Info: Read More
  • 中药标准品生产商,产品定制服务
  • 莱菔硫烷; 萝卜硫素

    Sulforaphane

    莱菔硫烷; 萝卜硫素
    产品编号 CFN90203
    CAS编号 4478-93-7
    分子式 = 分子量 C6H11NOS2 = 177.29
    产品纯度 >=98%
    物理属性 Oil
    化合物类型 Miscellaneous
    植物来源 The seeds of Brassica oleracea L. var. botrytis 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
    莱菔硫烷; 萝卜硫素 CFN90203 4478-93-7 1mg QQ客服:1457312923
    莱菔硫烷; 萝卜硫素 CFN90203 4478-93-7 5mg QQ客服:1457312923
    莱菔硫烷; 萝卜硫素 CFN90203 4478-93-7 10mg QQ客服:1457312923
    莱菔硫烷; 萝卜硫素 CFN90203 4478-93-7 20mg QQ客服:1457312923
    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
  • Tokyo Woman's Christian University (Japan)
  • Michigan State University (USA)
  • Korea Institute of Oriental Medicine (Korea)
  • University of Beira Interior (Portugal)
  • Universidade Católica Portuguesa (Portugal)
  • University of Maryland School of Medicine (USA)
  • Medizinische Universit?t Wien (Austria)
  • Kyushu University (Japan)
  • Research Unit Molecular Epigenetics (MEG) (Germany)
  • Universitas islam negeri Jakarta (Indonesia)
  • Universidad de Antioquia (Colombia)
  • University of Leipzig (Germany)
  • University of British Columbia (Canada)
  • John Innes Centre (United Kingdom)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Plant Archives2020, 2(1),2929-2934
  • Plant Pathology2022, 10.1111:ppa.13651.
  • Foods.2021, 10(6):1378.
  • Food and Fermentation Industries2018, 44(371)
  • Applied Biological Chem. 2020, 26(63).
  • J Funct Foods2019, 54:449-456
  • Biomolecules.2023, 13(2):227.
  • Food Chem.2020, 332:127412
  • Phytomedicine.2022, 110:154597.
  • Phytomedicine.2015, 22(4):498-503
  • J Traditional Thai Medical Res.2022, 8(1):pp1-14.
  • Int J Mol Sci.2020, 21(19),7070.
  • Int J Mol Sci.2019, 20(3):E651
  • Cytotechnology2022, s10616
  • Chin J Pharm Anal.2019, 39(7):1217-1228
  • J Nat Med.2018, 72(3):734-744
  • Nat Prod Commun.2018, 10.1177
  • Evid Based Complement Alternat Med.2018, 2018:3610494
  • Journal of Functional Foods2022, 96: 105216.
  • Gene.2022, 815:146178.
  • Plant Cell Tiss Org2017, 479-486
  • J Med Food.2020, 23(6):633-640.
  • The Korea Journal of Herbology2016, 29-35
  • ...
  • 生物活性
    Description: Sulforaphane is a cruciferous vegetable-derived isothiocyanate with promising antitumor, chemopreventive and therapeutic activities, it inhibits TPA-induced NF-κB activation and COX-2 expression in MCF-10A cells by blocking two distinct signaling pathways mediated by ERK1/2-IKKα and NAK-IKKβ. Sulforaphane may exert a significant neuroprotective effect on cholinergic deficit and cognitive impairment, it also has anti-inflammatory effect, at least ,in part,associated with interfering with the NF-κB pathway.
    Targets: Akt | ERK | TNF-α | p65 | NF-kB | IkB | COX | Nrf2 | HO-1 | Bcl-2/Bax | Caspase | AChR | IKK
    In vitro:
    J Biosci Bioeng. 2015 Jan;119(1):35-42.
    Sulforaphane down-regulates SKP2 to stabilize p27(KIP1) for inducing antiproliferation in human colon adenocarcinoma cells.[Pubmed: 25070589]
    Sulforaphane is a cruciferous vegetable-derived isothiocyanate with promising chemopreventive and therapeutic activities. Induction of proliferation arrest and apoptosis principally contribute to Sulforaphane's anticancer activity, but the precise molecular mechanisms remain elusive. The oncoprotein SKP2 is a key component of the SKP1-CULLIN1-F-box (SCF) E3 ligase complex and is responsible for directing SCF-mediated degradation of cyclin-dependent kinase inhibitor p27(KIP1) to promote cell proliferation.
    METHODS AND RESULTS:
    We herein provide the first evidence supporting the critical involvement of the SKP2-p27(KIP1) axis in Sulforaphane-induced antiproliferation in various human colon adenocarcinoma cell lines. Specifically, Sulforaphane markedly suppressed the levels of bromodeoxyuridine (BrdU) incorporation and clonogenicity in all tested cell lines, illustrating the antiproliferative effect of Sulforaphane. Of note, Sulforaphane-induced antiproliferation was accompanied with down-regulation of SKP2, leading to the stabilization and thus up-regulation of p27(KIP1). Additionally, Sulforaphane was found to down-regulate SKP2 mainly through transcriptional repression, as Sulforaphane lowered SKP2 mRNA expression and the SKP2 promoter activity. Furthermore, Sulforaphane treatment led to the activation of both AKT and ERK, thus ruling out the possibility that Sulforaphane down-regulates SKP2 by inhibiting AKT or ERK. Notably, Sulforaphane-elicited suppression of BrdU incorporation and clonogenicity were significantly rescued in the context of SKP2 overexpression or p27(KIP1) depletion, therefore highlighting the important role of SKP2 down-regulation and the ensuing stabilization of p27(KIP1) in Sulforaphane-induced antiproliferation.
