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  • 猪胆酸

    Hyocholic acid

    猪胆酸
    产品编号 CFN91626
    CAS编号 547-75-1
    分子式 = 分子量 C24H40O5 = 408.6
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Steroids
    植物来源
    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
    猪胆酸 CFN91626 547-75-1 1mg QQ客服:3257982914
    猪胆酸 CFN91626 547-75-1 5mg QQ客服:3257982914
    猪胆酸 CFN91626 547-75-1 10mg QQ客服:3257982914
    猪胆酸 CFN91626 547-75-1 20mg 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
    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
  • The University of Newcastle (Australia)
  • Institute of Bioorganic Chemistry Polish Academy of Sciences (Poland)
  • Worcester Polytechnic Institute (USA)
  • University of Liège (Belgium)
  • Florida A&M University (USA)
  • Vin?a Institute of Nuclear Sciences (Serbia)
  • Sant Gadge Baba Amravati University (India)
  • Sri Sai Aditya Institute of Pharmaceutical Sciences and Research (India)
  • Deutsches Krebsforschungszentrum (Germany)
  • Centrum Menselijke Erfelijkheid (Belgium)
  • Melbourne University (Australia)
  • Amity University (India)
  • John Innes Centre (United Kingdom)
  • Tokyo Woman's Christian University (Japan)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Natural Product Communications2020, doi: 10.1177.
  • Applied Biological Chem. 2020, 26(63).
  • The Journal of Supercritical Fluids2021, 176:105305.
  • Int. Conference on Med. Sci. and Bio.2017, 17973
  • Int J Oncol.2016, 49(4):1497-504
  • Int J Mol Sci.2020, 21(22):8816.
  • Biol Pharm Bull.2021, 44(12):1891-1893.
  • Curr Issues Mol Biol.2023, 45(3):2136-2156.
  • Environ Toxicol.2023, 23929.
  • J Pharm Biomed Anal.2016, 129:50-59
  • J of Health Science and Alternative Medicine2019, 1(1)
  • Cell.2022, 185(23):4298-4316.e21.
  • Planta Med.2018, 84(15):1101-1109
  • Comp. & Mathematical Methods in Med.2022, 5475559.
  • Environ Toxicol.2020, doi: 10.1002
  • Chin. Med.J.Res. Prac.2017, 31(4)
  • J Holistic Integrative Pharm.2023, 4(1):14-28
  • J Cell Mol Med.2023, jcmm.18071.
  • The Journal of Animal & Plant Sciences.2020, 30(6):1366-1373
  • AMB Express2020. 10(1):126.
  • US20170000760 A12016, 42740
  • Phytochem Anal.2022, doi: 10.1002
  • Food Chem.2017, 221:1135-1144
  • ...
  • 生物活性
    Description: Hyocholic acid(HCA) upregulates GLP-1 production and secretion in enteroendocrine cells and improves glucose homeostasis. Hyocholic acid has the effect of preventing and dissolving gallstones.
    In vitro:
    Hepatol Commun . 2021 Dec;5(12):2035-2051.
    Adjunct Fenofibrate Up-regulates Bile Acid Glucuronidation and Improves Treatment Response For Patients With Cholestasis[Pubmed: 34558841]
    Accumulation of cytotoxic bile acids (BAs) during cholestasis can result in liver failure. Glucuronidation, a phase II metabolism pathway responsible for BA detoxification, is regulated by peroxisome proliferator-activated receptor alpha (PPARα). This study investigates the efficacy of adjunct fenofibrate therapy to up-regulate BA-glucuronidation and reduce serum BA toxicity during cholestasis. Adult patients with primary biliary cholangitis (PBC, n = 32) and primary sclerosing cholangitis (PSC, n = 23), who experienced an incomplete response while receiving ursodiol monotherapy (13-15 mg/kg/day), defined as serum alkaline phosphatase (ALP) ≥ 1.5 times the upper limit of normal, received additional fenofibrate (145-160 mg/day) as standard of care. Serum BA and BA-glucuronide concentrations were measured by liquid chromatography-mass spectrometry. Combination therapy with fenofibrate significantly decreased elevated serum ALP (-76%, P < 0.001), aspartate transaminase, alanine aminotransferase, bilirubin, total serum BAs (-54%), and increased serum BA-glucuronides (+2.1-fold, P < 0.01) versus ursodiol monotherapy. The major serum BA-glucuronides that were favorably altered following adjunct fenofibrate include hyodeoxycholic acid-6G (+3.7-fold, P < 0.01), hyocholic acid-6G (+2.6-fold, P < 0.05), chenodeoxycholic acid (CDCA)-3G (-36%), and lithocholic acid (LCA)-3G (-42%) versus ursodiol monotherapy. Fenofibrate also up-regulated the expression of uridine 5'-diphospho-glucuronosyltransferases and multidrug resistance-associated protein 3 messenger RNA in primary human hepatocytes. Pearson's correlation coefficients identified strong associations between serum ALP and metabolic ratios of CDCA-3G (r2 = 0.62, P < 0.0001), deoxycholic acid (DCA)-3G (r2 = 0.48, P < 0.0001), and LCA-3G (r2 = 0.40, P < 0.001), in ursodiol monotherapy versus control. Receiver operating characteristic analysis identified serum BA-glucuronides as measures of response to therapy. Conclusion: Fenofibrate favorably alters major serum BA-glucuronides, which correlate with reduced serum ALP levels and improved outcomes. A PPARα-mediated anti-cholestatic mechanism is involved in detoxifying serum BAs in patients with PBC and PSC who have an incomplete response on ursodiol monotherapy and receive adjunct fenofibrate. Serum BA-glucuronides may serve as a noninvasive measure of treatment response in PBC and PSC.
