Taurocholic Acid (sodium salt)
(Synonyms: 牛磺胆酸钠,Sodium taurocholate; N-Choloyltaurine sodium) 目录号 : GC44993
A taurine-conjugated form of cholic acid
Cas No.:145-42-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Taurocholic acid (TCA) is a taurine-conjugated form of the primary bile acid cholic acid . Serum levels of TCA are decreased in patients with Crohn's disease and those with ulcerative colitis with no extraintestinal manifestations, but are increased in patients with ulcerative colitis accompanied by hepatobiliary disease.
| Cas No. | 145-42-6 | SDF | |
| 别名 | 牛磺胆酸钠,Sodium taurocholate; N-Choloyltaurine sodium | ||
| Canonical SMILES | O[C@@H]1C[C@]2([H])C[C@H](O)CC[C@]2(C)[C@]3([H])[C@]1([H])[C@@](CC[C@]4([H])[C@@H](CCC(NCCS([O-])(=O)=O)=O)C)([H])[C@]4(C)[C@@H](O)C3.[Na+] | ||
| 分子式 | C26H45NO7S•Na | 分子量 | 537.7 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 20 mg/ml,Ethanol: 2 mg/ml,PBS (pH 7.2): 3 mg/ml | 储存条件 | Store at 0-6°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.8598 mL | 9.2989 mL | 18.5977 mL |
| 5 mM | 0.372 mL | 1.8598 mL | 3.7195 mL |
| 10 mM | 0.186 mL | 0.9299 mL | 1.8598 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Protective effects of Taurocholic Acid on excessive hepatic lipid accumulation via regulation of bile acid metabolism in grouper
Food Funct 2022 Mar 7;13(5):3050-3062.PMID:35199809DOI:10.1039/d1fo04085e.
Dietary bile acid (BA) supplementation can notably ameliorate fatty liver disease caused by high dietary lipids, but the mechanism behind this is poorly understood. The present study was aimed at gaining insight into how TCA (Taurocholic Acid sodium) reduced hepatic lipid accumulation via the regulation of bile acid metabolism. We explored BA metabolism in juvenile hybrid grouper (Epinephelus fuscoguttatus♀ × E. lanceolatus♂). Three trials were: (1) fed the control, high lipid (HD) or gradient TCA diet; (2) fed a BA diet with or without antibiotics; and (3) injected with an agonist or antagonist of TGR5 (G protein-coupled bile acid receptor 1) and FXR (farnesoid X receptor). The results showed that the TCA diet (about 900 mg kg-1) significantly reduced lipid accumulation in the liver, thus improving liver health. The HD suppressed the abundance of bile-salt hydrolase (BSH) microbes, thus decreasing the concentration of unconjugated primary BAs. TCA administration altered the gut microbial composition and weakened the effects of the HD, thus increasing the level of unconjugated BAs. TCA treatment increased the transport and reabsorption of BAs by activating the TGR5 and FXR signaling pathways, and increased the BA pool size. Furthermore, the presence of microbiota in the intestine increased BA reabsorption and the BA pool size. Our study revealed that exogenous TCA alters the structure of intestinal microbiota and BA composition, then activated the FXR expression, thus regulating the BA metabolism via enhanced BA reabsorption. This, in turn, reduced lipid accumulation and improved the health of the liver in grouper.
Bile acid salt binding with colesevelam HCl is not affected by suspension in common beverages
J Pharm Sci 2006 Dec;95(12):2751-9.PMID:16937334DOI:10.1002/jps.20734.
It has been previously reported that anions in common beverages may bind to bile acid sequestrants (BAS), reducing their capacity for binding bile acid salts. This study examined the ability of the novel BAS colesevelam hydrochloride (HCl), in vitro, to bind bile acid sodium salts following suspension in common beverages. Equilibrium binding was evaluated under conditions of constant time and varying concentrations of bile acid salts in simulated intestinal fluid (SIF). A stock solution of sodium salts of glycochenodeoxycholic acid (GCDC), taurodeoxycholic acid (TDC), and glycocholic acid (GC), was added to each prepared sample of colesevelam HCl. Bile acid salt binding was calculated by high-performance liquid chromatography (HPLC) analysis. Kinetics experiments were conducted using constant initial bile acid salt concentrations and varying binding times. The affinity, capacity, and kinetics of colesevelam HCl binding for GCDC, TDC, and GC were not significantly altered after suspension in water, carbonated water, Coca-Cola, Sprite, grape juice, orange juice, tomato juice, or Gatorade. The amount of bile acid sodium salt bound as a function of time was unchanged by pretreatment with any beverage tested. The in vitro binding characteristics of colesevelam HCl are unchanged by suspension in common beverages.
