In vitro, in HEP G2 cell line, tauroursodeoxycholic acid has a protective effect against ethanol-induced human hepatocellular...
Cameron, R.G.; Neuman, M.G.; Shear, N.H.; Bellentani, S.; Tiribelli, C., 1994: In vitro, in HEP G2 cell line, tauroursodeoxycholic acid has a protective effect against ethanol-induced human hepatocellular damagehttps://eurekamag.com/research/031/866/031866200.php
tauroursodeoxycholic acid sodium salt Global Market and Forecast Research : ReportsnReports
[65 Pages Report] Check for Discount on tauroursodeoxycholic acid sodium salt Global Market and Forecast Research report by ChemReport. DescriptionWe provide independent and unbiased information on manufacturers, prices, production...http://www.reportsnreports.com/reports/599743-tauroursodeoxycholic-acid-sodium-salt-global-market-and-forecast-research.html
Abstract 409: Endoplasmic Reticulum Stress Mediates Fluid Balance and Metabolic Effects of the Brain Renin-Angiotensin System |...
Endoplasmic reticulum (ER) stress and the subsequent unfolded protein response (UPR) have been identified as important contributors to various neural diseases. We examined the role of ER stress and the UPR in the metabolic and fluid balance effects of brain angiotensin in two mouse models. The ER stress-reducing chemical chaperone tauroursodeoxycholic acid (TUDCA, 5.28 ug/day) or aCSF vehicle was infused into the lateral cerebral ventricle (ICV) of either C57Bl/6J mice treated for three weeks with high dietary sodium and chronic subcutaneous deoxycorticosterone acetate (the "DOCA-salt" model), or transgenic "sRA" mice that express human renin in neurons via the synapsin promoter and human angiotensinogen via its own promoter. Both the DOCA-salt and sRA models exhibit hyperactivity of the brain RAS, suppression of circulating RAS, hypertension, polydipsia, and an elevated resting metabolic rate. Forebrain, midbrain, and hindbrain regions of sRA mice exhibited a significant elevation of CHOP ...http://hyper.ahajournals.org/content/60/Suppl_1/A409
My Parkinson's Journey: Week 1: Off Tauroursodeoxycholic Acid
This was the first symptomatic improvement to happen after starting TUDCA, and as you can see, it was dramatic. On day two of taking it, suddenly I could solidly hit the low notes I used to be able to hit before PD came on the scene. It was a complete surprise to me as no medication had changed that. No amount of dopamine had improved it. So I wasn't even thinking about it as something to watch for. Because of this, I felt this symptom improvement could fairly certainly be ascribed to TUDCA because there's nothing Azilect could have done to regain that ability. All it does is allow the dopamine in your body to not breakdown as fast, and so it lasts longer and allows for more buildup as you pump more in via Sinemet ...http://rickspdjourney.blogspot.com/2015/01/week-1-off-tauroursodeoxycholic-acid.html
The porcine taurochenodeoxycholic acid 6alpha-hydroxylase (CYP4A21) gene: evolution by gene duplication and gene conversion |...
Porcine taurochenodeoxycholic acid 6α-hydroxylase, cytochrome P450 4A21 (CYP4A21), differs from other members of the CYP4A subfamily in terms of structural features and catalytic activity. CYP4A21 participates in the formation of hyocholic acid, a species-specific primary bile acid in the pig. The CYP4A21 gene was investigated and found to be approx. 13 kb in size and split into 12 exons. The intron-exon organization of the CYP4A21 gene corresponds to that of CYP4A fatty acid hydroxylase genes in other species. Comparison with a genomic segment of a pig CYP4A fatty acid hydroxylase gene (CYP4A24) revealed a sequence identity with CYP4A21 that extends beyond the exons, indicating a common origin by gene duplication. A pronounced sequence identity was found also within the proximal 5´-flanking regions, whereas the patterns of mRNA expression of CYP4A21 and CYP4A fatty acid hydroxylases in pig ...http://www.biochemj.org/content/378/3/1053
My Parkinson's Journey: Day 4: Tauroursodeoxycholic Acid
Likewise, as I was vacuuming, I often hang my left thumb on the left pants pocket to let my arm hang loose. That seems to help the dystonia some than if it is just hanging at my side. Today, I felt little need to do that. I believe I even noticed my left arm swinging a little when I walked instead of being stiff as a board. Stiffness and tremors have been noticeably reduced. The only time I noticed any was when I had some stress added like in straining to do something. We'll see if that holds up in the days ahead or whether this was just an exceptional day ...http://rickspdjourney.blogspot.com/2015/01/day-4-tauroursodeoxycholic-acid.html
Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR...
