Disease relevance of Ursodeoxycholyltaurine

• Tauroursodeoxycholic acid stimulates hepatocellular exocytosis and mobilizes extracellular Ca++ mechanisms defective in cholestasis [1].
• METHODS: Using anesthetized biliary fistula guinea pigs or rats, the ileum was perfused with ursodeoxycholyltaurine at a concentration causing maximal ileal transport of this bile acid; absorption was assessed by biliary recovery [2].
• Taurochenodeoxycholic acid and taurodeoxycholic acid infusions increased mesenteric arterial blood flow and conductance and induced systemic arterial hypotension, whereas tauroursodeoxycholic acid had no significant effect [3].
• The prevention of the hepatotoxic effects produced by intravenous infusion of taurochenodeoxycholic acid (TCDCA) by coinfusion with taurohyodeoxycholic acid (THDCA) was evaluated in bile fistula rats; the hepatoprotective effects of the latter were also compared with those of tauroursodeoxycholic acid (TUDCA) [4].
• Metabolism of orally administered tauroursodeoxycholic acid in patients with primary biliary cirrhosis [5].

Psychiatry related information on Ursodeoxycholyltaurine

• Tauroursodeoxycholic acid, a bile acid, is neuroprotective in a transgenic animal model of Huntington's disease [6].
• Tauroursodeoxycholic acid modulates p53-mediated apoptosis in Alzheimer's disease mutant neuroblastoma cells [7].

High impact information on Ursodeoxycholyltaurine

• To assess the effects of tauroursodeoxycholic acid (TUDCA) on bile excretory function, we examined whether TUDCA modulates vesicular exocytosis in the isolated perfused liver of normal rats in the presence of high (1.9 mM) or low (0.19 mM) extracellular Ca++ and in cholestatic rats 24 h after bile duct ligation [1].
• Tauroursodeoxycholic acid activates protein kinase C in isolated rat hepatocytes [8].
• UDCA is conjugated to taurine in vivo, and tauroursodeoxycholic acid (TUDCA) is a potent hepatocellular Ca2+ agonist and stimulates biliary exocytosis and hepatocellular Ca2+ influx, both of which are defective in experimental cholestasis [8].
• In feces, the proportion of lithocholate was 21.9% +/- 4.9% and 5.4% +/- 4.0% after ursodeoxycholic acid and tauroursodeoxycholic acid administration, respectively [9].
• Tauroursodeoxycholic acid reduces apoptosis and protects against neurological injury after acute hemorrhagic stroke in rats [10].

Chemical compound and disease context of Ursodeoxycholyltaurine

• Bile salt tauroursodeoxycholic acid modulation of Bax translocation to mitochondria protects the liver from warm ischemia-reperfusion injury in the rat [11].
• Ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) have been suggested as potential treatments for drug-induced cholestasis [12].
• Toxicity of ethanol and acetaldehyde in hepatocytes treated with ursodeoxycholic or tauroursodeoxycholic acid [13].

Biological context of Ursodeoxycholyltaurine

• Tauroursodeoxycholic acid (TUDCA), an endogenous bile acid, modulates cell death by interrupting classic pathways of apoptosis [10].
• In addition, TUDCA significantly reduced the number of TUNEL-positive brain cells, mitochondrial swelling, and partially inhibited caspase-3 processing and substrate cleavage [14].
• Tauroursodeoxycholic acid for the cytoprotection of liver grafts during cold storage: a new aspect of its anti-apoptotic properties [15]?
• Hydrophilic bile acid tauroursodeoxycholic acid (TUDC) had no effect on muscle contraction but prevented the TCDC-induced contraction and its inhibition on CCK-induced contraction [16].
• Apoptotic DNA fragmentation was significantly reduced by co-incubation with tauroursodeoxycholic acid [17].

Anatomical context of Ursodeoxycholyltaurine

• Tauroursodeoxycholic acid inserts the apical conjugate export pump, Mrp2, into canalicular membranes and stimulates organic anion secretion by protein kinase C-dependent mechanisms in cholestatic rat liver [18].
• Effect of tauroursodeoxycholic acid on endoplasmic reticulum stress-induced caspase-12 activation [19].
• Ca2+-dependent cytoprotective effects of ursodeoxycholic and tauroursodeoxycholic acid on the biliary epithelium in a rat model of cholestasis and loss of bile ducts [20].
• Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, is a strong modulator of apoptosis in both hepatic and nonhepatic cells, and appears to function by inhibiting mitochondrial membrane perturbation [14].
• Among these, damage to mitochondria matrix and crystae was significantly reduced in TUDCA-treated versus control grafts (P<0.01) [21].

Associations of Ursodeoxycholyltaurine with other chemical compounds

• Effects of tauroursodeoxycholic acid on cytosolic Ca2+ signals in isolated rat hepatocytes [22].
• The aim of this study was to explore the protective mechanisms of the taurine-conjugate of UDCA (tauroursodeoxycholic acid [TUDCA]) against glycochenodeoxycholic acid (GCDCA)-induced apoptosis in primary cultures of rat hepatocytes [23].
• Taurohyodeoxycholic acid (THDCA) and tauroursodeoxycholic acid (TUDCA) both induced CYP, reductase, and MFOs [24].
• Functional Modulation of Nuclear Steroid Receptors by Tauroursodeoxycholic Acid Reduces Amyloid {beta}-Peptide-Induced Apoptosis [25].
• Furthermore, primary cultures of rat hepatocytes were exposed to glycochenodeoxycholic acid (GCDCA), tauroursodeoxycholic acid (TUDCA), taurochenodeoxycholic acid (TCDCA) and to cytokines [26].

Gene context of Ursodeoxycholyltaurine

• We have recently shown that both ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) prevent transforming growth factor beta1 (TGF-beta1)-induced hepatocyte apoptosis by modulating the E2F-1/p53/Bax pathway [27].
• Tauroursodeoxycholic acid inserts the bile salt export pump into canalicular membranes of cholestatic rat liver [28].
• Inhibition of the E2F-1/p53/Bax pathway by tauroursodeoxycholic acid in amyloid beta-peptide-induced apoptosis of PC12 cells [29].
• Tauroursodeoxycholic acid prevents Bax-induced membrane perturbation and cytochrome C release in isolated mitochondria [30].
• GR and 5-HTR1A were unaffected by treatment with either IFN-gamma or tauroursodeoxycholic acid (TUDCA) [31].

Analytical, diagnostic and therapeutic context of Ursodeoxycholyltaurine

• Tauroursodeoxycholic acid administered 1 hour after ischemia resulted in significantly increased bile acid levels in the brain, improved neurologic function, and an approximately 50% reduction in infarct size 2 and 7 days after reperfusion [14].
• Cellular distribution of thrombomodulin as an early marker for warm ischemic liver injury in porcine liver transplantation: protective effect of prostaglandin I2 analogue and tauroursodeoxycholic acid [32].
• We investigated in the human liver transplantation setting the effect of the addition of TUDCA at time of liver harvesting and cold storage on the intra- and postoperative enzyme release and liver histopathology at the end of cold storage, at reperfusion, and 7 days after transplantation [21].
• Animals were divided into six groups (each group; n = 8); a non-ischemia sham group (CS), a control group without bile acids (CON), and 4 bile acid groups; 10 mg/kg and 50 mg/kg (U10, U50), taurocholic acid 10 mg/kg (CA10) and tauroursodeoxycholic acid 10 mg/kg (CD10) [33].
• OBJECTIVE: To determine whether tauroursodeoxycholic acid (TUDCA) would prevent or ameliorate the liver injury in neonates treated with total parenteral nutrition (TPN) [34].

References