    In vivo:
    Cell Metab . 2021 Apr 6;33(4):791-803.
    Hyocholic acid species improve glucose homeostasis through a distinct TGR5 and FXR signaling mechanism[Pubmed: 33338411]
    Hyocholic acid (HCA) and its derivatives are found in trace amounts in human blood but constitute approximately 76% of the bile acid (BA) pool in pigs, a species known for its exceptional resistance to type 2 diabetes. Here, we show that BA depletion in pigs suppressed secretion of glucagon-like peptide-1 (GLP-1) and increased blood glucose levels. HCA administration in diabetic mouse models improved serum fasting GLP-1 secretion and glucose homeostasis to a greater extent than tauroursodeoxycholic acid. HCA upregulated GLP-1 production and secretion in enteroendocrine cells via simultaneously activating G-protein-coupled BA receptor, TGR5, and inhibiting farnesoid X receptor (FXR), a unique mechanism that is not found in other BA species. We verified the findings in TGR5 knockout, intestinal FXR activation, and GLP-1 receptor inhibition mouse models. Finally, we confirmed in a clinical cohort, that lower serum concentrations of HCA species were associated with diabetes and closely related to glycemic markers.
    Can J Physiol Pharmacol . 1988 Aug;66(8):1028-1034.
    Effect of hyocholic acid on the prevention and dissolution of biliary cholesterol crystals in mice[Pubmed: 3179836]
    Gallstone prevention and dissolution were studied in a mouse model of cholesterol cholelithiasis using hyocholic acid (3 alpha, 6 alpha, 7 alpha-trihydroxy-5 beta-cholanic acid). Addition of hyocholic acid, 0.1 or 0.3%, in the lithogenic diet (1% cholesterol + 0.5% cholic acid) prevented the formation of cholesterol monohydrate crystals in 70 and 90% of cases, respectively. On the other hand, chow diet supplemented with 0.1 or 0.3% hyocholic acid dissolved cholesterol crystals in lithiasic mice in, respectively, 80 and 100% of cases within 12 days. In both protocols, biles were largely supersaturated with cholesterol; lecithin-cholesterol lamellar liquid crystals were responsible for the transport of the excess cholesterol content. The percentage of hydrophilic bile salts (hyocholic acid, hyodeoxycholic acid, beta-muricholic acid) in bile, although moderate (15-50% of total bile salts), appears to induce such liquid crystalline dispersion. This study demonstrates that the balance between hydrophilic and hydrophobic bile salts plays a major role in the prevention and dissolution of cholesterol crystals. It is also shown that the desaturation of biliary cholesterol is not a prerequisite for gallstone dissolution.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.4474 mL 12.2369 mL 24.4738 mL 48.9476 mL 61.1845 mL
    5 mM 0.4895 mL 2.4474 mL 4.8948 mL 9.7895 mL 12.2369 mL
    10 mM 0.2447 mL 1.2237 mL 2.4474 mL 4.8948 mL 6.1185 mL
    50 mM 0.0489 mL 0.2447 mL 0.4895 mL 0.979 mL 1.2237 mL
    100 mM 0.0245 mL 0.1224 mL 0.2447 mL 0.4895 mL 0.6118 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
    甘氨脱氧胆酸; Glycodeoxycholic acid CFN96947 360-65-6 C26H43NO5 = 449.63 20mg QQ客服:2159513211
    甘氨熊去氧胆酸; Glycoursodeoxycholic acid CFN89075 64480-66-6 C26H43NO5 = 449.63 20mg QQ客服:3257982914
    牛磺胆酸; Taurocholic acid CFN96646 81-24-3 C26H45NO7S = 515.70 5mg QQ客服:215959384
    牛磺熊去氧胆酸 ; Tauroursodeoxycholic acid CFN96645 14605-22-2 C26H45NO6S = 499.70 5mg QQ客服:3257982914
    牛磺鹅去氧胆酸钠; Sodium taurochenodeoxycholate CFN80241 6009-98-9 C26H44NNaO6S = 521.68 5mg QQ客服:1457312923
    熊去氧胆酸; Ursodeoxycholic acid CFN96464 128-13-2 C24H40O4 = 392.58 20mg QQ客服:2056216494
    鹅去氧胆酸; 鹅脱氧胆酸; Chenodeoxycholic acid CFN90478 474-25-9 C24H40O4 = 392.57 20mg QQ客服:2056216494
    胆酸; Cholic acid CFN99796 81-25-4 C22H40O5 = 408.57 20mg QQ客服:215959384
    猪胆酸; Hyocholic acid CFN91626 547-75-1 C24H40O5 = 408.6 5mg QQ客服:215959384
    去氧胆酸; Deoxycholic acid CFN99798 83-44-3 C24H40O4 = 392.57 20mg QQ客服:1457312923

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