Bile acid and bile salt disrupt gastric mucosal barrier in the dog by different mechanisms
Am J Physiol 1982 Feb;242(2):G95-9.PMID:7065146DOI:10.1152/ajpgi.1982.242.2.G95.
The present study was undertaken to assess the mechanism by which protonated Taurocholic Acid disrupts the gastric mucosal barrier. By the criterion of lecithin solubilization, the critical micellar concentration of Taurocholic Acid (pH 1) was 4.5 mM, as opposed to 3.0 mM for sodium taurocholate (pH 7). In canine Heidenhain pouches, Taurocholic Acid significantly increased net forward diffusion of Na+ and backdiffusion of H+ at concentrations of 9, 4.5, and 3.5 mM, indicating that micelle formation was not required for disruption of the gastric mucosal barrier by this bile acid. Saturation of the 9 mM Taurocholic Acid solution with lecithin (and cholesterol) did not prevent disruption of the gastric mucosal barrier. At 9 mM, Taurocholic Acid was absorbed from the pouches at a mean rate of 1,150 +/- 115 nmol/min in contrast to an absorption rate of 225 +/- 10 nmol/min for sodium taurocholate at the same concentration. These findings indicate that, unlike ionized bile salts, disruption of the gastric mucosal barrier by Taurocholic Acid is mediated largely by uptake of bile acid by the gastric mucosa rather than dissolution of mucosal membrane lipids.
Oral absorption mechanism and anti-angiogenesis effect of taurocholic acid-linked heparin-docetaxel conjugates
J Control Release 2014 Mar 10;177:64-73.PMID:24412572DOI:10.1016/j.jconrel.2013.12.034.
Oral delivery is the preferred route to deliver therapeutics via nanoparticles due to ease of administration and patient acceptance. Here, we report on the findings of the absorption pathway of Taurocholic Acid (TCA)-linked heparin and docetaxel (DTX) conjugate, which we refer to as HDTA. We studied the oral absorption of HDTA using a Caco-2 cell transport system and an animal model. We have also used other absorption enhancers, such as ethylene glycol tetraacetic acid (EGTA), or inhibitors, such as sodium azide, to compare the relative permeability of HDTA conjugates. In vivo comparative studies were conducted using free TCA as a pre-administration and exhibited the maximum absorption site of the organ after oral administration of HDTA conjugates. HDTA was found to be absorbed mainly in the ileum and Caco-2 cell monolayer through passive diffusion and bile acid transporters. High fluorescence intensity of HDTA in mice came from the ileum, and it was eliminated from the body through colon. This novel formulation could be further investigated by clinical trials to find the prospect of oral anti-cancer drug delivery through anti-angiogenic treatment strategies.
Recovery of Caco-2 Cell Monolayers to Normal from the Transport-enhanced State Induced by Capric Acid sodium salt and its Monoacylglycerol
Biosci Biotechnol Biochem 1999;63(4):680-7.PMID:27389102DOI:10.1271/bbb.63.680.
Caco-2 cell monolayers were used as a model of the intestinal epithelium to investigate the recovery profile from the transport-enhanced state induced by the transport enhancers, capric acid sodium salt (C10FANa) and capric acid monoacylglycerol (C10MG). The transepithelial electrical resistance, MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide) assay, and lactate dehydrogenase (LDH) release rate were investigated. The cell monolayer recovered depending on the concentration of the enhancer and on the exposure time. The MTT assay revealed that the cells recovered their mitochondrial dehydrogenase activity without proliferation. The cell monolayer exposed to C10FANa released LDH to both the apical and basolateral sides, but to C10MG, only to the apical side. The results were compared with those for SDS and Taurocholic Acid sodium salt, and the effect of C10FANa was found to be different. These results suggest that the damage by MCFA compounds is recoverable and that the recovery can be assessed by an MTT assay, but that the LDH-release behavior is different among the enhancers.