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  • 漆黄素; 紫铆素

    Butin

    漆黄素; 紫铆素
    产品编号 CFN97736
    CAS编号 492-14-8
    分子式 = 分子量 C15H12O5 = 272.25
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Flavonoids
    植物来源 The seeds of Cassia tora
    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
    漆黄素; 紫铆素 CFN97736 492-14-8 1mg QQ客服:1413575084
    漆黄素; 紫铆素 CFN97736 492-14-8 5mg QQ客服:1413575084
    漆黄素; 紫铆素 CFN97736 492-14-8 10mg QQ客服:1413575084
    漆黄素; 紫铆素 CFN97736 492-14-8 20mg QQ客服:1413575084
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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
  • Michigan State University (USA)
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  • Imperial College London (United Kingdom)
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  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Antioxidants (Basel).2021, 10(10):1620.
  • Molecules.2018, 23(12):E3103
  • Molecules.2020, 25(7):1625.
  • Research Square2021, March 3rd.
  • J Sep Sci.2018, 41(11):2488-2497
  • HortTechnology2016, 26(6):816-819
  • ACS Pharmacol. Transl. Sci.2023, 3c00129.
  • Applied Biological Chemistry2020, 63:37.
  • Molecules.2021, 26(9):2802.
  • J Mass Spectrom.2022, 57(2):e4810.
  • Biol Pharm Bull.2018, 41(1):65-72
  • Plant Physiol Biochem.2023, 201:107795.
  • Food Research International2023, 113792.
  • J Chromatogr B Analyt Technol Biomed Life Sci.2022, 1203:123307.
  • Eur Rev Med Pharmacol Sci.2020, 24(9):5127-5139.
  • Molecules.2020, 25(18),4089.
  • Inflammation.2022, 45(6):2529-2543.
  • Pharmacogn Mag.2015, 11(43):562-6
  • Anal Bioanal Chem.2018, 410(5):1561-1569
  • J. Pharm. Res. Int.2022, 34(58): pp.1-14.
  • Phytomedicine.2019, 61:152813
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  • Journal of Apicultural Research2021, 60(1).
  • ...
  • 生物活性
    Description: Butin has antioxidant activity, can protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction; it attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway.Butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway, enhancing the expression of phosphorylated Akt (active form of Akt), a regulator of OGG1.
    Targets: PI3K | Akt | Nrf2 | ROS | SOD | Calcium Channel | JNK | P450 (e.g. CYP17) | Bcl-2/Bax | Caspase | MAPK
    In vitro:
    J Cell Biochem. 2012 Jun;113(6):1987-97.
    The cytoprotective effect of butin against oxidative stress is mediated by the up-regulation of manganese superoxide dismutase expression through a PI3K/Akt/Nrf2-dependent pathway.[Pubmed: 22253095]
    Butin (7,3',4'-trihydroxydihydroflavone), a flavonoid with antioxidant activity, was recently reported to protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction. The objective of the present study was to elucidate the mechanism by which Butin protects mitochondria.
    METHODS AND RESULTS:
    The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79-4), the addition of Butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF-E2-related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant responsive element (ARE). Butin enhanced the nuclear translocation and ARE-binding activity of Nrf2, which was decreased by H2O2. The siRNA-mediated knockdown of Nrf2 attenuated Butin-induced Mn SOD expression and activity. Further, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) contributed to the ARE-driven Mn SOD expression. Butin activated PI3K/Akt and exposure to either LY294002 (a PI3K inhibitor), Akt inhibitor IV (an Akt-specific inhibitor), or Akt siRNA suppressed the Butin-induced activation of Nrf2, resulting in decreased Mn SOD expression and activity. Finally, the cytoprotective effect of Butin against H2O2-induced cell damage was suppressed by the siRNA-mediated knockdown of Mn SOD.
    CONCLUSIONS:
    These studies demonstrate that Butin attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway.
    Food Chem Toxicol. 2010 Mar;48(3):922-7.
    Butin reduces oxidative stress-induced mitochondrial dysfunction via scavenging of reactive oxygen species.[Pubmed: 20060874]
    This study investigated the cytoprotective effect of butin, a flavonoid, on hydrogen peroxide (H(2)O(2))-induced mitochondrial dysfunction.
    METHODS AND RESULTS:
    Electron spin resonance (ESR) spectrometry revealed butin's significant scavenging effects on superoxide radicals and hydroxyl radicals. When H(2)O(2) was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca(2+) levels that have been induced by H(2)O(2). Furthermore, butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H(2)O(2) treatment.
    CONCLUSIONS:
    We conclude these results suggest butin decreased mitochondrial ROS accumulation, balanced intracellular Ca(2+) levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
    Chem Biol Interact. 2009 Oct 30;181(3):338-42.
    Butin decreases oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1.[Pubmed: 19631197]
    In response to oxidative DNA base damage, oxoguanine glycosylase 1 (OGG1), in a base-excision repair (BER) pathway in mammals, plays a vital role in the repair of 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is a reliable marker of reactive oxygen species (ROS)-induced DNA base modification and contributes to the pathologic process of cancer.Recently, we have shown that butin (7,3',4'-trihydroxydihydroflavone) protects cells against hydrogen peroxide (H2O2)-induced damage of cellular components including DNA.
