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    Ursodeoxycholic acid
    Ursodeoxycholic acid
    Information
    CAS No. 128-13-2 Price $70 / 20mg
    Catalog No.CFN96464Purity>=98%
    Molecular Weight392.58Type of CompoundSteroids
    FormulaC24H40O4Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Ursodeoxycholic acid Description
    Source: The bile of bear.
    Biological Activity or Inhibitors: 1. Ursodeoxycholic acid as a chemopreventive agent in patients with ulcerative colitis and primary sclerosing cholangitis.
    2. Ursodeoxycholic acid aggravates bile infarcts and hepatocyte necroses in mice with biliary obstruction via disruption of cholangioles as a result of increased biliary pressure caused by its choleretic action.
    3. Ursodeoxycholic acid is a potent inhibitor of apoptosis, it prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation.
    4. Ursodeoxycholic acid can ameliorates experimental ileitis counteracting intestinal barrier dysfunction and oxidative stress.
    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.
    doi:10.1016/j.phymed.2017.12.030

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.5473 mL 12.7363 mL 25.4725 mL 50.945 mL 63.6813 mL
    5 mM 0.5095 mL 2.5473 mL 5.0945 mL 10.189 mL 12.7363 mL
    10 mM 0.2547 mL 1.2736 mL 2.5473 mL 5.0945 mL 6.3681 mL
    50 mM 0.0509 mL 0.2547 mL 0.5095 mL 1.0189 mL 1.2736 mL
    100 mM 0.0255 mL 0.1274 mL 0.2547 mL 0.5095 mL 0.6368 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.
    Ursodeoxycholic acid References Information
    Citation [1]

    Cell Death Differ. 1999 Sep;6(9):842-54.

    Ursodeoxycholic acid prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation.[Pubmed: 10510466 ]
    The hydrophilic bile salt Ursodeoxycholic acid (UDCA) is a potent inhibitor of apoptosis. In this paper, we further characterize the mechanism by which UDCA inhibits apoptosis induced by deoxycholic acid, okadaic acid and transforming growth factor beta1 in primary rat hepatocytes. Our data indicate that coincubation of cells with UDCA and each of the apoptosis-inducing agents was associated with an approximately 80% inhibition of nuclear fragmentation (P<0.001). Moreover, UDCA prevented mitochondrial release of cytochrome c into the cytoplasm by 70 - 75% (P<0.001), thereby, inhibiting subsequent activation of DEVD-specific caspases and cleavage of poly(ADP-ribose) polymerase. Each of the apoptosis-inducing agents decreased mitochondrial transmembrane potential and increased mitochondrial-associated Bax protein levels. Coincubation with UDCA was associated with significant inhibition of these mitochondrial membrane alterations. The results suggest that the mechanism by which UDCA inhibits apoptosis involves an interplay of events in which both depolarization and channel-forming activity of the mitochondrial membrane are inhibited.
    Citation [2]

    Gastroenterology. 2003 Apr;124(4):889-93.

    Ursodeoxycholic acid as a chemopreventive agent in patients with ulcerative colitis and primary sclerosing cholangitis.[Pubmed: 12671884 ]
    Ursodeoxycholic acid (UDCA) has shown effectiveness as a colon cancer chemopreventive agent in preclinical studies. In addition, a recent report suggests that it also may decrease the risk for developing colorectal dysplasia in patients with ulcerative colitis (UC) and primary sclerosing cholangitis (PSC). We sought to evaluate the effect of UDCA on colorectal neoplasia in a group of patients with UC and PSC enrolled in a randomized, placebo-controlled trial.UDCA significantly decreases the risk for developing colorectal dysplasia or cancer in patients with UC and PSC.
    Citation [3]

    Gastroenterology. 2002 Oct;123(4):1238-51.

    Ursodeoxycholic acid aggravates bile infarcts in bile duct-ligated and Mdr2 knockout mice via disruption of cholangioles.[Pubmed: 12360485]
    The effects of Ursodeoxycholic acid (UDCA) in biliary obstruction are unclear. We aimed to determine the effects of UDCA in bile duct-ligated and in Mdr2 knockout (Mdr2(-/-)) mice with biliary strictures.UDCA feeding in CBDL mice increased biliary pressure, with subsequent rupture of cholangioles and aggravation of hepatocyte necroses, resulting in significantly increased mortality. UDCA feeding in SBDL mice aggravated liver injury exclusively in the ligated lobe. Mdr2(-/-) mice developed liver lesions resembling sclerosing cholangitis characterized by biliary strictures and dilatations. UDCA induced bile infarcts in these animals. CONCLUSIONS: UDCA aggravates bile infarcts and hepatocyte necroses in mice with biliary obstruction via disruption of cholangioles as a result of increased biliary pressure caused by its choleretic action.
    Citation [4]

    Dig Dis Sci. 2004 Oct;49(10):1569-74.

    Ursodeoxycholic acid ameliorates experimental ileitis counteracting intestinal barrier dysfunction and oxidative stress.[Pubmed: 15573906]
    The aim of this study was to evaluate the effect of Ursodeoxycholic acid (UDCA) on intestinal permeability (IP) and reactive oxygen species (ROS) generation in indomethacin-induced enteropathy, a well-known experimental model of Crohn's disease. Seventy-eight male Wistar rats were randomly assigned to receive indomethacin, indomethacin + UDCA, or vehicles. Indomethacin induced a significant increase in the fraction of urinary excretion of 51Cr-EDTA following oral administration (7.9 +/- 1.3 vs 2.3 +/- 0.2%; P < 0.05) and lucigenin-amplified chemiluminescence in intestinal fragments ex vivo (10.1 +/- 1.9 vs 2.6 +/- 0.4 cpm x 10(3)/mg; P < 0.05) compared to controls. UDCA significantly reversed these effects (P < 0.05), without being incorporated in biliary bile acid composition (HPLC analysis). These findings support a local protective effect of UDCA in experimental ileitis by the modulation of intestinal barrier dysfunction and oxidative stress. In short, they provide insights into mechanisms of action of UDCA in intestinal inflammation and a new perspective on the treatment of Crohn's disease.