Disease relevance of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• Acini were resuspended thereafter in fresh buffer and further incubated for 30-90 min under various conditions [e.g., with pancreatic homogenates, ascites (from rats with pancreatitis induced by sodium taurocholate), pure pancreatic enzymes, and other factors] [1].
• Interactions between ionized calcium and sodium taurocholate: bile salts are important buffers for prevention of calcium-containing gallstones [2].
• Hemolysis induced by 50 mmol/L sodium-taurocholate was reduced by both lecithin and cholesterol in a concentration-dependent manner [3].
• Cyclosporine in doses of 0.5, 1.0 and 1.5 mg.kg-1.hr-1 were administered along with 18 mumol/min intravenous sodium taurocholate to dogs with chronic biliary and gastric fistulas [4].
• Cholestasis induced by estradiol-17 beta-D-glucuronide: mechanisms and prevention by sodium taurocholate [5].

Psychiatry related information on 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• T group was infused sodium taurocholate as above, and 0.6% ligustrazine was then administered via the femoral vein [6].

High impact information on 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• When sodium taurocholate was infused at the rate of 27 mumol/100 g rat per h (equivalent to the hourly hepatic bile-acid flux), bile-acid synthesis decreased 82% and cholesterol 7 alpha-hydroxylase activity declined 78% [7].
• The intestinal absorption of sodium taurocholate was studied in the near-term fetal and neonatal dog [8].
• Also, tauroursodeoxycholate (TUDC), which activates p38(MAP) kinase (p38(MAPK), increased BSEP-positive pseudocanaliculi by more than 50% in rat sodium taurocholate cotransporting peptide (Ntcp)-transfected but not in untransfected HepG2 cells [9].
• LPS administration resulted in a concordant 90% reduction of basolateral protein expression of the hepatocyte sodium taurocholate cotransporter and markedly diminished sodium-dependent taurocholate uptake [10].
• Cytoprotection was assessed in bile duct-obstructed rats and by incubating human erythrocytes with sodium taurocholate [11].

Chemical compound and disease context of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• Furthermore, since it has been postulated that sodium taurocholate (TC) may interfere with either uptake or biliary excretion of other steroid agents, we tested whether E-17G cholestasis could be modified by TC administration [5].
• Differential effects of hypoxia on the disposition of propranolol and sodium taurocholate by the isolated perfused rat liver [12].
• The susceptibility of the gastric mucosa to injury by topical sodium taurocholate (40 mmol/l) in hydrochloric acid (150 mmol/l) was studied in prehepatic and cirrhotic rat models of portal hypertension [13].
• Exposure of Salmonella enterica to sodium cholate, sodium deoxycholate, sodium chenodeoxycholate, sodium glychocholate, sodium taurocholate, or sodium glycochenodeoxycholate induces the SOS response, indicating that the DNA-damaging activity of bile resides in bile salts [14].
• The effect of a synthetic protease inhibitor, gabexate mesilate (GM), which was administered directly into the pancreatic duct, on acute pancreatitis induced by sodium taurocholate in dogs was investigated [15].

Biological context of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• Protein expression, messenger RNA levels, and tissue distribution of the bile acid transporters sodium taurocholate cotransporting protein (ntcp) and bile salt export pump (bsep) were also analyzed [16].
• Sodium taurocholate administered intravenously, either as a bolus or as an infusion at increasing submaximal rates, resulted in parallel increases of bile salt and alkaline phosphatase secretory rates into bile [17].
• From these results it was concluded that the primary active transport of sodium taurocholate is present in hepatocellular canalicular membranes [18].
• METHODS: The disintegration and DNA accessibility of conventional and fluorinated cationic lipoplexes and their in vitro transfection efficiency of human lung carcinoma epithelial A549 cells were studied in the presence of various concentrations of sodium taurocholate (STC), an anionic bile salt detergent [19].
• Gaucher's disease II. Studies on the kinetics of beta-glucosidase and the effects of sodium taurocholate in normal and Gaucher tissues [20].

