Taurochenodeoxycholic acid (12-Deoxycholyltaurine)
(Synonyms: 牛磺鹅去氧胆酸; 12-Deoxycholyltaurine) 目录号 : GC33825
A quantitative analytical standard guaranteed to meet MaxSpec identity, purity, stability, and concentration specifications
Cas No.:516-35-8
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Animal experiment: |
Rats: Male Wistar rats are divided into six groups of ten each. Group 1 is normal rat (Sham), Group 2 received FCA only, Group 3 and Group 4 received FCA+Taurochenodeoxycholic acid (0.1 g/kg) and FCA+Taurochenodeoxycholic acid (0.2 g/kg), respectively, Groups 3 and 4 are treated beginning from day 0 of injection of FCA, Group 5 and Group 6 received FCA+Taurochenodeoxycholic acid (0.1 g/kg) and FCA+Taurochenodeoxycholic acid (0.2 g/kg), respectively, Group 5 and Group 6 are treated from 14 days after induction. All animals are treated with intragastrical administration and sacrificed after 28 days of induction[4]. |
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References: [1]. Wang X, et al. Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway. Eur J Pharmacol. 2016 Sep 5;786:109-15. |
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Taurochenodeoxycholic acid (TCDCA) is a taurine-conjugated form of the primary bile acid chenodeoxycholic acid .1 Serum levels of TCDCA increase approximately 5-fold within two hours and begin to decrease within four hours during an oral lipid tolerance test in humans.2 Serum levels of TCDCA are increased in patients with liver cirrhosis and may serve as a marker of disease progression.3
TCDCA MaxSpec standard is a quantitative grade standard of TCDCA that has been prepared specifically for mass spectrometry and related applications where quantitative reproducibility is required. The solution has been prepared gravimetrically and is supplied in a deactivated glass ampule sealed under argon. The concentration was verified by comparison to an independently prepared calibration standard. The verified concentration is provided on the certificate of analysis. This TCDCA MaxSpec standard is guaranteed to meet identity, purity, stability, and concentration specifications and is provided with a batch-specific certificate of analysis. Ongoing stability testing is performed to ensure the concentration remains accurate throughout the shelf life of the product. Note: The amount of solution added to the vial is in excess of the listed amount. Therefore, it is necessary to accurately measure volumes for preparation of calibration standards. Follow recommended storage and handling conditions to maintain product quality.
牛磺酸基合成的原胆酸对羟基基团的一种共轭物质，称为牛磺酸基合成的降解胆酸，它是主要的胆汁酸之一。1 在口服脂质耐受性试验中，人体血清中的TCDCA水平在两小时内增加了约5倍，并在四小时内开始下降。2 肝硬化患者的血清TCDCA水平增加，可能作为疾病进展的标志物。3
TCDCA MaxSpec标准是一种定量级别的TCDCA标准，专门为质谱和相关应用而制备，需要量化重现性。该溶液经过重量法制备，密封在惰性气体氩气下的失活玻璃安瓿中提供。通过与独立制备的校准标准进行比较，已验证浓度。验证的浓度提供在分析证书上。该TCDCA MaxSpec标准保证符合标识、纯度、稳定性和浓度规范，并提供具有批次特异性的分析证书。持续进行稳定性测试以确保在产品的货架寿命期间浓度保持准确。注意：加入到小瓶中的溶液量超过了所列数量。因此，需要准确测量体积以准备校准标准。遵循推荐的存储和处理条件以维护产品质量。
1.Hoffman, A.F.The continuing importance of bile acids in liver and intestinal diseaseArch. Intern. Med.159(22)2647-2658(1999) 2.Schmid, A., Neumann, H., Karrasch, T., et al.Bile acid metabolome after an oral lipid tolerance test by liquid chromatography-tandem mass spectrometry (LC-MS/MS)PLoS One11(2)e0148869(2016) 3.Wang, X., Xie, G., Zhao, A., et al.Serum bile acids are associated with pathological progression of hepatitis B-induced cirrhosisJ. Proteome Res.15(4)1126-1134(2016)
| Cas No. | 516-35-8 | SDF | |
| 别名 | 牛磺鹅去氧胆酸; 12-Deoxycholyltaurine | ||
| Canonical SMILES | C[C@@]1([C@@]2([H])[C@H](C)CCC(NCCS(=O)(O)=O)=O)[C@](CC2)([H])[C@@]([C@@H](C[C@]3([H])C[C@H](O)CC4)O)([H])[C@]([C@]34C)([H])CC1 | ||
| 分子式 | C26H45NO6S | 分子量 | 499.7 |
| 溶解度 | DMSO : ≥ 25 mg/mL (50.03 mM) | 储存条件 | Store at RT |
| 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 | 2.0012 mL | 10.006 mL | 20.012 mL |
| 5 mM | 0.4002 mL | 2.0012 mL | 4.0024 mL |
| 10 mM | 0.2001 mL | 1.0006 mL | 2.0012 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。
Taurochenodeoxycholic acid mediates cAMP-PKA-CREB signaling pathway
Chin J Nat Med 2020 Dec;18(12):898-906.PMID:33357720DOI:10.1016/S1875-5364(20)60033-4.
