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  • 银杏内酯K

    Ginkgolide K

    银杏内酯K
    产品编号 CFN91009
    CAS编号 153355-70-5
    分子式 = 分子量 C20H22O9 = 406.4
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Diterpenoids
    植物来源 The leaves of Ginkgo biloba 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
    银杏内酯K CFN91009 153355-70-5 10mg QQ客服:2056216494
    银杏内酯K CFN91009 153355-70-5 20mg QQ客服:2056216494
    银杏内酯K CFN91009 153355-70-5 50mg QQ客服:2056216494
    银杏内酯K CFN91009 153355-70-5 100mg QQ客服:2056216494
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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
  • University of Minnesota (USA)
  • University of Illinois (USA)
  • Universite de Lille1 (France)
  • Hamdard University (India)
  • University of Wuerzburg (Germany)
  • Kazusa DNA Research Institute (Japan)
  • Sri Ramachandra University (India)
  • Medical University of Gdansk (Poland)
  • National Cancer Institute (USA)
  • The Australian National University (Australia)
  • Aveiro University (Portugal)
  • Kamphaengphet Rajabhat University (Thailand)
  • Universita' Degli Studi Di Cagliari (Italy)
  • Cancer Research Initatives Foundation(CARIF) (Malaysia)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Biochem Biophys Res Commun.2018, 505(1):194-200
  • Anal Biochem.2019, 569:10-15
  • Am J Chin Med.2022, 1-20.
  • J Cell Physiol.2020, 10.1002
  • South African J of Botany2020, 135:50-57
  • J Nat Prod.2019, 82(4):1002-1008
  • Molecules.2020, 25(23):5609.
  • J Bone Miner Res.2017, 32(12):2415-2430
  • Front Plant Sci.2022, 13: 905275.
  • PLoS One.2020, 15(2):e0220084.
  • Int J Biol Macromol.2020, 161:1230-1239.
  • Chemistry of Plant Raw Materials2019, 4:135-147
  • Int J Mol Sci.2023, 24(8):7442.
  • J of l. Chroma.&Related Tech2020, 43(11-12):414-423.
  • Appl. Sci. 2021, 11(22), 10552
  • J Ethnopharmacol.2020, 249:112396
  • Food Chem Toxicol.2023, 176:113802.
  • Korean J. Medicinal Crop Sci2021, 10:345-352.
  • Int J Mol Sci.2019, 20(23):E6071
  • Pharmaceuticals (Basel).2021, 14(7):633.
  • Korean Journal of Pharmacognosy.2020, 51(2):100-106
  • Phytochemistry Letters2021, 43:80-87.
  • Biomolecules.2020, 10(6):925.
  • ...
  • 生物活性
    Description: Ginkgolide K exerts anti-oxidative stress and neuroprotective effect on ischemic stroke, it has potentially anti- Parkinson's disease activity, it can promote the clearance of A53T mutation alpha-synuclein in SH-SY5Y cells. Ginkgolide K promotes angiogenesis after ischemia stroke through increasing the expression of HIF-1α/VEGF via JAK2/STAT3 pathway, it promotes astrocyte proliferation and migration after oxygen-glucose deprivation via inducing protective autophagy through the AMPK/mTOR/ULK1 signaling pathway. Ginkgolide K can inhibit PAF-induced platelet aggregation and improve nerve injury after cerebral ischemia-reperfusion.
    Targets: HIF | VEGFR | JAK | STAT | mTOR | AMPK | PAFR | ROS | Bcl-2/Bax | Caspase | SOD | PI3K | Calcium Channel | p65 | NF-kB | MMP(e.g.TIMP)
    In vitro:
    Cell Biol Toxicol. 2017 Dec 6.
    Ginkgolide K promotes the clearance of A53T mutation alpha-synuclein in SH-SY5Y cells.[Pubmed: 29214369]
    Alpha-synuclein (α-syn) is associated to Parkinson's disease (PD). The aggregated form of α-syn has potential neurotoxicity. Thus, the clearance of α-syn aggregation is a plausible strategy to delay disease progression of PD.
    METHODS AND RESULTS:
    In our study, we found that the treatment of Ginkgolide B (GB) and Ginkgolide K (GK) reduced cell death, and enhanced cell proliferation in SH-SY5Y cells, which overexpressed A53T mutant α-syn. Surprisingly, GK, but not GB, promoted the clearance of A53T α-syn, which can be abolished by autophagy inhibitor 3-methyladenine, indicating that GK-induced autophagy intervened in the clearance of A53T α-syn. However, GK did not affect the NEDD4 that belongs to the ubiquitin ligase in the endosomal-lysosomal pathway. Furthermore, GK treatment inhibited the p-NF-kB/p65 and induced the PI3K, BDNF, and PSD-95.
    CONCLUSIONS:
    Taken together, GK increased the clearance of α-syn, reduced cell death, and triggered complex crosstalk between different signaling pathways. Although our results show a potentially new therapeutic candidate for PD, the details of this mechanism need to be further identified.
    Neurotoxicology. 2012 Jan;33(1):59-69.
    Neuroprotective effect of ginkgolide K on glutamate-induced cytotoxicity in PC 12 cells via inhibition of ROS generation and Ca(2+) influx.[Pubmed: 22120026 ]