Anatomical context of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• Effect of sodium taurocholate on the human gastric mucosa at acid and neutral pH's [21].
• The influence of sodium taurocholate on bile canalicular contractions was examined by time-lapse cinephotomicrography of isolated rat hepatocytes in primary monolayer cultures [22].
• The effect of low concentrations of sodium taurocholate on the secretory and electrical activity of isolated rabbit fundic mucosa has been studied [23].
• Bovine trypsin, with or without sodium taurocholate, was infused intraduodenally into conscious rats deprived of bile-pancreatic juice and the recovery of trypsin activity from the small intestine determined [24].
• Effect of mast cell degranulation on gastric mucosal damage produced by sodium taurocholate in the rat [25].

Associations of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid with other chemical compounds

• When back diffusion of H+ was induced by establishing a concentration gradient of H+ from S leads to N or by exposing the secretory surface to sodium taurocholate with secretory pH 2.25, the burimamide-inhibited tissue demonstrated significantly greater depression of the electrical parameters than the secreting mucosae [26].
• Prophylactic administration of FOY-305 had a significantly favorable effect on the course of the sodium taurocholate-induced disease and on the survival rate of the treated group [27].
• Optimal enzyme assay conditions required both Triton X-100 and sodium taurocholate, pH 4 [28].
• Cholic acid shows similar changes in the apparent pKa, being approximately 5.2 in sodium taurocholate micelles and at least 6.8 in phospholipid vesicles [29].
• Pure ACAT-1 dispersed in mixed micelles containing sodium taurocholate, phosphatidylcholine, and cholesterol remains catalytically active [30].

Gene context of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• Bile salts are rapidly removed from the circulation by the liver-specific sodium/taurocholate cotransporter (SLC10A1) [31].
• We investigated the serial changes in CCK-1R mRNA and protein levels and their immunolocalization after acute haemorrhagic pancreatitis induced in male Wistar rats by retrograde intraductal infusion of 4% sodium taurocholate (100 micro L 100 g(-1) body weight) [32].
• Furthermore, the significance of variable doses of the endothelin receptor antagonist LU13 (1 mg/kg, 3 mg/kg and 100 mg/kg) was determined in a 4% sodium taurocholate model and in a cerulein pancreatitis model [33].
• RESULTS: PACAP augmented caerulein-induced pancreatitis and failed to ameliorate sodium taurocholate-induced pancreatitis [34].
• The lipase activity increased 42 times in the presence of 10 mM sodium taurocholate, which for the first time provides direct evidence that a bile salt-activated lipase (bp-BAL) was isolated from bovine pancreas [35].

Analytical, diagnostic and therapeutic context of 2-[4-[(3R,7R,12S)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoylamino]ethanesulfonic acid

• In one set of experiments, the bile acid pool was depleted, and during a continuous i.v. infusion of sodium taurocholate (20 mumol/min), duodenal bile acid delivery was assessed over 6 h by a marker perfusion technique [36].
• Canalicular membrane vesicles were purified from the livers of Sprague-Dawley rats, and the uptake of tritiated sodium taurocholate into canalicular membrane vesicles was determined by rapid filtration technique [18].
• METHODS: Oedematous pancreatitis was induced by continuous intravenous infusion of caerulein and haemorrhagic pancreatitis by retrograde injection of sodium taurocholate into the biliopancreatic duct [37].
• Decreased sterol biosynthesis in vivo was elicited by feeding sodium taurocholate or by fasting the rats, whereas increased synthesis was induced by biliary ligation or feeding cholestyramine, a bile salt binding resin; these effects were monitored by assay of mucosal 3-hydroxy-3-methylglutaryl coenzyme A reductase [38].
• In male Sprague-Dawley rats, a bile-duct cannula was inserted to collect bile, and sodium taurocholate was infused (100 nmol/min per 100 g) for 60 min [39].

References