Cholic acid sodium
(Synonyms: 胆酸钠) 目录号 : GC39670
A primary bile acid
Cas No.:361-09-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cholic acid is a primary bile acid.1 It is formed from cholesterol via a multistep process catalyzed by the cytochrome P450 (CYP) isoforms CYP7A1, CYP8B1, and CYP27A1. Cholic acid is conjugated to glycine or taurine by bile acid-CoA:amino acid N-acyltransferase (BAAT) to produce glycocholic acid and taurocholic acid , respectively, in the liver, and is transformed into the secondary bile acid deoxycholic acid by intestinal microbiota.1,2,3 It induces C. difficile colony formation in an agar dilution assay when used at a concentration of 0.1% w/v.4 Dietary administration of cholic acid (0.4% w/w) increases serum cholesterol levels, biliary phospholipid secretion, and fecal DCA levels in rats.5
1.?arenac, T.M., and Mikov, M.Bile acid synthesis: From nature to the chemical modification and synthesis and their applications as drugs and nutrientsFront. Pharmacol.9939(2018) 2.Hunt, M.C., Siponen, M.I., and Alexson, S.E.H.The emerging role of acyl-CoA thioesterases and acyltransferases in regulating peroxisomal lipid metabolismBiochim. Biophys. Acta1822(9)1397-1410(2012) 3.Staley, C., Weingarden, A.R., Khoruts, A., et al.Interaction of gut microbiota with bile acid metabolism and its influence on disease statesAppl. Microbiol. Biotechnol.101(1)47-64(2017) 4.Sorg, J.A., and Sonenshein, A.L.Bile salts and glycine as cogerminants for Clostridium difficile sporesJ. Bacteriol.190(7)2505-2512(2008) 5.Uchida, K., Nomura, Y., and Takeuchi, N.Effects of cholic acid, chenodeoxycholic acid, and their related bile acids on cholesterol, phospholipid, and bile acid levels in serum, liver, bile, and feces of ratsJ. Biochem.87(1)187-194(1980)
| Cas No. | 361-09-1 | SDF | |
| 别名 | 胆酸钠 | ||
| Canonical SMILES | C[C@H](CCC(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])C[C@H](O)[C@@]21C.[Na+] | ||
| 分子式 | C24H40NaO5 | 分子量 | 431.56 |
| 溶解度 | DMSO: 86 mg/mL (199.74 mM) | 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3172 mL | 11.5859 mL | 23.1717 mL |
| 5 mM | 0.4634 mL | 2.3172 mL | 4.6343 mL |
| 10 mM | 0.2317 mL | 1.1586 mL | 2.3172 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。
Effects of Dietary Astragalus Polysaccharide Supplementation on the Th17/Treg Balance and the Gut Microbiota of Broiler Chickens Challenged With Necrotic Enteritis
Front Immunol 2022 Feb 21;13:781934.PMID:35265068DOI:10.3389/fimmu.2022.781934.
This study aimed to investigate the effects of dietary astragalus polysaccharide (APS) supplementation on the immune function, gut microbiota and metabolism of broiler chickens challenged with necrotic enteritis (NE). Two hundred forty Arbor Acres broiler chicks (one day old) were randomly assigned using a 2 × 2 factorial arrangement into two groups fed different levels of dietary APS (0 or 200 ppm of diet) and two disease challenge groups (control or NE challenged). The results showed that NE infection significantly increased FCR, mortality rate, Th17/Treg (Th17 cells% in blood and ileum, Th17/Treg, IL-17 and IL-17/IL-10 in blood), NO, lysozyme activity and IL-1β in blood, intestinal immune cell proportion and activity (Tc%, Treg% and monocyte phagocytic activity in ileum), intestinal inflammatory cytokines (TLR2, NF-κB, TNF-α and IL- 6) gene expression levels, and the number of Clostridium perfringens in cecum. NE infection significantly reduced body weight gain, thymus index, lymphocyte proliferation activity in blood and ileum, villus height and V/C in jejunum, Th cells% and Mucin2 gene expression in ileum. Dietary APS supplementation significantly increased body weight, feed intake, proportion of immune cells (T cells in blood and Tc, Treg in ileum), lymphocyte proliferation activity, V/C in jejunum, and ZO-1 gene expression in ileum. Dietary APS supplementation significantly reduced FCR and mortality rate, Th17/Treg, Th17%, intestinal pathology scores, intestinal inflammatory cytokine gene expression levels, and the number of Clostridium perfringens in cecum. In addition, broilers challenged with NE significantly increased Staphylococcus and Turicibacter and reduced α diversity of microbiota in ileum. Dietary APS supplementation significantly increased α diversity, Romboutsia, Halomonas, propionic acid, butyric acid, formononetin, taurine, Cholic acid and equol and downregulated uric acid, L-arginine and serotonin in ileum. Spearman's correlation analysis revealed that Romboutsia, Turicibacter, Staphylocpccus, Halomonas, Streptococcus, Escherichia-Shigella, Prevotella, uric acid, L-arginine, jerivne, sodium cholate and Cholic acid were related to inflammation and Th17/Treg balance. In conclusion, APS alleviated intestinal inflammation in broilers challenged with NE probably by regulating intestinal immune, Th17/Treg balance, as well as intestinal microbiota and metabolites.