    CONCLUSIONS:
    Collectively, these data expand our molecular understanding about how Sulforaphane elicits proliferation arrest, but also implicate the application of Sulforaphane in therapeutic modalities targeting SKP2.
    J Nutr Biochem. 2014 Aug;25(8):824-33.
    Sulforaphane reduces vascular inflammation in mice and prevents TNF-α-induced monocyte adhesion to primary endothelial cells through interfering with the NF-κB pathway.[Pubmed: 24880493]
    Sulforaphane, a naturally occurring isothiocyanate present in cruciferous vegetables, has received wide attention for its potential to improve vascular function in vitro. However, its effect in vivo and the molecular mechanism of Sulforaphane at physiological concentrations remain unclear.
    METHODS AND RESULTS:
    Here, we report that a Sulforaphane concentration as low as 0.5 μM significantly inhibited tumor necrosis factor-α (TNF-α)-induced adhesion of monocytes to human umbilical vein endothelial cells, a key event in the pathogenesis of atherosclerosis both in static and under flow conditions. Such physiological concentrations of Sulforaphane also significantly suppressed TNF-α-induced production of monocyte chemotactic protein-1 and adhesion molecules including soluble vascular adhesion molecule-1 and soluble E-selectin, key mediators in the regulation of enhanced endothelial cell-monocyte interaction. Furthermore, Sulforaphane inhibited TNF-α-induced nuclear factor (NF)-κB transcriptional activity, Inhibitor of NF-κB alpha (IκBα) degradation and subsequent NF-κB p65 nuclear translocation in endothelial cells, suggesting that Sulforaphane can inhibit inflammation by suppressing NF-κB signaling. In an animal study, Sulforaphane (300 ppm) in a mouse diet significantly abolished TNF-α-increased ex vivo monocyte adhesion and circulating adhesion molecules and chemokines in C57BL/6 mice. Histology showed that Sulforaphane treatment significantly prevented the eruption of endothelial lining in the intima layer of the aorta and preserved elastin fibers' delicate organization, as shown by Verhoeff-van Gieson staining. Immunohistochemistry studies showed that Sulforaphane treatment also reduced vascular adhesion molecule-1 and monocyte-derived F4/80-positive macrophages in the aorta of TNF-α-treated mice.
    CONCLUSIONS:
    In conclusion, Sulforaphane at physiological concentrations protects against TNF-α-induced vascular endothelial inflammation, in both in vitro and in vivo models. This anti-inflammatory effect of Sulforaphane may be, at least in part, associated with interfering with the NF-κB pathway.
    In vivo:
    Pharmacol Res. 2014 Jul;85:23-32.
    Sulforaphane alleviates scopolamine-induced memory impairment in mice.[Pubmed: 24836869]
    Sulforaphane, an organosulfur compound present in cruciferous vegetables, has been shown to exert neuroprotective effects in experimental in vitro and in vivo models of neurodegeneration.
    METHODS AND RESULTS:
    To determine whether Sulforaphane can preserve cognitive function, we examined its effects on scopolamine-induced memory impairment in mice using the Morris water maze test. Sulforaphane (10 or 50mg/kg) was administered to C57BL/6 mice by oral gavage for 14 days (days 1-14), and memory impairment was induced by intraperitoneal injection of scopolamine (1mg/kg) for 7 days (days 8-14). Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity in the hippocampus and frontal cortex, as indicated by a decreased acetylcholine (ACh) level and an increased acetylcholinesterase (AChE) activity. Sulforaphane significantly attenuated the scopolamine-induced memory impairment and improved cholinergic system reactivity, as indicated by an increased ACh level, decreased AChE activity, and increased choline acetyltransferase (ChAT) expression in the hippocampus and frontal cortex. These effects of Sulforaphane on cholinergic system reactivity were confirmed in vitro. Sulforaphane (10 or 20μM) increased the ACh level, decreased the AChE activity, and increased ChAT expression in scopolamine-treated primary cortical neurons.
    CONCLUSIONS:
    These observations suggest that Sulforaphane might exert a significant neuroprotective effect on cholinergic deficit and cognitive impairment.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.6405 mL 28.2024 mL 56.4048 mL 112.8095 mL 141.0119 mL
    5 mM 1.1281 mL 5.6405 mL 11.281 mL 22.5619 mL 28.2024 mL
    10 mM 0.564 mL 2.8202 mL 5.6405 mL 11.281 mL 14.1012 mL
    50 mM 0.1128 mL 0.564 mL 1.1281 mL 2.2562 mL 2.8202 mL
    100 mM 0.0564 mL 0.282 mL 0.564 mL 1.1281 mL 1.4101 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
    山梨酸; Sorbic acid CFN90061 110-44-1 C6H8O2 = 112.13 20mg QQ客服:2056216494
    正庚醛肟; Heptanal oxime CFN90121 629-31-2 C7H15NO = 129.20 5mg QQ客服:1457312923
    二烯丙基二硫醚; Diallyl disulfide CFN93237 2179-57-9 C6H10S2 = 146.3 20mg QQ客服:2159513211
    大蒜素; Allicin CFN90201 539-86-6 C6H10S2O = 162.27 20mg QQ客服:1413575084
    莱菔硫烷; 萝卜硫素; Sulforaphane CFN90203 4478-93-7 C6H11NOS2 = 177.29 5mg QQ客服:3257982914
    硫辛酸; Lipoic acid CFN99192 62-46-4 C8H14O2S2 = 206.3 20mg QQ客服:1457312923
    顺铂; Cisplatin CFN93261 15663-27-1 Cl2H6N2Pt = 300.05 5mg 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