Bile acids are synthesized from cholesterol in the liver and further metabolized by the gut microbiota into secondary bile acids. Bile acid synthesis is under negative feedback control through activation of the nuclear receptor farnesoid X receptor (http://www.biomedsearch.com/nih/Gut-Microbiota-Regulates-Bile-Acid/23395169.html
Ursodiol in Huntington's Disease - Full Text View - ClinicalTrials.gov
Huntington's disease is an inherited neurodegenerative disease that causes a movement disorder, dementia, and psychiatric and behavioral disturbance in affected individuals.. Tauroursodeoxycholic acid (TUDCA) is a bile acid synthesized in the liver by the conjugation of taurine to ursodeoxycholic acid (UDCA). It is thought to function as an anti-apoptotic agent in HD, evidenced by studies in toxic cell models and both toxic and transgenic rodent models of the disease.. Ursodiol is a commercially-available exogenous form of UDCA, the precursor of TUDCA. Although the compound has an established dosing, safety, tolerability and efficacy profile in patients with hepatobiliary disorders, gaps exist in the understanding of the pharmacokinetics / pharmacodynamics of the compound, particularly in patients with normal gastrointestinal function, and no human data exist for its therapeutic use in neurodegenerative disorders. The specific aims of this study are:. ...https://clinicaltrials.gov/ct2/show/NCT00514774?cond=%22Huntington+disease%22&rank=9
Ursodiol in Huntington's Disease - Full Text View - ClinicalTrials.gov
Huntington's disease is an inherited neurodegenerative disease that causes a movement disorder, dementia, and psychiatric and behavioral disturbance in affected individuals.. Tauroursodeoxycholic acid (TUDCA) is a bile acid synthesized in the liver by the conjugation of taurine to ursodeoxycholic acid (UDCA). It is thought to function as an anti-apoptotic agent in HD, evidenced by studies in toxic cell models and both toxic and transgenic rodent models of the disease.. Ursodiol is a commercially-available exogenous form of UDCA, the precursor of TUDCA. Although the compound has an established dosing, safety, tolerability and efficacy profile in patients with hepatobiliary disorders, gaps exist in the understanding of the pharmacokinetics / pharmacodynamics of the compound, particularly in patients with normal gastrointestinal function, and no human data exist for its therapeutic use in neurodegenerative disorders. The specific aims of this study are:. ...https://clinicaltrials.gov/ct2/show/NCT00514774?term=Chorea&rank=15
Abstract 17023: Endoplasmic Reticulum Stress Regulates Protein-Tyrosine Phosphatase 1B Expression and Cellular Glucose Uptake...
Obesity is associated with an increased risk of developing insulin resistance and type-2 diabetes. Sustained obesity overwhelms the capacity of endoplasmic reticulum (ER) for the folding of proteins leading to insulin resistance. Protein tyrosine-phosphatase 1B (PTP1B) is a negative regulator of insulin signaling. Because PTP1B is localized in the ER, this study was undertaken to test the hypothesis that ER stress upregulates PTP1B leading to insulin resistance. Leptin deficient obese mice and PTP1B knockout mice were used for in vivo studies. For in vitro studies cultured, differentiated C2C12 myotubes were treated with the ER-stressor tunicamycin and insulin-stimulated deoxyglucose uptake was assessed. Obese mice exhibited higher expression levels of ER stress markers and PTP1B in the liver and gastrocnemius muscle compared to age and sex-matched lean control mice. Oral administration of ER-chaperone tauroursodeoxycholic acid (TUDCA, 50 mg/kg/d) attenuated the PTP1B expression in obese ...http://circ.ahajournals.org/content/126/Suppl_21/A17023
Chaperona química - Wikipedia
Uma chaperona química (ou chaperona farmacológica) é uma pequena molécula que entra na célula, por meio de uma droga, auxiliando em processos de enovalmento protéico de proteínas com suas conformações incorretas. Mutações em proteínas podem causar problemas no enovelamento, resultando em problemas celulares. Essas drogas já vem sendo utilizadas em alguns modelos de estudo de doenças, como Diabetes mellitus tipo 2. 4-Fenilbutirato TUDCA Umut Özcan et al. Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes Science 25 August 2006: Vol. 313 no. 5790 pp. 1137-1140 Welch WJ, Brown CR. Influence of molecular and chemical chaperones on protein folding. Cell Stress Chaperones. 1996 Jun;1(2):109-15. Qing Xie et al. Effect of tauroursodeoxycholic acid on endoplasmic reticulum stress-induced caspase-12 activation. Hepatology Volume 36, Issue 3, pages 592-601, September ...https://pt.wikipedia.org/wiki/Chaperona_qu%C3%ADmica
Repositório da Universidade de Lisboa: Binding studies of bile acids using the native fluorescence of the tryptophan residue of...
