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  • 蛇床子素

    Osthol

    蛇床子素
    产品编号 CFN98765
    CAS编号 484-12-8
    分子式 = 分子量 C15H16O3 = 244.3
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Coumarins
    植物来源 The fructus of Cnidium monnieri (L.) Cusson
    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
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    产品名称 产品编号 CAS编号 包装 QQ客服
    蛇床子素 CFN98765 484-12-8 10mg QQ客服:215959384
    蛇床子素 CFN98765 484-12-8 20mg QQ客服:215959384
    蛇床子素 CFN98765 484-12-8 50mg QQ客服:215959384
    蛇床子素 CFN98765 484-12-8 100mg QQ客服:215959384
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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
  • Vin?a Institute of Nuclear Sciences (Serbia)
  • Universitas Airlangga (Indonesia)
  • Indian Institute of Science (India)
  • Sanford Burnham Prebys Medical Discovery Institute (USA)
  • University of Queensland (Australia)
  • University of Toulouse (France)
  • Universite de Lille1 (France)
  • Northeast Normal University Changchun (China)
  • University of Ioannina (Greece)
  • Technical University of Denmark (Denmark)
  • Kitasato University (Japan)
  • Massachusetts General Hospital (USA)
  • University of Otago (New Zealand)
  • Biotech R&D Institute (USA)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Korean J. Medicinal Crop Sci.2021, 29(1):45-50.
  • Biotechnol Bioeng.2020, 117(7):2198-2208.
  • Int Immunopharmacol.2021, 100:108073.
  • Antioxidants (Basel).2020, 9(2): E119
  • J Cell Mol Med.2022, 26(23):5807-5819.
  • J Pharmacol Sci.2021, 147(2):184-191.
  • Molecules.2019, 24(16):E2985
  • Microchemical Journal2022, 182: 107874.
  • Int J Mol Sci.2022, 23(21):13406.
  • Key Engineering Materials2022, 931(47-53).
  • Toxicol In Vitro.2019, 59:161-178
  • Molecules.2022, 27(7):2116.
  • J Food Sci.2022, 87(11):4905-4916.
  • Earth Environ. Sci. 2021, 905:012080.
  • Cell Biochem Funct.2018, 36(6):303-311
  • Int J Mol Sci.2021, 22(8):4211.
  • J Agric Food Chem.2019, 67(27):7748-7754
  • Pharm Biol.2016, 54(7):1255-62
  • Int J Oncol.2016, 49(4):1497-504
  • Exp Ther Med.2019, 18(6):4388-4396
  • Biochem Biophys Res Commun.2018, 505(1):261-266
  • BMC Complement Med Ther.2023, 23(1):264.
  • Sains Malaysiana2022, 51(4):1143-1154
  • ...
  • 生物活性
    Description: Osthol is a natural antihistamine alternative, may be a potential inhibitor of histamine H1 receptor activity. Osthol has toxicity, may be used as bio-pesticides. Osthol is an inhibitor of human Pgp and multidrug efflux pumps of Staphylococcus aureus , reversing the resistance against frontline antibacterial drugs.Osthol has anti-allergic, antiosteoporosis, anti-fatty liver, antitumor, and cardioprotective effects. Osthol inhibits hepatic SREBP-1c/2 mRNA expressions and subsequent modulation of SREBP-1c/2-mediated target genes such as FAS, CYP7A and LDL receptor; it can stimulate the osteoblastic differentiation of rat calvarial osteoblast cultures by the BMP-2/p38MAPK/Runx-2/osterix pathway.
    Targets: PPAR | LDL | P450 (e.g. CYP17) | P-gp | p38MAPK | FAS | BMP-2 | Runx-2 | Histamine H1 receptor
    In vitro:
    Environ Health Toxicol. 2014 Dec 10;29:e2014020.
    Acute toxicity assessment of Osthol content in bio-pesticides using two aquatic organisms.[Pubmed: 25518842]
    This study focused on the assessment of acute toxicity caused by Osthol, a major component of environment-friendly biological pesticides, by using two aquatic organisms.
    METHODS AND RESULTS:
    The assessment of acute toxicity caused by Osthol was conducted in Daphnia magna and by examining the morphological abnormalities in Danio rerio embryos. The median effective concentration value of Osthol in D. magna 48 hours after inoculation was 19.3 μM. The median lethal concentration of D. rerio embryo at 96 hours was 30.6 μM. No observed effect concentration and predicted no effect concentration values of Osthol in D. magna and D. rerio were calculated as 5.4 and 0.19 μM, respectively. There was an increase in the morphological abnormalities in D. rerio embryo due to Osthol over time. Coagulation, delayed hatching, yolk sac edema, pericardial edema, and pigmentation were observed in embryos at 24-48 hours. Symptoms of scoliosis and head edema occurred after 72 hours. In addition, bent tails, ocular defects, and symptoms of collapse were observed in fertilized embryo tissue within 96 hours. Ocular defects and pigmentation were the additional symptoms observed in this study.