    METHODS AND RESULTS:
    In the present study, we examined the possible protective effect of butin on oxidative stress-induced DNA base modification, especially 8-OHdG. Hydrogen peroxide significantly increased the level of 8-OHdG, which was detected by 8-OHdG ELISA and confocal microscopy, but butin decreased this level. Suppression of 8-OHdG formation by butin was related to the enhanced mRNA and protein expression of OGG1, which was detected by RT-PCR and Western blot analysis. Butin also increased the transcriptional activity of OGG1, which was suppressed by H2O2 treatment; this transcriptional activity was detected by OGG1 promoter luciferase assay. Butin enhanced the expression of phosphorylated Akt (active form of Akt), a regulator of OGG1, which was decreased by H2O2 treatment.
    CONCLUSIONS:
    A PI3K-specific inhibitor, LY294002, abolished the phosphorylated Akt and OGG1 expressions induced by butin, suggesting that OGG1 induction by butin involves the PI3K/Akt pathway.
    In vivo:
    Sci Rep . 2017 Jan 27;7:41491.
    Protective effect of butin against ischemia/reperfusion-induced myocardial injury in diabetic mice: involvement of the AMPK/GSK-3β/Nrf2 signaling pathway[Pubmed: 28128361]
    Abstract Hyperglycemia-induced reactive oxygen species (ROS) generation contributes to development of diabetic cardiomyopathy (DCM). This study was designed to determine the effect of an antioxidant butin (BUT) on ischemia/reperfusion-induced myocardial injury in diabetic mice. Myocardial ischemia/reperfusion (MI/R) was induced in C57/BL6J diabetes mice. Infarct size and cardiac function were detected. For in vitro study, H9c2 cells were used. To clarify the mechanisms, proteases inhibitors or siRNA were used. Proteins levels were investigated by Western blotting. In diabetes MI/R model, BUT significantly alleviated myocardial infarction and improved heart function, together with prevented diabetes-induced cardiac oxidative damage. The expression of Nrf2, AMPK, AKT and GSK-3β were significantly increased by BUT. Furthermore, in cultured H9c2 cardiac cells silencing Nrf2 gene with its siRNA abolished the BUT's prevention of I/R-induced myocardial injury. Inhibition of AMPK and AKT signaling by relative inhibitor or specific siRNA decreased the level of BUT-induced Nrf2 expression, and diminished the protective effects of BUT. The interplay relationship between GSK-3β and Nrf2 was also verified with relative overexpression and inhibitors. Our findings indicated that BUT protected against I/R-induced ROS-mediated apoptosis by upregulating the AMPK/Akt/GSK-3β pathway, which further activated Nrf2-regulated antioxidant enzymes in diabetic cardiomyocytes exposed to I/R.
    Transl Neurosci . 2018 May 8;9:7-12.
    Butin Attenuates Brain Edema in a Rat Model of Intracerebral Hemorrhage by Anti Inflammatory Pathway[Pubmed: 29755784]
    Abstract Background: This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). Methodology: ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. Result: Neurological scoring significantly increased and hemorrhagic lesion volume decreased in butin treated group of rats compared to ICH group. However, treatment with butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the butin treated group than ICH group. In addition butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. Conclusion: Our study concludes that butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response. Keywords: Brain edema; Butin; Cytokines; Inflammation; Intracerebral hemorrhage.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.6731 mL 18.3655 mL 36.7309 mL 73.4619 mL 91.8274 mL
    5 mM 0.7346 mL 3.6731 mL 7.3462 mL 14.6924 mL 18.3655 mL
    10 mM 0.3673 mL 1.8365 mL 3.6731 mL 7.3462 mL 9.1827 mL
    50 mM 0.0735 mL 0.3673 mL 0.7346 mL 1.4692 mL 1.8365 mL
    100 mM 0.0367 mL 0.1837 mL 0.3673 mL 0.7346 mL 0.9183 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
    黄苏木素; Plathymenin CFN96496 492-12-6 C15H12O6 = 288.25 5mg QQ客服:3257982914
    圣草酚; Eriodictyol CFN99719 552-58-9 C15H12O6 = 288.25 20mg QQ客服:215959384
    7-O-甲基圣草酚; 7-O-Methyleriodictyol CFN98833 51857-11-5 C16H14O6 = 302.3 5mg QQ客服:1413575084
    高圣草素; Homoeriodictyol CFN96489 446-71-9 C16H14O6 = 302.28 5mg QQ客服:1457312923
    槲寄生新甙III; Viscumneoside III CFN89421 118985-27-6 C27H32O15 = 596.53 10mg QQ客服:2056216494
    圣草酚 7,3'-二甲醚; Eriodictyol 7,3'-dimethyl ether CFN89533 54352-60-2 C17H16O6 = 316.30 5mg QQ客服:2159513211
    橙皮素; Hesperetin CFN98842 520-33-2 C16H14O6 = 302.3 20mg QQ客服:215959384
    橙皮素-7-甲醚; Hesperetin-7-methyl ether CFN90876 N/A C17H16O6 = 316.3 10mg QQ客服:1457312923
    圣草酚 7,3',4'-三甲醚; 7,3',4'-Tri-O-methyleriodictyol CFN89491 70987-96-1 C18H18O6 = 330.33 5mg QQ客服:2056216494
    (2S)-5,7,3'4'-四甲氧基二氢黄酮; (2S)-5,7,3',4'-tetramethoxyflavanone CFN95406 74628-43-6 C19H20O6 = 344.4 10mg QQ客服:2159513211

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