Ursodeoxycholic acid (UDCA) and its taurine-conjugate, tauroursodeoxycholic acid (TUDCA), play a unique role in modulating the apoptotic threshold in cells. The mechanism is thought to involve, in part, inhibition of translocation for Bax from the ...http://repositorio.ul.pt/handle/10451/21084
Kanamycin Monosulfate - Drugs.com
Kanamycin Monosulfate is a medicine available in a number of countries worldwide. A list of US medications equivalent to Kanamycin Monosulfate is available on the Drugs.com website.https://www.drugs.com/international/kanamycin-monosulfate.html
6 alpha-hydroxylation of taurochenodeoxycholic acid and lithocholic acid by CYP3A4 in human liver microsomes
The aim of the present study was to identify the enzymes in human liver catalyzing hydroxylations of bile acids. Fourteen recombinant expressed cytochrome P450 (CYP) enzymes, human liver microsomes from different donors, and selective cytochrome P450 inh. ...http://uu.diva-portal.org/smash/record.jsf?pid=diva2:112787
"Studies of Sulfur Reduction of Taurine and Taurine-Conjugated Bile Aci" by Jiang Qian
Bile acids are C24 steroids that are derived in the liver from cholesterol and secreted into the intestinal lumen to aid in emulsification of dietary lipids and lipid-soluble vitamins. The indigenous intestinal microflora modify bile acids, producing up to 20 unique bile acid metabolites. The 7α-dehydroxylation of the bile acids is the most physiologically important bile acid biotransformation. All known intestinal bacteria capable of bile acid 7α-dehydroxylation are anaerobic, gram-positive rods of the genera Clostridium and Eubcicterium. Bile acid 7α-dehydroxylating bacteria often contain bile salt hydrolase, which hydrolyzes the peptide bond in taurine-conjugated bile acids to yield a free bile acid and taurine. Taurine is an organosulfonate containing a sulfite moiety. There have been no published reports indicating whether 7α-dehydroxylating bacteria ...https://digitalcommons.wku.edu/theses/694/
CAS # 25389-94-0, Kanamycin sulfate, Kanamytrex, Kantrex, Kantrim, Kanamycin A monosulfate
chemBlink provides information about CAS # 25389-94-0, Kanamycin sulfate, Kanamytrex, Kantrex, Kantrim, Kanamycin A monosulfate, molecular formula: C18H36N4O11.H2SO4;C18H38N4O15S.http://www.chemblink.com/products/25389-94-0.htm
Bile acids mimic oxidative stress induced upregulation of thioredoxin reductase in colon cancer cell lines : Carcinogenesis - oi
Bile acids have been suggested to play an important role in the etiology of colon and gastric cancer after gastrectomy, but the molecular biology of these effects is poorly understood. We evaluated the effect of different bile acids on human gastric and colon carcinoma cells and identified genes by RNA arbitrarily primed PCR for differential display that are modulated following treatment with hydrophobic bile acids. Thioredoxin reductase (TR) mRNA was upregulated after treatment with taurochenodeoxycholic acid (TCDCA) in St 23132 cells. This raised the question whether deoxycholic acid (DCA) would have regulative effects on TR in HT-29 cells. After an incubation time of 6 h with DCA, TR mRNA expression was increased up to threefold. Ursodeoxycholic acid had no influence on TR mRNA expression. The upregulation of TR after DCA incubation was almost identical to incubation with ...http://oxfordindex.oup.com/view/10.1093/carcin/23.8.1281
