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  • 白藜芦醇

    Resveratrol

    白藜芦醇
    产品编号 CFN98791
    CAS编号 501-36-0
    分子式 = 分子量 C14H12O3 = 228.2
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Phenols
    植物来源 The rhizomes of Polygonum cuspidatum Sieb. et Zucc.
    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
    白藜芦醇 CFN98791 501-36-0 10mg QQ客服:1148253675
    白藜芦醇 CFN98791 501-36-0 20mg QQ客服:1148253675
    白藜芦醇 CFN98791 501-36-0 50mg QQ客服:1148253675
    白藜芦醇 CFN98791 501-36-0 100mg QQ客服:1148253675
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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
  • Aarhus University (Denmark)
  • University of Illinois (USA)
  • University of Vienna (Austria)
  • Universidad Miguel Hernández (Spain)
  • CSIRO - Agriculture Flagship (Australia)
  • Vin?a Institute of Nuclear Sciences (Serbia)
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  • University of Dicle (Turkey)
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  • Universidade da Beira Interior (Germany)
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  • Shanghai Institute of Biochemistry and Cell Biology (China)
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  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Neurochem Int.2018, 121:114-124
  • J Ethnopharmacol.2018, 210:88-94
  • J Ginseng Res.2020, 44(4):611-618.
  • Process Biochemistry2019, 85:106-115
  • Kor. J. Pharmacogn.2016, 47(1):62-72
  • Food Chem.2019, 275:746-753
  • RSC Adv.2018, 32621-32636
  • Food Analytical Methods2020, 1-10
  • Korea Institute of Oriental Medicine2020, doi: 10.21203.
  • Acta Physiologiae Plantarum2016, 38:7
  • J Control Release.2021, 336:159-168.
  • J. Food Composition and Anal.2022, V 109:104482.
  • bioRxiv2021, 458409.
  • Food Science and Biotechnology2022, 10.1007.
  • Front Plant Sci.2021, 12:673337.
  • J Ethnopharmacol.2019, 236:31-41
  • Nutrients.2019, 12(1)
  • Sci Rep. 2017, 8207(7)
  • Applied Biological Chemistry2021, 64(4)
  • J Ethnopharmacol.2019, 244:112074
  • Sci Rep.2018, 8:9267
  • Antibiotics.2022, 11(4), 510.
  • Current Traditional Medicine, 2021, 7:326-335(10).
  • ...
  • 生物活性
    Description: Resveratrol, a natural polyphenol that possesses anti-oxidant, anti-inflammatory, cardioprotective, blood-sugar-lowering, antiaging, and anti-cancer properties. It has a wide spectrum of targets including cyclooxygenases(i.e. COX, IC50=1.1 μM), lipooxygenases(LOX, IC50=2.7 μM, kinases, sirtuins, c-IAP1, c-IAP2, livin and XIAP. Resveratrol regulates gene transcription via activation of the stimulus-regulated protein kinases Raf and ERK and the stimulus-responsive transcription factors TCF and Egr-1.
    Targets: MMP(e.g.TIMP) | Akt | Caspase | AMPK | Raf | ERK | NO | NOS | cAMP | PDE | Calcium Channel | LOX | COX | Egr-1 | TCF
    In vitro:
    Environ Mol Mutagen. 2015 Apr;56(3):333-46.
    Resveratrol protects against arsenic trioxide-induced oxidative damage through maintenance of glutathione homeostasis and inhibition of apoptotic progression.[Pubmed: 25339131]
    Arsenic trioxide (As2 O3 ) is commonly used to treat acute promyelocytic leukemia and solid tumors. However, the clinical application of the agent is limited by its cyto- and genotoxic effects on normal cells. Thus, relief of As2 O3 toxicity in normal cells is essentially necessary for improvement of As2 O3 -mediated chemotherapy.
    METHODS AND RESULTS:
    In this study, we have identified a series of protective effects of resveratrol against As2 O3 -induced oxidative damage in normal human bronchial epithelial (HBE) cells. We showed that treatment of HBE cells with resveratrol significantly reduced cellular levels of DNA damage, chromosomal breakage, and apoptosis induced by As2 O3 . The effect of resveratrol against DNA damage was associated with a decreased level of reactive oxygen species and lipid peroxidation in cells treated by As2 O3 , suggesting that resveratrol protects against As2 O3 toxicity via a cellular anti-oxidative stress pathway. Further analysis of the roles of resveratrol demonstrated that it modulated biosynthesis, recycling, and consumption of glutathione (GSH), thereby promoting GSH homeostasis in HBE cells treated by As2 O3 . This was further supported by results showing that resveratrol prevented an increase in the activities and levels of caspases, Fas, Fas-L, and cytochrome c proteins induced by As2 O3 .
    CONCLUSIONS:
    Our study indicates that resveratrol relieves As2 O3 -induced oxidative damage in normal human lung cells via maintenance of GSH homeostasis and suppression of apoptosis.
    Anticancer Res. 2015 Jan;35(1):273-81.