    Glutamate is considered to be responsible for the pathogenesis of cerebral ischemia disease. [Ca(2+)](i) influx and reactive oxygen species (ROS) production are considered to be involved in glutamate-induced apoptosis process.
    METHODS AND RESULTS:
    In this study, we investigated the neuroprotective effects of Ginkgolide K in the glutamate-induced rat's adrenal pheochromocytoma cell line (PC 12 cells) and the possible mechanism. Glutamate cytotoxicity in PC 12 cells was accompanied by an increment of malondialdehyde (MDA) content and lactate dehydrogenase (LDH) release, as well as Ca(2+) influx, bax/bcl-2 ratio, cytochrome c release, caspase-3 protein and ROS generation, and reduction of cell viability and mitochondrial membrane potential (MMP). Moreover, treatment with glutamate alone resulted in decrease activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activity. However, pretreatment with Ginkgolide K significantly reduced MDA content, LDH release, as well as Ca(2+) influx, cytochrome c release, bax/bcl-2 ratio, caspase-3 protein and ROS production, and attenuated the decrease of cells viability and MMP. In addition, Ginkgolide K remarkedly up-regulated SOD and GSH-PX activities.
    CONCLUSIONS:
    All these findings indicated that Ginkgolide K protected PC12 cells against glutamate-induced apoptosis by inhibiting Ca(2+) influx and ROS production. Therefore, the present study supports the notion that Ginkgolide K may be a promising neuroprotective agent for the treatment of cerebral ischemia disease.
    In vivo:
    Eur J Pharmacol. 2018 Jun 8;833:221-229.
    Ginkgolide K promotes angiogenesis in a middle cerebral artery occlusion mouse model via activating JAK2/STAT3 pathway.[Pubmed: 29890157]
    Ginkgolide K (GK) is a new compound extracted from the leaves of Ginkgo biloba, which has been recognized to exert anti-oxidative stress and neuroprotective effect on ischemic stroke. While whether it plays an enhanced effect on angiogenesis during ischemic stroke remains unknown.
    METHODS AND RESULTS:
    The aim of this study was to investigate the effect of ginkgolide K on promoting angiogenesis as well as the protective mechanism after cerebral ischemia-reperfusion. Using the transient middle cerebral artery occlusion (tMCAO) mouse model, we found that GK (3.5, 7.0, 14.0 mg/kg, i.p., bid., 2 weeks) attenuated neurological impairments, and promoted angiogenesis of injured ipsilateral cortex and striatum after 14 days of cerebral ischemia-reperfusion in mice. Further, GK (3.5 mg/kg in vivo, 10 μM in vitro) significantly up-regulated the expressions of HIF-1α and VEGF in tMCAO mouse brains and in b End3 cells after OGD/R, and GK-induced upregulation of HIF-1α and VEGF in b End3 cells could be abolished by JAK2/STAT3 inhibitor AG490.
    CONCLUSIONS:
    Our results demonstrate that GK promotes angiogenesis after ischemia stroke through increasing the expression of HIF-1α/VEGF via JAK2/STAT3 pathway, which provide an insight into the novel clinical application of GK and its analogs in ischemic stroke therapy in future.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.4606 mL 12.3031 mL 24.6063 mL 49.2126 mL 61.5157 mL
    5 mM 0.4921 mL 2.4606 mL 4.9213 mL 9.8425 mL 12.3031 mL
    10 mM 0.2461 mL 1.2303 mL 2.4606 mL 4.9213 mL 6.1516 mL
    50 mM 0.0492 mL 0.2461 mL 0.4921 mL 0.9843 mL 1.2303 mL
    100 mM 0.0246 mL 0.123 mL 0.2461 mL 0.4921 mL 0.6152 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
    Gopherenediol; Gopherenediol CFN96287 916236-79-8 C20H34O2 = 306.5 5mg QQ客服:2056216494
    闹羊花毒素II; Rhodojaponin II CFN90674 26116-89-2 C22H34O7 = 410.51 10mg QQ客服:2159513211
    闹羊花毒素III; Rhodojaponin III CFN90673 26342-66-5 C20H32O6 = 368.47 10mg QQ客服:1413575084
    闹羊花毒素V; Rhodojaponin V CFN90670 37720-86-8 C22H34O7 = 410.5 10mg QQ客服:1457312923
    20-脱羟基伊桐素B; Itol A CFN99049 1033747-78-2 C20H32O6 = 368.5 5mg QQ客服:1413575084
    银杏内酯A; Ginkgolide A CFN99638 15291-75-5 C20H24O9 = 408.4 20mg QQ客服:1413575084
    银杏内酯J; Ginkgolide J CFN99149 107438-79-9 C20H24O10 = 424.40 20mg QQ客服:2159513211
    银杏内酯B; Ginkgolide B CFN99640 15291-77-7 C20H24O10 = 424.4 20mg QQ客服:1413575084
    银杏内酯C; Ginkgolide C CFN99639 15291-76-6 C20H24O11 = 440.4 20mg QQ客服:2056216494
    银杏内酯K; Ginkgolide K CFN91009 153355-70-5 C20H22O9 = 406.4 20mg QQ客服:2159513211

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