Taurochenodeoxycholic acid (TCDCA) is one of the main effective components of bile acid, playing critical roles in apoptosis and immune responses through the TGR5 receptor. In this study, we reveal the interaction between TCDCA and TGR5 receptor in TGR5-knockdown H1299 cells and the regulation of inflammation via the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA)-cAMP response element binding (CREB) signal pathway in NR8383 macrophages. In TGR5-knockdown H1299 cells, TCDCA significantly activated cAMP level via TGR5 receptor, indicating TCDCA can bind to TGR5; in NR8383 macrophages TCDCA increased cAMP content compared to treatment with the adenylate cyclase (AC) inhibitor SQ22536. Moreover, activated cAMP can significantly enhance gene expression and protein levels of its downstream proteins PKA and CREB compared with groups of inhibitors. Additionally, TCDCA decreased tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-8 and IL-12 through nuclear factor kappa light chain enhancer of activated B cells (NF-κB) activity. PKA and CREB are primary regulators of anti-inflammatory and immune response. Our results thus demonstrate TCDCA plays an essential anti-inflammatory role via the signaling pathway of cAMP-PKA-CREB induced by TGR5 receptor.
Taurochenodeoxycholic acid inhibits the proliferation and invasion of gastric cancer and induces its apoptosis
J Food Biochem 2022 Mar;46(3):e13866.PMID:34278593DOI:10.1111/jfbc.13866.
Taurochenodeoxycholic acid (TCDCA) is the principal ingredient of Compound Shougong Powder. Despite traditional Chinese medicine (TCM) research demonstrates that Compound Shougong Powder can restrict tumor growth, whether TCDCA exerts a role in suppressing cancer as the major ingredient of Compound Shougong Powder remains unknown. This study aims to clarify the regulatory mechanism of TCDCA on gastric cancer. Gastric cancer cells SGC-7901 were cultured to investigate the effects of TCDCA on proliferation and apoptosis. Furthermore, a subcutaneously implanted tumor model was established using SGC-7901 cells in BALB/C nude mice and tumor volume was measured under low and high dose treatment of TCDCA. Cell proliferation, apoptosis, and invasion were subjected to 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, flow cytometry, and transwell assay. Differentially expressed genes were screened by transcriptome sequencing. Nude mouse tumorigenicity assay was initiated to identify the effect of TCDCA on both tumor volume and weight, and the expression of candidate genes screened by transcriptome sequencing was determined by real-time fluorescence quantification (qPCR) and Western blot. The experiments revealed that TCDCA could significantly inhibit the proliferation and invasion of gastric cancer cells and induce apoptosis of these cells. Meanwhile, test findings via in vivo indicated that TCDCA severely diminished the volume and weight of tumors. This study first demonstrated that TCDCA inhibited the proliferation and invasion of gastric cancer and induced apoptosis, which is expected to serve as an experimental basis for the application of TCM in tumor therapeutic options. PRACTICAL APPLICATIONS: Through this study, the inhibitory effect of Taurochenodeoxycholic acid on gastric cancer can be clarified, which provides a new research basis for the application of traditional Chinese medicine (TCM) and TCM monomer in cancer. In addition, this study can further promote the research and application of Chinese traditional medicine, which has important application value and economic benefits.
6alpha-hydroxylation of Taurochenodeoxycholic acid and lithocholic acid by CYP3A4 in human liver microsomes
Biochim Biophys Acta 1999 Apr 19;1438(1):47-54.PMID:10216279DOI:10.1016/s1388-1981(99)00031-1.
