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  • 毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷

    Calycosin-7-O-beta-D-glucoside

    毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷
    产品编号 CFN99141
    CAS编号 20633-67-4
    分子式 = 分子量 C22H22O10 = 446.40
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Flavonoids
    植物来源 The herbs of Astragalus membranaceus Bge. var. mongholicus.
    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
    毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷 CFN99141 20633-67-4 10mg QQ客服:3257982914
    毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷 CFN99141 20633-67-4 20mg QQ客服:3257982914
    毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷 CFN99141 20633-67-4 50mg QQ客服:3257982914
    毛蕊异黄酮-7-O-beta-D-葡萄糖苷; 毛蕊异黄酮苷 CFN99141 20633-67-4 100mg QQ客服:3257982914
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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
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  • University of Beira Interior (Portugal)
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  • John Innes Centre (United Kingdom)
  • Medical University of Gdansk (Poland)
  • Charles University in Prague (Czech Republic)
  • Julius Kühn-Institut (Germany)
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  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Medicinal Chemistry Research 2021, 30:1117-1124.
  • J. Soc. Cosmet. Sci. Korea2021, 47(1):57-63
  • Nutrients2020, 12(2):488
  • Nutrients.2019, 12(1)
  • BMC Complement Med Ther.2023, 23(1):264.
  • Korean J Acupunct2020, 37:104-121
  • Biochem Biophys Res Commun.2018, 495(1):1271-1277
  • Toxicol In Vitro.2023, 86:105521.
  • Metab Eng.2022, 75:143-152.
  • Horticulturae2020, 6(4),76.
  • Phytomedicine Plus2022, 2(1):100207.
  • Microchemical Journal2022, 182: 107874.
  • Front Pharmacol.2021, 12:764297.
  • Planta Med.2022, a-1876-3009.
  • Neurochem Res.2021, s11064-021-03449-0
  • J Cancer.2019, 10(23):5843-5851
  • Pharmacol Rep.2022, 74(1):175-188.
  • Korean Herb. Med. Inf. 2016, 4(1):35-42
  • J Sci Food Agric.2018, 98(3):1153-1161
  • Br J Pharmacol.2020, 10.1111
  • Journal of Food Hygiene and Safety2019, 34(5):413-420
  • J Ethnopharmacol.2018, 210:88-94
  • Phytomedicine.2018, 40:37-47
  • ...
  • 生物活性
    Description: Calycosin-7-O-beta-D-glucoside, a melanin biosynthesis inhibitor, can protect BBB integrity in experimental cerebral ischemia–reperfusion injury via regulating NO/cav-1/MMPs pathway. It attenuates ischemia-reperfusion injuryin vivovia activation of the PI3K/Akt pathway, and has effects on cell apoptosis in cervical cancer HeLa cells and expression of Bcl-2/Bax.
    Targets: NO | MMP(e.g.TIMP) | Bcl-2/Bax | PI3K | VEGFR | Akt | Rho | ROCK | Caspase | ROS
    In vitro:
    Bmc Compl. Altern. M., 2015, 15(1):1-11.
    Calycosin-7-O-β-D-glucoside promotes oxidative stress-induced cytoskeleton reorganization through integrin-linked kinase signaling pathway in vascular endothelial cells.[Pubmed: 26346982 ]
    Dysfunction of vascular endothelium is implicated in many pathological situations. Cytoskeleton plays an importance role in vascular endothelial permeability barrier and inflammatory response. Many Chinese herbs have the endothelial protective effect, of which, "Astragalus membranaceus" is a highly valued herb for treatment of cardiovascular and renal diseases in traditional Chinese medicine, In this study, we tested whether calycosin-7-O-β-D-glucoside (Calycosin), a main effective monomer component of "Astragalus membranaceus", could protect endothelial cells from bacterial endotoxin (LPS)-induced cell injury.
    METHODS AND RESULTS:
    Endothelial cell injury was induced by exposing human umbilical vein endothelial cells (HUVECs) to LPS. The effects of calycosin on LPS-induced changes in cell viability, apoptosis rate, cell migration, nitric oxide synthase (NOS), generationof intracellular reactive oxygen species (ROS) and cytoskeleton organization were determined. Microarray assay was employed to screen the possible gene expression change. Based on the results of microarray assay, the expression profile of genes involved in Rho/ROCK pathway and AKT pathway were further evaluated with quantitative real-time RT-PCR or western blot methods. Calycosin improved cell viability, suppressed apoptosis and protected the cells from LPS-induced reduction in cell migration and generation of ROS, protein level of NOS at a comparable magnitude to that of Y27632 and valsartan. Similar to Y27632 and valsartan, Calycosin, also neutralized LPS-induced actomyosin contraction and vinculin protein aggregation. Microarray assay, real-time PCR and western blot results revealed that LPS induced expression of FN, ITG A5, RhoA, PI3K (or PIP2 in western blotting), FAK, VEGF and VEGF R2, and inhibited expression of MLCP. We believed multiple pathways involved in the regulation of calycosin on HUVECs. Calycosin are considered to be able to activate MLCP through promoting the generation of NO, decreasing PMLC, suppressing the cytoskeleton remodeling caused by activation of Rho/ROCK pathway and inhibiting AKT pathway by decreasing VEGF, VEGF R2 and PI3K level.