    Resveratrol at anti-angiogenesis/anticancer concentrations suppresses protein kinase G signaling and decreases IAPs expression in HUVECs.[Pubmed: 25550561 ]
    Resveratrol increases nitric oxide (NO) production via increased expression and activation of endothelial-form-NO-synthase (eNOS) in endothelial cells. However, the role of downstream cGMP/protein kinase G (PKG) signaling, a pathway activated by NO/eNOS, in pro- and anti-angiogenic effects of resveratrol is still unclear.
    METHODS AND RESULTS:
    Endogenous NO/cGMP/PKG pathway and downstream cell-survival proteins (Inhibitor of Apoptosis Proteins, IAPs) were studied in relation to pro- and anti-angiogenic effects of resveratrol in human umbilical vein endothelial cells (HUVECs). Resveratrol at higher/anti-angiogenic concentrations inhibits HUVEC tube formation and cell migration/invasion (indices of angiogenesis). Resveratrol at lower concentrations stimulates proliferation and protects HUVECs against spontaneous apoptosis. 8-Br-cGMP, a direct activator of PKG, protects against pro-apoptotic effects of high-concentration resveratrol. Western blot analyses showed that anti-angiogenic concentrations of resveratrol suppress endogenous PKG kinase activity and decrease the expression of four cell-survival proteins, c-IAP1, c-IAP2, livin and XIAP.
    CONCLUSIONS:
    Resveratrol-induced anti-angiogenesis/pro-apoptosis induced suppression of PKG signaling and decreased expression of the cell-survival proteins c-IAP1, c-IAP2, livin and XIAP.
    Biochem Pharmacol . 2016 May 15;108:75-89.
    Baicalein exhibits anti-inflammatory effects via inhibition of NF-κB transactivation[Pubmed: 27019135]
    NF-κB is a crucial mediator of inflammatory and immune responses and a number of phytochemicals that can suppress this immune-regulatory transcription factor are known to have promising anti-inflammatory potential. However, we report that inducer of pro-inflammatory transcription factor NF-κB functions as an anti-inflammatory agent. Our findings reveal that a plant derived flavonoid baicalein could suppress mitogen induced T cell activation, proliferation and cytokine secretion. Treatment of CD4+ T cells with baicalein prior to transfer in to lymphopenic allogenic host significantly suppressed graft versus host disease. Interestingly, addition of baicalein to murine splenic lymphocytes induced DNA binding of NF-κB but did not suppress Concanavalin A induced NF-κB. Since baicalein did not inhibit NF-κB binding to DNA, we hypothesized that baicalein may be suppressing NF-κB trans-activation. Thioredoxin system is implicated in the regulation of NF-κB trans-activation potential and therefore inhibition of thioredoxin system may be responsible for suppression of NF-κB dependent genes. Baicalein not only inhibited TrxR activity in cell free system but also suppressed mitogen induced thioredoxin activity in the nuclear compartment of lymphocytes. Similar to baicalein, pharmacological inhibitors of thioredoxin system also could suppress mitogen induced T cell proliferation without inhibiting DNA binding of NF-κB. Further, activation of cellular thioredoxin system by the use of pharmacological activator or over-expression of thioredoxin could abrogate the anti-inflammatory action of baicalein. We propose a novel strategy using baicalein to limit NF-κB dependent inflammatory responses via inhibition of thioredoxin system.
    Drug Des Devel Ther . 2016 Apr 18;10:1419-41.
    Baicalein suppresses metastasis of breast cancer cells by inhibiting EMT via downregulation of SATB1 and Wnt/β-catenin pathway[Pubmed: 27143851]
    Abstract Background: The flavonoid baicalein, a historically used Chinese herbal medicine, shows a wide range of biological and pharmaceutical effects, among which its potent antitumor activity has raised great interest in recent years. However, the molecular mechanism involved in the antimetastatic effect of baicalein remains poorly understood. This study aimed to verify the inhibitory effects of baicalein on metastasis of MDA-MB-231 human breast cancer cells both in vitro and in vivo, as well as to investigate the related mechanisms. Methods: MTT assay was used to examine the inhibition of baicalein on proliferation of MDA-MB-231 cells. Wound healing assay and the in vitro invasion assay was carried out to investigate the effects of baicalein on migration and invasion of MDA-MB-231 cells, respectively. In order to explore the effects of baicalein on tumor metastasis in vivo, xenograft nude mouse model of MDA-MB-231 cells was established. Animals were randomly divided into four groups (control, therapy group, and low-dose and high-dose prevention group, n=6), and treated with baicalein as designed. Following sacrifice, their lungs and livers were collected to examine the presence of metastases. qRT-PCR and Western blot were performed to study the effects of baicalein on expression of SATB1, EMT-related molecules, and Wnt/β-catenin signaling components of MDA-MB-231 cells as well as the metastatic tissue. Effects of baicalein on the expression of target proteins in vivo were also analyzed by immunohistochemistry. Results: Our results indicated that baicalein suppressed proliferation, migration, and invasion of MDA-MB-231 cells in a time- and dose-dependent manner. Based on assays carried out in xenograft nude mouse model, we found that baicalein inhibited tumor metastasis in vivo. Furthermore, baicalein significantly decreased the expression of SATB1 in MDA-MB-231 cells. It suppressed the expression of vimentin and SNAIL while enhancing the expression of E-cadherin. Baicalein also downregulated the expression of Wnt1 and β-catenin proteins and transcription level of Wnt/β-catenin-targeted genes. Conclusion: Our results demonstrate that baicalein has the potential to suppress breast cancer metastasis, possibly by inhibition of EMT, which may be attributed to downregulation of both SATB1 and the Wnt/β-catenin pathway. Taken together, baicalein may serve as a promising drug for metastasis treatment of breast cancer. Keywords: EMT; SATB1; Wnt/β-catenin pathway; baicalein; breast cancer; metastasis.
