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    Taurocholic acid
    Taurocholic acid
    CAS No. 81-24-3 Price
    Catalog No.CFN96646Purity>=98%
    Molecular Weight515.70Type of CompoundSteroids
    FormulaC26H45NO7SPhysical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Taurocholic acid Description
    Source: From snake bile.
    Biological Activity or Inhibitors: 1. Rectal administration of taurocholic acid can stimulate glucagon-like peptide-1 and peptide YY by TGR5 receptor activation, which may have potential for the management of type 2 diabetes and obesity.
    2. Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway.
    3. Taurocholic acid feeding shows cytoprotective effects on the biliary tree after adrenergic denervation of the liver.
    4. High concentraction of taurocholic acid can induce apoptosis in HTR-8/SVneo cells via overexpression of ERp29 and activation of p38.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

    PMID: 29149595

    Scientific Reports 2017 Dec 11;7(1):17332.
    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

    Molecules. 2017 Oct 27;22(11). pii: E1829.
    doi: 10.3390/molecules22111829.

    PMID: 29077044

    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.9391 mL 9.6956 mL 19.3911 mL 38.7822 mL 48.4778 mL
    5 mM 0.3878 mL 1.9391 mL 3.8782 mL 7.7564 mL 9.6956 mL
    10 mM 0.1939 mL 0.9696 mL 1.9391 mL 3.8782 mL 4.8478 mL
    50 mM 0.0388 mL 0.1939 mL 0.3878 mL 0.7756 mL 0.9696 mL
    100 mM 0.0194 mL 0.097 mL 0.1939 mL 0.3878 mL 0.4848 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.
    Taurocholic acid References Information
    Citation [1]

    Diabetes Obes Metab. 2013 May;15(5):474-7.

    Effects of rectal administration of taurocholic acid on glucagon-like peptide-1 and peptide YY secretion in healthy humans.[Pubmed: 23181598 ]
    Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), secreted by enteroendocrine L-cells located most densely in the colon and rectum, are of fundamental importance in blood glucose and appetite regulation. In animal models, colonic administration of bile acids can stimulate GLP-1 and PYY by TGR5 receptor activation. We evaluated the effects of Taurocholic acid (TCA), administered as an enema, on plasma GLP-1 and PYY, as well as gastrointestinal sensations in 10 healthy male subjects, and observed that rectal administration of TCA promptly stimulated secretion of both GLP-1 and PYY, and increased fullness, in a dose-dependent manner. These observations confirm that topical application of bile acids to the distal gut may have potential for the management of type 2 diabetes and obesity.
    Citation [2]

    Exp Biol Med (Maywood). 2007 Jul;232(7):942-9.

    Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway.[Pubmed: 17609511]
    We also have shown that Taurocholic acid both in vivo and in vitro stimulates cholangiocyte proliferation. We hypothesize that Taurocholic acid feeding protects cholangiocytes against TNF-alpha -induced apoptosis through a phosphatidylinositol-3-kinase (PI3K)-dependent pathway. Immediately after BDL, rats were fed Taurocholic acid or control diet in the absence/presence of daily injections of wortmannin for 1 week. Seven days later, control-fed or Taurocholic acid-fed rats were treated with a single intraperitoneal injection of actinomycin D + TNF-alpha . Twenty-four hours later we evaluated: (i) cholangiocyte apoptosis and proliferation in liver sections and (ii) basal and secretin-stimulated bile and bicarbonate secretion in bile fistula rats. Taurocholic acid feeding prevented TNF-alpha -induced increases in cholangiocyte apoptosis and decreases in growth and secretin-stimulated bile and bicarbonate secretion, changes that were blocked by PI3K inhibition. The PI3K survival pathway is important in bile acid protection against immune-mediated cholangiocyte injury in cholestatic liver diseases.
    Citation [3]

    Liver Int. 2007 May;27(4):558-68.

    Cytoprotective effects of taurocholic acid feeding on the biliary tree after adrenergic denervation of the liver.[Pubmed: 17403196 ]
    Cholangiopathies impair the balance between proliferation and apoptosis of cholangiocytes leading to the disappearance of bile ducts and liver failure. Taurocholic acid (TC) is essential for cholangiocyte proliferative and functional response to cholestasis. Bile acids and neurotransmitters co-operatively regulate the biological response of the biliary epithelium to cholestasis. Adrenergic denervation of the liver during cholestasis results in the damage of bile ducts. TC prevented the induction of cholangiocyte apoptosis induced by adrenergic denervation. TC also restored cholangiocyte proliferation and functional activity, reduced after adrenergic denervation. TC prevented AKT dephosphorylation induced by adrenergic denervation. The cytoprotective effects of TC were abolished by the simultaneous administration of wortmannin.
    Citation [4]

    Placenta. 2014 Jul;35(7):496-500.

    High concentraction of taurocholic acid induced apoptosis in HTR-8/SVneo cells via overexpression of ERp29 and activation of p38.[Pubmed: 24780196 ]
    Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific disease associated with a significant risk of fetal complications. Our previous study using an iTRAQ-based proteomics approach showed that ERp29 was overexpressed in the placenta tissue of ICP patients, which was an apoptosis-related protein and has not been investigated in the pathogenesis of ICP. The aim of this study was to explore the role of ERp29 in the mechanism of apoptosis in the placenta of ICP. HTR-8/SVneo cells were cultured and treated with different concentrations of Taurocholic acid (TCA) (0, 10, 50 and 100 μM). The apoptotic index and cell cycle were detected by flow cytometry; furthermore, the expression levels of ERp29 and p-p38 were detected by western blot. The ERp29-siRNA was also used to confirm the role of ERp29 in TCA induced-apoptosis. RESULTS: ERp29 expression and the apoptotic index were significantly increased in HTR-8/SVneo cells exposed to 100 μM TCA; so were p-p38 and caspase-3 activity, compared with the 50 μM, 10 μM TCA groups and negative control group (P < 0.05, respectively). The induction of apoptosis by TCA and the expression of p-p38 were reduced in HTR-8/SVneo cells after treatment with ERp29-siRNA, compared with controls (P < 0.05, respectively). CONCLUSIONS: This study suggested that overexpression of ERp29 may play a key role in TCA-induced apoptosis in HTR-8/SVneo cells via activation of p38, which may participate in the pathogenesis of ICP and may represent a novel target for ICP treatment.