Bilirubin inhibits bile acid induced apoptosis in rat hepatocytes | Gut
Although our understanding of the pathogenesis of cholestatic liver disease is incomplete, it is generally believed that accumulation of toxic hydrophobic bile acids, such as deoxycholic acid conjugates, within the hepatocyte can contribute to liver injury by inducing hepatocyte apoptosis.7,3 Antioxidants, such as α-tocopherol or lazaroid, reduce both the generation of ROS and cell injury in freshly isolated hepatocytes treated with GCDC4,10 as well as in the intact rat infused with taurochenodeoxycholic acid.22 Bilirubin, the yellow pigment which accumulates in the plasma of patients with cholestasis, was recognised as an antioxidant of possible physiological importance approximately 15 years ago, and its activity as a free radical scavenger was demonstrated in model membrane systems, being equal to or even surpassing that of α-tocopherol.13,14 As bilirubin interacts with biomembranes, it was postulated that this pigment could prevent lipid ...http://gut.bmj.com/content/52/12/1774
Effect of bile acids on DNA synthesis by the regenerating liver was investigated in mice in vivo after partial hepatectomy (PH). Radioactivity incorporation into DNA after [14C]thymidine intraperitoneal administration peaked at 48 h after PH. At this time a significant taurocholate-induced dose-dependent reduction in DNA synthesis without changes in total liver radioactivity content was found (half-maximal effect at approximately 0.1 mumol/g body wt). Effect of taurocholate (0.5 mumol/g body wt) was mimicked by chocolate, ursodeoxycholate, deoxycholate, dehydrocholate, tauroursodeoxycholate, taurochenodeoxycholate, and taurodeoxycholate. In contrast, chenodeoxycholate, glycocholate, glycochenodeoxycholate, glycoursodeoxycholate, glycodeoxycholate, 5 beta-cholestane, bromosulfophthalein, and free taurine lacked this effect. No relationship between hydrophobic-hydrophilic balance and inhibitory effect was observed. Analysis by high-performance liquid chromatography indicated that inhibition of ...http://ajpgi.physiology.org/content/268/6/G1051
These data are consistent with the current model of multiple overlapping binding sites on MRP2 (Ito et al., 2001a; Bodo et al., 2003; Zelcer et al., 2003), where transport activity can be markedly stimulated by numerous endogenous and exogenous compounds. Thus, taurocholate, glycocholate, glycochenodeoxycholate, taurochenodeoxycholate, and taurodeoxycholate can activate transport of E217G by MRP2 expressed in Sf9 cell membrane vesicles; glycocholate may also be transported in the presence of E217G (Bodo et al., 2003; Zelcer et al., 2003). Here, we examined a range of concentrations of UDC, TUDC, and GUDC to provide an in-depth mathematical assessment of the nature of the binding and to obtain good fits to a pharmacologically meaningful model. We also corrected for endogenous transport (i.e., transport in EV membranes) to obtain more accurate kinetic parameters of the modulation of MRP2-mediated transport. The present data confirm the previous studies (Bodo et al., 2003; Zelcer et al., 2003) and ...http://jpet.aspetjournals.org/content/320/2/893
Reestablishment of rabbit gallbladder epithelial cells in collagen gel culture and their alterations by cytochalasin B and...
