Nordeoxycholic Acid
(Synonyms: 去甲脱氧氯酸,23-NDCA, 23-Nordeoxycholic Acid) 目录号 : GC47792A metabolite of norcholic acid and derivative of deoxycholic acid
Cas No.:53608-86-9
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nordeoxycholic acid is a metabolite of the bile acid norcholic acid and a 23-carbon derivative of deoxycholic acid .1 Levels of nordeoxycholic acid are decreased in the liver of rats in a high-fat diet model of non-alcoholic fatty liver disease (NAFLD) and serum levels are lower in men compared with women.2,3 Nordeoxycholic acid has commonly been used as an internal standard for the quantification of bile acids in various sample types by GC- and LC-MS.4,5
1.Nakatomi, F., Kihira, K., Kuramoto, T., et al.Intestinal absorption and metabolism of norcholic acid in ratsJ. Pharmacobiodyn8(7)557-563(1985) 2.Tang, Y., Zhang, J., Li, J., et al.Turnover of bile acids in liver, serum and caecal content by high-fat diet feeding affects hepatic steatosis in ratsBiochim. Biophys. Acta Mol. Cell Biol. Lipids1864(10)1293-1304(2019) 3.Xie, G., Wang, Y., Wang, X., et al.Profiling of serum bile acids in a healthy Chinese population using UPLC-MS/MSJ. Proteome Res.14(2)850-859(2015) 4.Bergeron, A., Furtado, M., and Garofolo, F.Importance of using highly pure internal standards for successful liquid chromatography/tandem mass spectrometric bioanalytical assaysRapid Commun. Mass Spectrom.23(9)1287-1197(2009) 5.Evrard, E., and Janssen, G.Gas-liquid chromatographic determination of human fecal bile acidsJ. Lipid Res.9(2)226-236(1968)
| Cas No. | 53608-86-9 | SDF | |
| 别名 | 去甲脱氧氯酸,23-NDCA, 23-Nordeoxycholic Acid | ||
| 化学名 | (3α,5β,12α)- 3,12- dihydroxy-24- norcholan -23- oic acid | ||
| Canonical SMILES | C[C@H](CC(O)=O)[C@@]1([H])CC[C@@]2([H])[C@]3([H])CC[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@@]21C | ||
| 分子式 | C23H38O4 | 分子量 | 378.6 |
| 溶解度 | DMF: 15mg/mL,DMF:PBS (pH 7.2) (1:4): 0.2mg/mL,DMSO: 10mg/mL,Ethanol: 10mg/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。 |
||
| 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 | 2.6413 mL | 13.2066 mL | 26.4131 mL |
| 5 mM | 0.5283 mL | 2.6413 mL | 5.2826 mL |
| 10 mM | 0.2641 mL | 1.3207 mL | 2.6413 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。
Interpretation of enantioresolution in Nordeoxycholic Acid channels based on the four-location model
Chirality 2003 Jan;15(1):53-9.PMID:12467043DOI:10.1002/chir.10159.
Nordeoxycholic Acid (NDCA) forms three kinds of host frameworks, M1, M2, and M3, with channels where aliphatic alcohols (1-7) are accommodated. (13)C-NMR studies clarified that racemic alcohols 1- or 2-6 are enclosed in the M1- or M2-type channel with lower than 15% enantiomeric excess, respectively, while 3-methyl-2-pentanol (7) is done in the M3-type with 47% ee. These inclusion phenomena can be explained due to the Difference Fourier maps of electron densities of their enantiomers in the channels. In addition, analysis of the manner of packing indicates that four locations in the channels should be fixed for the enantioresolution of the alcohols. These results support the four-location model, which has been proposed by Mesecar et al.(20) with respect to enantioresolution on protein surfaces.
Intestinal absorption and metabolism of norcholic acid in rats
J Pharmacobiodyn 1985 Jul;8(7):557-63.PMID:4067817DOI:10.1248/bpb1978.8.557.
Intestinal absorption and hepatic and intestinal bacterial biotransformations of norcholic acid, the C23 homologue of cholic acid, were studied in the rats. Norcholic acid, like cholic acid, was efficiently absorbed from the intestine and quickly secreted into the bile. Unlike the C24 bile acid, however, which is secreted by rat liver as its taurine conjugate, the C23 bile acid appeared in the bile predominantly as the unconjugated form. conjugated form. Bacterial modification of norcholic acid was similar to but less extensive than that of cholic acid. A considerable part of norcholic acid was left unchanged during its passage through the intestinal tract. A major bacterial metabolite of norcholic acid was the 7-dehydrogenation product, 7-ketonordeoxycholic acid, rather than the 7-dehydroxylation product, Nordeoxycholic Acid, though the reverse is true for cholic acid.
Dietary Macroalgae Saccharina japonica Ameliorates Liver Injury Induced by a High-Carbohydrate Diet in Swamp Eel ( Monopterus albus)
Front Vet Sci 2022 Jun 14;9:869369.PMID:35774985DOI:10.3389/fvets.2022.869369.
