Taurochenodeoxycholic Acid (sodium salt)
(Synonyms: 牛磺鹅去氧胆酸钠盐; 12-Deoxycholyltaurine sodium) 目录号 : GC44992A taurine-conjugated form of chenodeoxycholic acid
Cas No.:6009-98-9
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Taurochenodeoxycholic acid (TCDCA) is a taurine-conjugated form of the primary bile acid chenodeoxycholic acid . Serum levels of TCDCA increase approximately 5-fold in within two hours and begin to decrease within four hours during an oral lipid tolerance test in humans. Serum levels of TCDCA are increased in patients with liver cirrhosis and may serve as a marker of disease progression.
Cas No. | 6009-98-9 | SDF | |
别名 | 牛磺鹅去氧胆酸钠盐; 12-Deoxycholyltaurine sodium | ||
Canonical SMILES | C[C@H](CCC(NCCS([O-])(=O)=O)=O)[C@@]1([H])CC[C@@]2([H])[C@]3([H])[C@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])CC[C@@]21C.[Na+] | ||
分子式 | C26H44NO6S•Na | 分子量 | 521.7 |
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 -20°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 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 1.9168 mL | 9.5841 mL | 19.1681 mL |
5 mM | 0.3834 mL | 1.9168 mL | 3.8336 mL |
10 mM | 0.1917 mL | 0.9584 mL | 1.9168 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 | ||||||||||
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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。
Endogenous bile acid disposition in rat and human sandwich-cultured hepatocytes
Toxicol Appl Pharmacol 2012 May 15;261(1):1-9.PMID:22342602DOI:10.1016/j.taap.2012.02.002.
Sandwich-cultured hepatocytes (SCH) are used commonly to investigate hepatic transport protein-mediated uptake and biliary excretion of substrates. However, little is known about the disposition of endogenous bile acids (BAs) in SCH. In this study, four endogenous conjugated BAs common to rats and humans [taurocholic acid (TCA), glycocholic acid (GCA), Taurochenodeoxycholic Acid (TCDCA), and glycochenodeoxycholic acid (GCDCA)], as well as two BA species specific to rodents (α- and β-tauromuricholic acid; α/β TMCA), were profiled in primary rat and human SCH. Using B-CLEAR® technology, BAs were measured in cells+bile canaliculi, cells, and medium of SCH by LC-MS/MS. Results indicated that, just as in vivo, taurine-conjugated BA species were predominant in rat SCH, while glycine-conjugated BAs were predominant in human SCH. Total intracellular BAs remained relatively constant over days in culture in rat SCH. Total BAs in control (CTL) cells+bile, cells, and medium were approximately 3.4, 2.9, and 8.3-fold greater in human than in rat. The estimated intracellular concentrations of the measured total BAs were 64.3±5.9 μM in CTL rat and 183±56 μM in CTL human SCH, while medium concentrations of the total BAs measured were 1.16±0.21 μM in CTL rat SCH and 9.61±6.36 μM in CTL human SCH. Treatment of cells for 24h with 10 μM troglitazone (TRO), an inhibitor of the bile salt export pump (BSEP) and the Na⁺-taurocholate cotransporting polypeptide (NTCP), had no significant effect on endogenous BAs measured at the end of the 24-h culture period, potentially due to compensatory mechanisms that maintain BA homeostasis. These data demonstrate that BAs in SCH are similar to in vivo, and that SCH may be a useful in vitro model to study alterations in BA disposition if species differences are taken into account.
Potential tumor-promoting activity of bile acids in rat glandular stomach
Jpn J Cancer Res 1987 Jan;78(1):32-9.PMID:3102436doi
The potential tumor-promoting and -initiating activities of bile acids in the glandular stomach mucosa of F344 rats after administration by gastric intubation were studied. Taurocholic acid sodium salt at doses of 300 to 1200 mg/kg body weight and glycocholic acid sodium salt at doses of 400 to 1200 mg/kg body weight induced up to 100-fold increases in ornithine decarboxylase activity with maxima after 4 hr and up to 10-fold increases in replicative DNA synthesis with maxima after 16-17 hr in the pyloric mucosa of the stomach. Taurodeoxycholic acid sodium salt, Taurochenodeoxycholic Acid sodium salt and glycocholic acid also induced high ornithine decarboxylase activity, and glycodeoxycholic acid sodium salt and glycochenodeoxycholic acid sodium salt caused slight induction of ornithine decarboxylase activity, but taurolithocholic acid sodium salt did not induce ornithine decarboxylase activity at all in the pyloric mucosa of the stomach. Glycocholic acid sodium salt did not induce unscheduled DNA synthesis in the pyloric mucosa of the stomach. The present results suggest that six bile acids, but not taurolithocholic acid sodium salt, have potential tumor-promoting activities in the pyloric mucosa of rat stomach and that glycocholic acid sodium salt has no potential tumor-initiating activity in the pyloric mucosa of rat stomach.
Inhibition of endoplasmic reticulum stress combined with activation of angiotensin-converting enzyme 2: novel approach for the prevention of endothelial dysfunction in type 1 diabetic rats
Can J Physiol Pharmacol 2022 Mar;100(3):234-239.PMID:34587465DOI:10.1139/cjpp-2021-0170.