We previously developed a model in which rabbit gall bladder epithelial cells in collagen gels proliferated and formed multicellular spherical cysts after 2 to 4 days. In the present study, we examined in depth the dynamic processes of loss and reestablishment of cell polarity of rabbit gallbladder epithelial cells isolated and cultured in collagen gel. Six hours after being place in culture, the isolated epithelial cells had lost the morphologic features and phenotypic markers inherent in the in vivo gallbladder mucosa, and autophagic vacuoles appeared transiently, reflecting epithelial cell injury, or remodelling, or both. After 12 hours, mucin dots appeared in clumps of epithelial cells and gradually became larger, and the epithelial cell clumps were transformed into multicellular cysts after 1 to 2 days. The luminal surfaces of the mucin dots (intracytoplasmic inclusions or small lumens sealed by several epithelial cells) and multicellular cysts were covered by microvilli and presented profiles ofhttps://www.semanticscholar.org/paper/Reestablishment-of-rabbit-gallbladder-epithelial-c-Yoshida-Katayanagi/e1bff04316630201f62809d2f3a0a5f8d87eaecb
106 Gallbladder carcinomas carry poor prognosis and difficulties with treatment, often due to late stage diagnosis, highly malignant nature, and limited knowledge regarding the pathogenesis. Overexpression of erbB2 in gallbladder epithelial cells in BK5.erbB2 transgenic mice leads to development of adenocarcinoma in 90% of the homozygous transgenic mice. This transgenic mouse model provided a useful tool for investigating the mechanism of erbB2 induced development of gallbladder carcinoma. We detected that erbB2 overexpression in transgenic gallbladder epithelial cells was associated with a high level of EGFR and both erbB2 and EGFR were constitutively activated. We further analyzed the downstream of erbB2/EGFR signaling in gallbladder epithelial cells from BK5.erbB2 mice to investigate the mechanism of carcinogenesis. Immunohistochemical analysis revealed that activated Akt was predominantly nuclear in gallbladder epithelial cells from the transgenic mice, but not in nontransgenic mice. Western ...http://cancerres.aacrjournals.org/content/67/9_Supplement/106
Functional and ultrastructural features of ethanol/bile salts interaction in the isolated perfused rat liver - Alvaro - 1995 -...
We investigated whether bile salts (BS) with different hydrophobic-hydrophilic properties interact with ethanol on bile secretion, enzyme (aspartate transaminase [AST], lactate dehydrogenase [LDH]) release in the perfusate, liver ultrastructure, and vesicular exocytosis in the isolated perfused rat liver. Ethanol (0.1 or 1%) promoted a rapid decrease of bile flow and BS secretion in livers perfused with taurocholate (TCA), the physiologic BS in the rat (−28% decrease of baseline values with 0.1% and −34% with 1% ethanol). The inhibitory effect of ethanol on bile flow and BS secretion was significantly (P , .02) attenuated by perfusing liver with the hydrophilic BS, tauroursodeoxycholate (TUDCA), and it was exacerbated (P , .02) by perfusion with the hydrophobic BS, taurodeoxycholate (TDCA). The release of AST and LDH in the perfusate was unaffected by 0.1% ethanol, but increased threefold to fivefold by 1% ethanol in TCA-perfused livers. This cytolitic effect of ethanol was not observed in ...http://onlinelibrary.wiley.com/doi/10.1002/hep.1840210435/abstract
TOM CLARK: Jorge Luis Borges: El hilo de la fábula / The thread of the story
Taurine is conjugated via its amino terminal group with chenodeoxycholic acid and cholic acid to form the bile salts sodium taurochenodeoxycholate and sodium taurocholate. The low pKa of taurine's sulfonic acid group ensures this moiety is negatively charged in the pH ranges normally found in the intestinal tract and, thus, improves the surfactant properties of the cholic acid conjugate. Taurine crosses the blood-brain barrier and has been implicated in a wide array of physiological phenomena including inhibitory neurotransmission, long-term potentiation in the striatum/hippocampus, membrane stabilization, feedback inhibition of neutrophil/macrophage respiratory burst, adipose tissue regulation and possible prevention of obesity, calcium homeostasis, recovery from osmotic shock, protection against glutamate excitotoxicity and prevention of epileptic seizures ...http://tomclarkblog.blogspot.com/2011/03/jorge-luis-borges-el-hilo-de-la-fabula.html?showComment=1301319207610
A chronic voluntary exercise paradigm, which mimics the exercise pattern of many humans, influences the hepatic clearance of several organic anions and a bile acid, whereas a neutral organic compound is seemingly unaffected. To extend these observations, the present work has evaluated in female Sprague-Dawley rats the effect of 6 weeks of voluntary running on the hepatobiliary elimination of endogenous bile acids and glutathione and exogenously injected rose bengal, digoxin, and acetaminophen. Inactive rats had mobility limited to their cages, whereas exercised rats had free access to a 44-in running wheel. In comparison to weight-matched sedentary rats, the exercised rats ran 4.3 +/- 0.3 miles/day, consumed 45% more food daily, had slightly greater liver/body weight ratios, and slightly elevated basal bile flow rates. Biliary excretion of endogenous bile acids was increased significantly, and excretion of reduced and oxidized glutathione was increased in ...http://dmd.aspetjournals.org/content/22/4/537