    CONCLUSIONS:
    Because Osthol showed considerable toxicity levels continuous toxicity evaluation in agro-ecosystems is necessary when bio-pesticides containing Osthol are used.
    Phytother Res. 2007 Mar;21(3):226-30.
    Antitumor effects of Osthol from Cnidium monnieri: an in vitro and in vivo study.[Pubmed: 17154232 ]
    Cnidium monnieri (L.) Cusson is a Chinese medicine which is used widely by traditional medicine doctors. Osthol is a major bio-activity compound of the herb.
    METHODS AND RESULTS:
    In this study, osthol was isolated from C. monnieri and its in vitro and in vivo antitumor effects studied. The results of the in vitro study showed: that osthol inhibited the growth of HeLa, in a time- and concentration-dependent manner, with IC(50) values of 77.96 and 64.94 microm for 24 and 48 h, respectively; that osthol had lower cytotoxic effects in primary cultured normal cervical fibroblasts; and that increased DNA fragmentation and activated PARP in HeLa after treatment with osthol which could induce apoptosis. The results of the in vivo model showed that the survival days of the P-388 D1 tumor-bearing CDF(1) mice were prolonged (ILS% = 37) after osthol (30 mg/kg) was given once a day for 9 days.
    CONCLUSIONS:
    Based on these results, it is suggested that osthol could inhibit P-388 D1 cells in vivo and induce apoptosis in HeLa cells in vitro, and that osthol is good lead compound for developing antitumor drugs. However, C. formosanum Yabe of Taiwan's endemic plants contained little osthol, with no imperatorin, and its major components were different from that of C. monnieri. Therefore, it is suggested that C. formosanum also may possess economic worth.
    In vivo:
    World J Gastroenterol. 2014 Sep 7;20(33):11753-61.
    Osthol attenuates hepatic steatosis via decreased triglyceride synthesis not by insulin resistance.[Pubmed: 25206279]
    To evaluate the effects of osthol on intrahepatic fat synthesis, β-oxidation, inflammation, and insulin resistance by multifaceted analysis.
    METHODS AND RESULTS:
    Sprague-Dawley rats (n = 30) were randomly divided into control, non-alcoholic fatty liver disease (NAFLD), and osthol groups. NAFLD and osthol groups were fed with a high-fat diet for 14 wk. After 8 wk of the high-fat diet, the osthol group also received osthol 20 mg/kg orally 5 times/wk. To assess the insulin resistance, oral glucose tolerance was performed at the end of 14 wk. Immunohistochemical (4-HNE, F4/80) and hematoxylin and eosin (HE) staining were performed on liver tissue extracts after animal sacrifice at 14 wk. SREBP1c, FAS, SCD-1, PPAR-α, CROT, MCP-1, IRS-1, and IRS-2 mRNA expressions were assessed with reverse transcription-polymerase chain reaction. HE staining revealed that, compared with the NAFLD group, the osthol group showed significantly decreased intrahepatic fat content (39.4% vs 21.0%; P = 0.021). SREBP1c expression in the NAFLD group increased compared to controls (P = 0.0001), while osthol treatment decreased SREBP1c expression compared with the NAFLD group (P = 0.0059). In the osthol group, intrahepatic FAS and SCD-1, which act downstream of SREBP1c, decreased significantly compared with the NAFLD group. Moreover, PPAR-α expression in the osthol group was also significantly higher than in the NAFLD group (P = 0.0147).
    CONCLUSIONS:
    Osthol treatment attenuated liver steatosis by decreasing de novo liver triglyceride synthesis and had nominal effects on insulin resistance and liver inflammation.
    Lipids. 2012 Oct;47(10):987-94.
    Reduction of rat cardiac hypertrophy by osthol is related to regulation of cardiac oxidative stress and lipid metabolism.[Pubmed: 22918576]
    The objective of this study was to examine the therapeutic effect of osthol, a coumarin compound isolated from the fruit of Cnidium monnieri (L.) Cusson, on cardiac hypertrophy in rats and investigate its potential mechanisms.
    CONCLUSIONS:
    The rats with cardiac hypertrophy induced by renovascular hypertension were given osthol orally by gavage for 4 weeks. The results showed that in the osthol 20 mg/kg group, the blood pressure, heart weight index and myocardial malondialdehyde content were lowered (p < 0.001, p = 0.002 and p = 0.025, respectively), the myocardial superoxide dismutase and glutathione peroxidase contents were increased (p < 0.001), and the elevated unesterified fatty acids and triacylglycerols in myocardial tissues were decreased (p = 0.017 and p = 0.004, respectively). At the same time, the myocardial peroxisome proliferator-activated receptor (PPAR)-α and carnitine palmitoyltransferase (CPT)-1a mRNA expressions were increased and the myocardial diacylglycerol acyltransferase (DGAT) mRNA expression was decreased in the osthol 20 mg/kg group (p < 0.001). Osthol treatment was associated with a decreased cross-sectional area of cardiomyocytes (p < 0.001).
