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Taurocholic acid


CAS No. : 81-24-3

(Synonyms: N-Choloyltaurine)

81-24-3
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Cat. No. : HY-B1788
M.Wt: 515.70
Formula: C26H45NO7S
Purity: >98 %
Solubility: H2O : 100 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic)
Introduction of 81-24-3 :

Taurocholic acid (N-Choloyltaurine) has marked bioactive effects such as an inhibitory potential against hepatic artery ligation induced biliary damage by upregulation of VEGF-A expression. Taurocholic acid has immunoregulation effect[1]. In Vitro:Taurocholic acid (100 μM, 24 h) decreases the proportion of CD3+CD8+ T and NK cells in isolated PBMCs from HBeAg-positive CHB patients[2].
Taurocholic acid (100 μM, 24 h) decreases IFN-α stimulated cytokine and cytotoxic granule levels (IFN-γ, TNF-α, granzyme B) in CD3+CD8+ T and NK cells[2].
In Vivo:Taurocholic acid (oral gavage, 100 mg/kg, 2 weeks) sodium promotes HBV replication by reducing the percentage of NK and CD3+CD8+ T cells in C57BL/6 mice with tail vein injection with rAAV8-1.3HBV[2].
Taurocholic acid (1% in diet, 1 week) sodium prevents hepatic artery ligation (HAL)-induced cholangiocyte damage in rats by upregulation of VEGF-A expression[3].
Taurocholic acid can be used in animal modeling to create stress-induced gastric injury models and pancreatitis models[3][4][5].
Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

1. Induction of stress-induced gastric injury[3]
Background
Both in humans and experimental animals, Taurocholic acid irritates the gastric mucosa and causes the reverse diffusion of acid through the broken barrier.
Specific Modeling Methods
Rat: Donryu strain rats • male • 230-240 g
Administration: 30-300 mg/kg • p.o • single dose.
Note
After rats have fasted for 24 hours, their pylorus is ligated under ether anesthesia. Fifteen minutes after pylorus ligation, medication is administered to the rats.
The pylorus-ligated rats are then placed in cages with restricted movement.
Subsequently, the cages are immersed in a water bath maintained at 23°C until the water level reaches the xiphoid process of the rats, lasting for 7 hours.
Seven hours later, the animals are sacrificed under ether anesthesia, and the stomach of each animal is removed. The gastric contents are collected through the esophagus and analyzed for volume and acidity.
Modeling Indicators
Molecular Changes: Significant reductions in acidity and pepsin activity were observed, along with an increase in Na+ concentration. However, there was no effect on gastric juice volume or K+ concentration.
Correlated Product(s): Aspirin (HY-14654)
Opposite Product(s): L-Glutamine (HY-N0390)
2. Induction of Acute Pancreatitis[4]
Background
Taurocholic acid induced the formation of interstitial edema and caused acinar cell vacuolization in the pancreatic lobules. Taurocholic acid also increased serum amylase and lipase activities. Interstitial edema becomes one of the most important criteria for assessing pancreatic damage in acute pancreatitis[4].
Specific Modeling Methods
Rat: Wistar • male • weighing 220-240 g
Administration: 1 mL/kg • retrograde infusion into the common pancreaticobiliary duct • at a speed of 0.25 mL/min[4]
Mice: Balb/c and Wistar • male • weighing 25-30 g and 250-300 g[5]
Administration: 1 mL/kg • retrograde infusion • perfusion for 8 h[5]
Note
(1) Before administration, mice were kept at room temperature of 23±1°C and 50-60 % relative humidity with free access to water and chow on a 12-h light/dark cycle. They were allowed to adapt to this environment for 5 days before the experiment, and received no nourishment and free access to water for 12 h preoperatively[1][2].
(2) Pancreatic acinar cells were isolated freshly from Balb/c or C57/BL6J mice using a collagenase IV. Cells were treated under room temperature, and used within 4 hours after isolation[2].
Modeling Indicators
Histological analysis: Taurocholic acid administration caused the formation of interstitial edema in the pancreas and an increase of pancreas weight. Acinar cell vacuolization was evident in the pancreatic lobules, accompanied by some foci of pancreatic hemorrhage and marked peritoneal ascites. A pyknotic nucleus was in the center of necrotic acinar cell with a bright border. Taurocholic acid administration induced marked oedema, inflammatory cell infiltration and acinar cell necrosis[1][2].
Biochemical Analysis: Taurocholic acid administration increased serum amylase and lipase activities[1].
Correlated Product(s): Neuronostatin; Flavonoids 1

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