A high-carbohydrate diet lowers the rearing cost and decreases the ammonia emission into the environment, whereas it can induce liver injury, which can reduce harvest yields and generate economic losses in reared fish species. Macroalgae Saccharina japonica (SJ) has been reported to improve anti-diabetic, but the protective mechanism of dietary SJ against liver injury in fish fed a high-carbohydrate diet has not been studied. Therefore, a 56-day nutritional trial was designed for swamp eel Monopterus albus, which was fed with the normal diet [20% carbohydrate, normal carbohydrate (NC)], a high carbohydrate diet (32% carbohydrate, HC), and a HC diet supplemented with 2.5% SJ (HC-S). The HC diet promoted growth and lowered feed coefficient (FC), whereas it increased hepatosomatic index (HSI) when compared with the NC diet in this study. However, SJ supplementation increased iodine contents in muscle, reduced HSI, and improved liver injury, such as the decrease of glucose (GLU), total bile acid (TBA), and alanine aminotransferase (ALT) in serum, and glycogen and TBA in the liver. Consistently, histological analysis showed that SJ reduced the area of lipid droplet, glycogen, and collagen fiber in the liver (p < 0.05). Thoroughly, the underlying protective mechanisms of SJ supplementation against HC-induced liver injury were studied by liver transcriptome sequencing coupled with pathway analysis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differentially expressed genes (DEGs), such as the acetyl-coenzyme A synthetase (acss1), alcohol dehydrogenase (adh), interferon-induced protein with tetratricopeptide repeats 1 (ifit1), aldo-keto reductase family 1 member D1 (akr1d1), cholesterol 7-alpha-monooxygenase (cyp7a1), and UDP-glucuronosyltransferase (ugt), indicated that the pathway of glycolysis/gluconeogenesis was the main metabolic pathway altered in the HC group compared with the NC group. Meanwhile, hepatitis C, primary BA biosynthesis, and drug metabolism-cytochrome P450 were the three main metabolic pathways altered by SJ supplementation when compared with the HC group. Moreover, the BA-targeted metabolomic analysis of the serum BA found that SJ supplementation decreased the contents of taurohyocholic acid (THCA), taurochenodeoxycholic acid (TCDCA), taurolithocholic acid (TLCA), Nordeoxycholic Acid (NorDCA), and increased the contents of ursocholic acid (UCA), allocholic acid (ACA), and chenodeoxycholic acid (CDCA). In particular, the higher contents of UCA, ACA, and CDCA regulated by SJ were associated with lower liver injury. Overall, these results indicate that the 2.5% supplementation of SJ can be recommended as a functional feed additive for the alleviation of liver injury in swamp eel-fed high-carbohydrate diets.
Salvia-Nelumbinis naturalis extract protects mice against MCD diet-induced steatohepatitis via activation of colonic FXR-FGF15 pathway
Biomed Pharmacother 2021 Jul;139:111587.PMID:33865013DOI:10.1016/j.biopha.2021.111587.
Salvia-Nelumbinis naturalis (SNN) formula is a traditional Chinese medicine prescription, and has been confirmed to be effective in treating non-alcoholic steatohepatitis (NASH), but the underlying mechanisms are still unknown. Here we showed that 4-week SNN administration alleviated methionine-choline-deficiency (MCD) diet-induced hepatic steatosis and inflammation as well as serum levels of alanine transaminase (ALT) increase in C57BL/6 mice. Fecal 16S rDNA sequencing indicated that SNN altered the structure of gut microbiota and partially reversed the gut dysbiosis. Simultaneously, we analyzed the fecal BA profile using liquid chromatography coupled with triple quadrupole mass spectrometry (UPLC-TQMS) -based metabolomics, and found that SNN modulated fecal BA profile, predominantly increased the microbiomes related BA species (e.g. Nordeoxycholic Acid) which in turn, activated farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) signaling pathway in the colon but not the ileum. The activation of intestinal FXR-FGF15 signaling was accompanied by increase of liver protein kinase B (PKB/Akt) phosphorylation, and decrease of p-65 subunit of NF-κB phosphorylation, resulting in less liver CD68 positive macrophages, and inflammatory cytokine IL-1β and TNF-α expression. Our results established the link between SNN treatment, gut microbiota, BA profile and NASH, which might shed light into the mechanisms behind the beneficial effects of SNN on NASH, thus provide evidence for the clinical application of SNN.
A single-injection targeted metabolomics profiling method for determination of biomarkers to reflect tripterygium glycosides efficacy and toxicity
Toxicol Appl Pharmacol 2020 Jan 15;389:114880.PMID:31945383DOI:10.1016/j.taap.2020.114880.
Metabolomics is a powerful tool for studying physiological state of the system. In this study, we proposed a single-injection targeted metabolomics method to identify reliable tripterygium glycosides efficacy and toxicity related biomarkers based on ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Through careful optimization of the UHPLC-MS/MS conditions, a total of 289 metabolites can be quantified in single-injection of 27 min using both positive and negative scanning modes with rapid polarity switching. Tripterygium glycosides is widely used in clinical for its excellent anti-inflammatory and immunosuppressive functions. However, it is the most common drug that can cause hepatotoxicity. In this study, the established metabolomics method was used for determination of biomarkers to reflect tripterygium glycosides efficacy and toxicity. Two different dosages were designed in the animal experiment, including therapeutic dosage and toxic dosage. Statistical analysis based on metabolite concentrations showed that the glutathione metabolism and pyrimidine metabolism were the obvious interfering pathways. This was highly consistent with previous studies. A total of 22 and 47 metabolites were screened as potential biomarkers related to the efficacy and hepatotoxicity of tripterygium glycosides, respectively. Receiver operating characteristic curve (ROC) analysis showed that ten metabolites, including cytosine, 5-methyluridine, deoxyuridine, 5-methylcytidine, deoxycytidine triphosphate (DCTP), keto-glutarate, d-ribose, dihydrofolate, Nordeoxycholic Acid and isodeoxycholic acid possessed area under the curve (AUC) of 1. The metabolites filtered here can better distinguish tripterygium glycosides treated rats from the control rats compared with the traditional blood indicators of liver function.