    CONCLUSIONS:
    These findings suggest that osthol may exert a therapeutic effect on cardiac hypertrophy in rats, and its mechanisms may be related to the improvement of myocardial oxidative stress and lipid metabolism via regulation of PPARα-mediated target gene expressions including an increase in CPT-1a mRNA expression and a decrease in DGAT mRNA expression.
    Acta Pharmacol Sin . 2017 Aug;38(8):1120-1128
    Osthole pretreatment alleviates TNBS-induced colitis in mice via both cAMP/PKA-dependent and independent pathways[Pubmed: 28603288]
    Abstract Osthole, a natural coumarin found in traditional Chinese medicinal plants, has shown multiple biological activities. In the present study, we investigated the preventive effects of osthole on inflammatory bowel disease (IBD). Colitis was induced in mice by infusing TNBS into the colonic lumen. Before TNBS treatment, the mice received osthole (100 mg·kg-1·d-1, ip) for 3 d. Pretreatment with osthole significantly ameliorated the clinical scores, colon length shortening, colonic histopathological changes and the expression of inflammatory mediators in TNBS-induced colitis. Pretreatment with osthole elevated serum cAMP levels; but treatment with the PKA inhibitor H89 (10 mg·kg-1·d-1, ip) did not abolish the beneficial effects of osthole on TNBS-induced colitis. In mouse peritoneal macrophages, pretreatment with osthole (50 μmol/L) significantly attenuated the LPS-induced elevation of cytokines at the mRNA level; inhibition of PKA completely reversed the inhibitory effects of osthole on IL-1β, IL-6, COX2, and MCP-1 but not on TNFα. In Raw264.7 cells, the p38 inhibitor SB203580 markedly suppressed LPS-induced upregulation of the cytokines, whereas the PKA inhibitors H89 or KT5720 did not abolish the inhibitory effects of SB203580. Moreover, in LPS-stimulated mouse peritoneal macrophages, SB203580 strongly inhibited the restored expression of IL-1β, IL-6, COX2, and MCP-1, which was achieved by abolishing the suppressive effects of osthole with the PKA inhibitors. Western blot analysis showed that osthole significantly suppressed the phosphorylation of p38, which was induced by TNBS in mice or by LPS in Raw264.7 cells. Inhibition of PKA partially reversed the suppressive effects of osthole on p38 phosphorylation in LPS-stimulated cells. Collectively, our results suggest that osthole is effective in the prevention of TNBS-induced colitis by reducing the expression of inflammatory mediators and attenuating p38 phosphorylation via both cAMP/PKA-dependent and independent pathways, among which the cAMP/PKA-independent pathway plays a major role.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.0933 mL 20.4666 mL 40.9333 mL 81.8666 mL 102.3332 mL
    5 mM 0.8187 mL 4.0933 mL 8.1867 mL 16.3733 mL 20.4666 mL
    10 mM 0.4093 mL 2.0467 mL 4.0933 mL 8.1867 mL 10.2333 mL
    50 mM 0.0819 mL 0.4093 mL 0.8187 mL 1.6373 mL 2.0467 mL
    100 mM 0.0409 mL 0.2047 mL 0.4093 mL 0.8187 mL 1.0233 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
    蛇床子素; Osthol CFN98765 484-12-8 C15H16O3 = 244.3 20mg QQ客服:2159513211
    橙皮内酯; Meranzin CFN98249 23971-42-8 C15H16O4 = 260.3 5mg QQ客服:1457312923
    水合蛇床子素; Osthol hydrate CFN90848 69219-24-5 C15H18O4 = 262.3 10mg QQ客服:3257982914
    3'-O-Methylmurraol; 3'-O-Methylmurraol CFN89183 1891097-17-8 C16H18O4 = 274.31 5mg QQ客服:1457312923
    酸橙素烯醇; Auraptenol CFN99340 1221-43-8 C15H16O4 = 260.3 5mg QQ客服:1413575084
    九里香酮; Murrayone CFN98505 19668-69-0 C15H14O4 = 258.27 10mg QQ客服:1413575084
    异橙皮内酯 ; Isomeranzin CFN99090 1088-17-1 C15H16O4 = 260.3 20mg QQ客服:1413575084
    橙皮内酯水合物; Meranzin hydrate CFN98994 5875-49-0 C15H18O5 = 278.3 20mg QQ客服:1457312923
    (S)-8-(3-乙氧基-2-羟基-3-甲基丁基)-7-甲氧基-2H-1-苯并吡喃-2-酮; 8-(3-Ethoxy-2-hydroxy-3-methylbutyl)-7-methoxycoumarin CFN99362 125072-68-6 C17H22O5 = 306.4 5mg QQ客服:215959384
    8-(二甲基烯丙基)-7-羟基-6-甲氧基香豆素; Cedrelopsin CFN89410 19397-28-5 C15H16O4 = 260.28 5mg QQ客服:2056216494

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