Persistent hyperglycemia in type 1 diabetes triggers numerous signaling pathways, which may prove deleterious to the endothelium. As hyperglycemia damages the endothelial layer via multiple signaling pathways, including enhanced oxidative stress, downregulation of angiotensin-converting enzyme 2 signaling, and exacerbation of endoplasmic reticulum (ER) stress, it becomes difficult to prevent injury using monotherapy. Thus, the present study was conceived to evaluate the combined effect of ER stress inhibition along with angiotensin-converting enzyme 2 activation, two major contributors to hyperglycemia-induced endothelial dysfunction, in preventing endothelial dysfunction associated with type 1 diabetes. Streptozotocin-induced diabetic animals were treated with either diminazene aceturate (5 mg·kg-1 per day, p.o.) or tauroursodeoxycholic acid, sodium salt (200 mg·kg-1 per day i.p.), or both for 4 weeks. Endothelial dysfunction was evaluated using vasoreactivity assay, where acetylcholine-induced relaxation was assessed in phenylephrine pre-contracted rings. Combination therapy significantly improved vascular relaxation when compared with diabetic control as well as monotherapy. Restoration of nitrite levels along with prevention of collagen led to improved vasodilatation. Moreover, there was an overall reduction in aortic oxidative stress. We conclude that by simultaneously inhibiting ER stress and activating angiotensin-converting enzyme 2 deleterious effects of hyperglycemia on endothelium were significantly alleviated. This could serve as a novel strategy for the prevention of endothelial dysfunction.
Dietary Bile Salt Types Influence the Composition of Biliary Bile Acids and Gut Microbiota in Grass Carp
Front Microbiol 2018 Sep 18;9:2209.PMID:30279683DOI:10.3389/fmicb.2018.02209.
Lipid metabolism can influence host's health. There is increasing evidence for interplay between two key regulating factors in lipid metabolism: bile acids (BAs) and gut microbiota. However, very little is known about how types of different diet-supplemented bile salts (BS) influence this interaction in vivo. We sought to explore these relationships using grass carp (Ctenopharyngodon idellus), which often suffers functional disorder of liver and gallbladder. We studied fluctuations of BAs in the gall and changes of microbial communities in the gut in response to seven different diets: five different BS, chelating BS agent, and control. The BS comprised two primary BS [sodium taurochololate (TCAS) and sodium taurochenodeoxycholate (TCDCAS)], sodium tauroursodeoxycholate (TUDCAS), and two secondary BS [sodium taurodeoxycholate (TDCAS) and sodium taurolithocholate (TLCAS)]. Supplementation of primary BS caused a more significant fluctuation of biliary BAs than secondary BS, and TCAS caused a more prominent increase than TCDCAS and TUDCAS. For the gut microbiota, primary BS tended to increase their diversity and induce community succession, secondary BS resulted in a higher firmicutes/bacteroidetes ratio, while TUDCAS had no significant effects. Changes of the gut microbiota triggered by different types of BS caused alteration in BAs biotransformation. Two-obesity-associated families, Lachnospiraceae and Ruminococcaceae were positively correlated with biliary cholic acid (CA), Taurochenodeoxycholic Acid (TCDCA), and deoxycholic acid (DCA). As both primary and secondary BS resulted in increased synthesis of toxic secondary Bas by the gut microbiota, future studies should pay closer attention to gut microbiota when considering BA treatment.
Ingestion of whey protein and β-conglycinin exerts opposite effects on intestinal FGF15 and serotonin secretion in mice
Front Endocrinol (Lausanne) 2023 Jan 27;14:1080790.PMID:36777350DOI:10.3389/fendo.2023.1080790.
Farnesoid X receptor (FXR) and Takeda G protein-coupled Receptor 5 (TGR5), the intestinal bile acid (BA) receptors, regulate the gut-derived hormones including fibroblast growth factor 15/19 (FGF15/19) and serotonin (5-hydrooxytryptamine, 5-HT). Here we show that ingestion of whey protein isolate, a milk protein, significantly decreased expression of heteromeric organic solute transporter Ostα and Ostβ, which is the basolateral BA transporter in the enterocyte, and increased the expression of FXR and FGF15 in C57BL6J mouse ileum and plasma FGF15 levels. In addition, the ingestion of whey protein isolate significantly suppressed expression of hepatic cholesterol-7α hydroxylase (CYP7A1), which induces the primary BA synthesis, bile salt export pump (BSEP) and sodium-taurocholate cotransporting polypeptide (NTCP), which are the key transporters for the BA excretion and uptake in the liver, and genes involved in gluconeogenesis, and decreased the primary BAs including cholic acid, taurocholic acid, glycocholic acid, and Taurochenodeoxycholic Acid in the liver compared with controls. Moreover, ingestion of whey protein isolate significantly decreased the expression of TGR5, glucagon-like peptide 1 (GLP-1), and tryptophan hydroxylase1 (Tph1) in the small intestine, leading to decreases in plasma 5-HT and insulin levels. On the other hand, ingestion of the soy protein β-conglycinin significantly increased the expression of Ostα and Ostβ, and decreased the expression of FGF15 in the ileum and plasma FGF15 levels, leading to the increases in expression of hepatic CYP7A1, BSEP, NTCP, and genes involved in gluconeogenesis, and the primary BAs in the liver. Moreover, ingestion of β-conglycinin significantly increased the expression of intestinal TGR5, GLP-1, and Tph1, leading to increases in plasma 5-HT and insulin levels. These findings suggest that whey protein and β-conglycinin have opposite effects on intestinal FGF15 and 5-HT secretion in mice.