    In vivo:
    Biochem Biophys Res Commun. 2015 Feb 27;458(1):86-91.
    Resveratrol restores the circadian rhythmic disorder of lipid metabolism induced by high-fat diet in mice.[Pubmed: 25640840]
    Circadian rhythmic disorders induced by high-fat diet are associated with metabolic diseases. Resveratrol could improve metabolic disorder, but few reports focused on its effects on circadian rhythm disorders in a variety of studies.
    METHODS AND RESULTS:
    The aim of the present study was to analyze the potential effects of resveratrol on high-fat diet-induced disorders about the rhythmic expression of clock genes and clock-controlled lipid metabolism. Male C57BL/6 mice were divided into three groups: a standard diet control group (CON), a high-fat diet (HFD) group and HFD supplemented with 0.1% (w/w) resveratrol (RES). The body weight, fasting blood glucose and insulin, plasma lipids and leptin, whole body metabolic status and the expression of clock genes and clock-controlled lipogenic genes were analyzed at four different time points throughout a 24-h cycle (8:00, 14:00, 20:00, 2:00). Resveratrol, being associated with rhythmic restoration of fasting blood glucose and plasma insulin, significantly decreased the body weight in HFD mice after 11 weeks of feeding, as well as ameliorated the rhythmities of plasma leptin, lipid profiles and whole body metabolic status (respiratory exchange ratio, locomotor activity, and heat production). Meanwhile, resveratrol modified the rhythmic expression of clock genes (Clock, Bmal1 and Per2) and clock-controlled lipid metabolism related genes (Sirt1, Pparα, Srebp-1c, Acc1 and Fas). The response pattern of mRNA expression for Acc1 was similar to the plasma triglyceride.
    CONCLUSIONS:
    All these results indicated that resveratrol reduced lipogenesis and ultimately normalized rhythmic expression of plasma lipids, possibly via its action on clock machinery.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.3821 mL 21.9106 mL 43.8212 mL 87.6424 mL 109.553 mL
    5 mM 0.8764 mL 4.3821 mL 8.7642 mL 17.5285 mL 21.9106 mL
    10 mM 0.4382 mL 2.1911 mL 4.3821 mL 8.7642 mL 10.9553 mL
    50 mM 0.0876 mL 0.4382 mL 0.8764 mL 1.7528 mL 2.1911 mL
    100 mM 0.0438 mL 0.2191 mL 0.4382 mL 0.8764 mL 1.0955 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
    虎杖甙; Polydatin CFN99159 27208-80-6 C20H22O8 = 390.40 20mg QQ客服:3257982914
    白藜芦醇-3-O-β-D-(2''-O-没食子酰)-葡萄糖苷; Pieceid-2''-O-gallate CFN95226 105304-51-6 C27H26O12 = 542.5 10mg QQ客服:3257982914
    二氢藜芦醇; Dihydroresveratrol CFN98987 58436-28-5 C14H14O3 = 230.3 20mg QQ客服:1413575084
    二氢白藜芦醇3-O-葡萄糖甙; Dihydroresveratrol 3-O-glucoside CFN99021 100432-87-9 C20H24O8 = 392.4 5mg QQ客服:2932563308
    去氧土大黄苷元; Desoxyrhapontigenin CFN90854 33626-08-3 C15H14O3 = 242.3 10mg QQ客服:1148253675
    去氧土大黄苷; Desoxyrhaponticin CFN90911 30197-14-9 C21H24O8 = 404.4 20mg QQ客服:215959384
    土大黄苷 6''-O-没食子酸酯; Rhaponticin 6''-O-gallate CFN91099 94356-23-7 C28H28O13 = 572.51 5mg QQ客服:2932563308
    土大黄苷 2''-O-没食子酸酯; Rhaponticin 2''-O-gallate CFN91100 94356-24-8 C28H28O13 = 572.51 5mg QQ客服:2159513211
    2,3,5,4-四羟基二苯乙烯葡萄糖苷; 2,3,5,4'-Tetrahydroxyl diphenylethylene-2-O-glucoside CFN99995 82373-94-2 C20H22O9 = 406.39 20mg QQ客服:1413575084
    松茋; Pinostilbene CFN98662 42438-89-1 C15H14O3 = 242.3 5mg QQ客服:2159513211

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