The aim of the present study was to identify the enzymes in human liver catalyzing hydroxylations of bile acids. Fourteen recombinant expressed cytochrome P450 (CYP) enzymes, human liver microsomes from different donors, and selective cytochrome P450 inhibitors were used to study the hydroxylation of Taurochenodeoxycholic acid and lithocholic acid. Recombinant expressed CYP3A4 was the only enzyme that was active towards these bile acids and the enzyme catalyzed an efficient 6alpha-hydroxylation of both Taurochenodeoxycholic acid and lithocholic acid. The Vmax for 6alpha-hydroxylation of Taurochenodeoxycholic acid by CYP3A4 was 18.2 nmol/nmol P450/min and the apparent Km was 90 microM. Cytochrome b5 was required for maximal activity. Human liver microsomes from 10 different donors, in which different P450 marker activities had been determined, were separately incubated with Taurochenodeoxycholic acid and lithocholic acid. A strong correlation was found between 6alpha-hydroxylation of Taurochenodeoxycholic acid, CYP3A levels (r2=0.97) and testosterone 6beta-hydroxylation (r2=0.9). There was also a strong correlation between 6alpha-hydroxylation of lithocholic acid, CYP3A levels and testosterone 6beta-hydroxylation (r2=0.7). Troleandomycin, a selective inhibitor of CYP3A enzymes, inhibited 6alpha-hydroxylation of Taurochenodeoxycholic acid almost completely at a 10 microM concentration. Other inhibitors, such as alpha-naphthoflavone, sulfaphenazole and tranylcypromine had very little or no effect on the activity. The apparent Km for 6alpha-hydroxylation of taurochenodeoxycholic by human liver microsomes was high (716 microM). This might give an explanation for the limited formation of 6alpha-hydroxylated bile acids in healthy humans. From the present results, it can be concluded that CYP3A4 is active in the 6alpha-hydroxylation of both Taurochenodeoxycholic acid and lithocholic acid in human liver.
Taurochenodeoxycholic acid Increases cAMP Content via Specially Interacting with Bile Acid Receptor TGR5
Molecules 2021 Nov 23;26(23):7066.PMID:34885648DOI:10.3390/molecules26237066.
Taurochenodeoxycholic acid (TCDCA) is one of the main components of bile acids (BAs). TCDCA has been reported as a signaling molecule, exerting anti-inflammatory and immunomodulatory functions. However, it is not well known whether those effects are mediated by TGR5. This study aimed to elucidate the interaction between TCDCA and TGR5. To achieve this aim, first, the TGR5 eukaryotic vector was constructed. The expression level of TGR5 in 293T cells was determined by immunofluorescence, real-time quantitative PCR (RT-PCR, qPCR), and Western blot. The luciferase assay, fluorescence microscopy, and enzyme-linked immunosorbent assay (ELISA) were recruited to check the interaction of TCDCA with TGR5. TCDCA treatment in 293T cells resulted in TGR5 internalization coupled with a significant increase in cAMP luciferase expression. Our results demonstrated that TCDCA was able to bind to the TGR5 receptor and activate it. These results provide an excellent potential therapeutic target for TCDCA research. Moreover, these findings also provide theoretical evidence for further TCDCA research.
Taurochenodeoxycholic acid ameliorates and ursodeoxycholic acid exacerbates small intestinal inflammation
Am J Physiol 1997 May;272(5 Pt 1):G1249-57.PMID:9176237DOI:10.1152/ajpgi.1997.272.5.G1249.
Intraluminal bacteria, food intake, and bile play important roles in indomethacin-induced small intestinal inflammation in rats. Tauroursodeoxycholic acid (TUDCA) and ursodeoxycholic acid (UDCA) inhibit hydrophobic bile acid-induced damage in various types of cells. We investigated the effects of these bile acids along with the possible influence of other bile acids on this model of inflammation. Clinical and intestinal inflammatory parameters and bile secretion were assessed after 7-day dietary bile acid pretreatments and subsequent indomethacin injections. UDCA significantly enhanced indomethacin-associated reductions in food intake and body weight, increases in gross inflammatory scores and myeloperoxidase activity, and the shortening of small intestinal length. Taurochenodeoxycholic acid (TCDCA) significantly normalized the clinical inflammatory parameters, prevented indomethacin-induced increases in the biliary contents of secondary bile acids and hydrophobicity index, and tended to attenuate the intestinal inflammation. Although elevated biliary levels of muricholic acids and a decreased hydrophobicity index were evident before indomethacin injection in the TCDCA case, these alterations could not explain the TCDCA-mediated protection. Dietary TCDCA attenuates whereas UDCA exacerbates intestinal inflammation in this model. Alterations in the bile composition (increases in UDCA and chenodeoxycholic acid) may explain the observed modification effects.