    CONCLUSIONS:
    Calycosin protected HUVEC from LPS-induced endothelial injury, possibly through suppression of Rho/ROCK pathway and regulation of AKT pathway.
    Neural Plast . 2019 Dec 1;2019:8798069.
    Calycosin-7- O- β- D-glucoside Attenuates OGD/R-Induced Damage by Preventing Oxidative Stress and Neuronal Apoptosis via the SIRT1/FOXO1/PGC-1 α Pathway in HT22 Cells[Pubmed: 31885537]
    Abstract Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke.
    Neural Plast . 2019 Dec 1;2019:8798069.
    Calycosin-7- O- β- D-glucoside Attenuates OGD/R-Induced Damage by Preventing Oxidative Stress and Neuronal Apoptosis via the SIRT1/FOXO1/PGC-1 α Pathway in HT22 Cells[Pubmed: 31885537]
    Abstract Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke.
    In vivo:
    Mol Med Rep. 2016 Jan; 13(1): 633–640.
    Calycosin-7-O-β-d-glucoside attenuates ischemia-reperfusion injury in vivo via activation of the PI3K/Akt pathway[Pubmed: 26648122]
    The aim of the present study was to investigate the effects and mechanisms of calycosin‑7‑O‑β‑D‑glucoside (CG) on ischemia‑reperfusion (I/R) injury in vivo.
    METHODS AND RESULTS:
    Hemodynamic parameters, including ejection fraction (EF), fractional shortening (FS), left ventricular end‑systolic pressure (LVESP) and left ventricular end‑diastolic pressure (LVEDP) were monitored using an ultrasound system, and infarct size was measured using Evans blue/tetrazolium chloride double staining. The activities of serum creatine kinase (CK), lactate dehydrogenase (LDH) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) were determined to assess the degree of myocardial injury and oxidative stress‑induced damage. The protein expression levels of cleaved‑caspase‑3, cleaved‑caspase‑9, phosphorylated (p)‑phosphatidylinositol 3‑kinase (PI3K) p85, PI3K p85, p‑Akt and Akt were determined using western blotting. The results demonstrated that pretreatment with high dose (H)‑CG markedly improved cardiac function, as evidenced by upregulated EF, FS and LVESP, and downregulated LVEDP. In addition, administration of CG resulted in significant decreases in infarct size in the I/R+low dose‑CG and I/R+H‑CG groups, compared with the I/R group. The activities of CK and LDH, and the levels of MDA in the I/R+H‑CG group were reduced, compared with those in the I/R group, whereas SOD activity was elevated. Treatment with CG inhibited the cleavage and activity of caspase‑3 and caspase‑9, and enhanced the phosphorylation of PI3K p85 and Akt. Notably, administration of the PI3K inhibitor, LY294002, markedly lowered the levels of p‑PI3K p85/p‑Akt, and eradicated the inhibitory effects of H‑CG on infarct size, myocardial injury and oxidative stress‑induced damage.
    CONCLUSIONS:
    Taken together, the results suggested that CG may alleviate I/R injury by activating the PI3K/Akt signaling pathway.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.2401 mL 11.2007 mL 22.4014 mL 44.8029 mL 56.0036 mL
    5 mM 0.448 mL 2.2401 mL 4.4803 mL 8.9606 mL 11.2007 mL
    10 mM 0.224 mL 1.1201 mL 2.2401 mL 4.4803 mL 5.6004 mL
    50 mM 0.0448 mL 0.224 mL 0.448 mL 0.8961 mL 1.1201 mL
    100 mM 0.0224 mL 0.112 mL 0.224 mL 0.448 mL 0.56 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
    染料木素-7-O-β-D-葡萄糖苷-4’-O-[α-L-鼠李糖基-(1-2)-β-D-葡萄糖苷]; Genistein 7-O-beta-D-glucopyranoside-4'-O-[alpha-L-rhamnopyranosyl-(1->2)-beta-D-glucopyranoside] CFN95159 70404-42-1 C33H40O19 = 740.7 10mg QQ客服:1457312923
    染料木苷; Genistin CFN90250 529-59-9 C21H20O10 = 432.38 20mg QQ客服:215959384
    金雀异黄素7-O-葡糖苷酸; Genistein 7-O-glucuronide CFN70353 38482-81-4 C21H18O11 = 446.4 5mg QQ客服:2159513211
    4''-甲氧基染料木苷; 4''-methyloxy-Genistin CFN93006 950910-16-4 C22H22O10 = 446.40 5mg QQ客服:3257982914
    Ambocin; Ambocin CFN89471 108044-05-9 C26H28O14 = 564.49 5mg QQ客服:1457312923
    新化合物IV; New compound 4 CFN95185 N/A C27H30O14 = 578.5 5mg QQ客服:3257982914
    澳白檀苷; Lanceolarin CFN95166 15914-68-8 C27H30O14 = 578.5 5mg QQ客服:215959384
    鸡豆黄素配糖物; 印度黄檀苷; Sissotrin CFN97005 5928-26-7 C22H22O10 = 446.4 5mg QQ客服:215959384
    染料木素-7,4'-二-O-β-D-葡萄糖苷; Genistein 7,4'-di-O-beta-D-glucopyranoside CFN90953 36190-98-4 C27H30O15 = 594.52 20mg QQ客服:2056216494
    丙二酰染料木苷; 6''-O-Malonylgenistin CFN90631 51011-05-3 C24H22O13 = 518.42 5mg QQ客服:1457312923

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