regulated the expression of some phenotype molecules. In Ca(2+)-independent or -dependent antigen stimulation, although B1 had different inhibitive patterns on CD69 expression stimulated by phorbol 12-myristate 13-acetate (PMA) or Ca2+ ionophore, it inhibited T-cell proliferation induced by CD3/CD28 or PMA/ionomycin and partially blocked that induced by PMA/CD28. Interestingly, an additive inhibition between B1 and tacrolimus (FK506) was found in the CD69 expression stimulated by PMA/CD28 and PMA/ionomycin. Similarly, this immunosuppression by combination therapy was observed in a heart transplantation model in vivo and might act through an immunosuppressive mechanism different from FK506.
    CONCLUSIONS:
    B1, whose mechanism of action is not similar to that of FK506, has selectively immunosuppressive effects on T-cell and B-cell activation in vitro and effectively prevents rat heart allograft rejection in vivo.
    Biochemistry . 2014 Dec 9;53(48):7562-9.
    Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression[Pubmed: 25407882]
    Abstract More than 90 percent of cancer-mediated deaths are due to metastasis, but the mechanisms that control metastasis remain poorly understood. Thus, the therapy targeting this process has been challenged constantly, but no therapy has yet been approved. CXC chemokine receptor 4 (CXCR4), a Gi protein-coupled receptor for the CXC chemokine ligand (CXCL) 12/stromal cell derived factor (SDF) 1α, is known to be expressed in various tumors. Recently, the CXCL12/CXCR4 axis has emerged as a key mediator of tumor metastasis; therefore, the possibility that identification of CXCR4 inhibitors can be a promising strategy for abrogating metastasis has been considered. In this report, we investigate baohuoside I, a component of Epimedium koreanum, as a regulator of CXCR4 expression as well as function in cervical cancer and breast cancer cells. We observed that baohuoside I downregulated CXCR4 expression in a dose- and time-dependent manner in HeLa cells. Treatment with a pharmacological proteasome and lysosomal inhibitors did not have a substantial effect on baohuoside I's ability to suppress CXCR4 expression. When we investigated the molecular mechanism of action, it was observed that the suppression of CXCR4 expression occurred at the level of mRNA. The decrease in the level of CXCR4 expression caused by baohuoside I was correlated with inhibition of the CXCL12-induced invasion of both cervical and breast cancer cells. Overall, our results show that baohuoside I exerts its antimetastatic effect through the downregulation of CXCR4 expression and, thus, has the potential to play a role in the suppression of cancer metastasis.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.9436 mL 9.7178 mL 19.4356 mL 38.8712 mL 48.589 mL
    5 mM 0.3887 mL 1.9436 mL 3.8871 mL 7.7742 mL 9.7178 mL
    10 mM 0.1944 mL 0.9718 mL 1.9436 mL 3.8871 mL 4.8589 mL
    50 mM 0.0389 mL 0.1944 mL 0.3887 mL 0.7774 mL 0.9718 mL
    100 mM 0.0194 mL 0.0972 mL 0.1944 mL 0.3887 mL 0.4859 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
    朝藿苷E; Caohuoside E CFN95016 174286-23-8 C43H54O22 = 922.9 5mg QQ客服:3257982914
    朝藿定K; Epimedin K CFN95019 174286-13-6 C45H56O23 = 964.9 5mg QQ客服:1457312923
    淫羊藿次苷; Icariside I CFN92550 56725-99-6 C27H30O11 = 530.5 20mg QQ客服:3257982914
    茂藿苷A; Maohuoside A CFN98523 128988-55-6 C27H32O12 = 548.5 5mg QQ客服:1457312923
    大花淫羊藿苷F; Ikarisoside F CFN90138 113558-14-8 C31H36O14 = 632.62 5mg QQ客服:2159513211
    淫羊藿属苷A; Epimedoside A CFN90762 39012-04-9 C32H38O15 = 662.7 10mg QQ客服:3257982914
    宝藿苷V; Baohuoside V CFN90763 118544-18-6 C38H48O19 = 808.8 5mg QQ客服:215959384
    宝藿苷I; Baohuoside I CFN98525 113558-15-9 C27H30O10 = 514.52 20mg QQ客服:215959384
    箭藿苷B; Sagittatoside B CFN90211 118525-36-3 C32H38O14 = 646.64 10mg QQ客服:2056216494
    2''-O-鼠李糖基淫羊藿次苷II; 2''-O-Rhamnosylicariside II CFN92551 135293-13-9 C33H40O14 = 660.7 10mg QQ客服:3257982914

    信息支持


    公司简介
    订购流程
    付款方式
    退换货政策

    ChemFaces提供的产品仅用于科学研究使用,不用于诊断或治疗程序。

    联系方式


    电机:027-84237783
    传真:027-84254680
    在线QQ: 1413575084
    E-Mail:manager@chemfaces.com

    湖北省武汉沌口经济技术开区车城南路83号1号楼第三层厂房


    ChemFaces为科学家,科研人员与企业提供快速的产品递送。我们通过瑞士SGS ISO 9001:2008质量体系认证天然化合物与对照品的研发和生产