Induction of sodium-dependent bile acid transporter messenger RNA, protein, and activity in rat ileum by Cholic acid
Gastroenterology 1997 Nov;113(5):1599-608.PMID:9352862DOI:10.1053/gast.1997.v113.pm9352862.
Background & aims: The ileal sodium-dependent bile acid transporter reclaims bile acids from the intestinal lumen to preserve their enterohepatic recirculation. The present studies sought to determine the possible role of enteric bile acids in the molecular regulation of the apical bile acid transporter in rat ileal mucosa. Methods: Paired rats were fed a control diet or control diet plus Cholic acid (1%) or ursodeoxycholic acid (1%) for 10 days. Other paired rats underwent biliary diversion for 72 hours, followed by intraduodenal infusion of taurocholate or fluid/electrolytes. Transporter protein, messenger RNA (mRNA), and activity were determined in the distal 15 cm of ileal mucosa. Results: Transporter protein and mRNA levels in cholic acid-fed rats increased approximately threefold above levels in paired rats fed the control diet (P < 0.02). Similarly, sodium-dependent [3H]taurocholate uptake into membrane vesicles from cholic acid-fed rats increased twofold above uptake into vesicles from control-fed rats because of a twofold increase in maximal transport velocity. In biliary-diverted rats (72-96 hours), transporter protein decreased to 57% +/- 5% of paired controls with intact enterohepatic circulation (P < 0.0001). The intraduodenal infusion of taurocholate (24 hours) in biliary-diverted rats resulted in a time-dependent reinduction of transporter protein expression (3.5-fold). Conclusions: The expression of the ileal apical bile acid transporter is induced at a pretranslational level by free or taurine-conjugated Cholic acid within the small intestine.
Spermicidal and antiviral properties of Cholic acid: contraceptive efficacy of a new vaginal sponge (Protectaid) containing sodium cholate
Hum Reprod 1993 Jun;8(6):866-9.PMID:7688380DOI:10.1093/oxfordjournals.humrep.a138156.
Cholic acid (sodium cholate) exhibits a strong spermicidal and antiviral [anti-human immunodeficiency virus (HIV)-1] activity. The same effects are observed for F-5 Gel, the active mixture of a new contraceptive sponge (Protectaid), which contains sodium cholate in association with low concentrations (0.5%) of nonoxynol-9 and benzalkonium chloride. Both Cholic acid and the F-5 Gel exert a dose-dependent, in-vitro inhibitory effect (i) on the activity of HIV-1 associated reverse transcriptase in an acellular system and (ii) on the potential of HIV-1 efficiently to infect human lymphocytes. During 12 months use, the contraceptive efficacy of the 'Protectaid' sponge was 100% in 20 young women who had chosen this method for reasons of both contraception and anti-sexually transmitted disease. No side-effects were recorded throughout this period. Cervical cultures at 6-month intervals showed the presence of Mycoplasma hominis and Candida albicans in one or two cases. The combined spermicidal and anti-HIV properties of Cholic acid reported in this paper and used in the 'Protectaid' sponge offer a new and modern protective method of contraception.
Fluorescent benzofurazan-cholic acid conjugates for in vitro assessment of bile acid uptake and its modulation by drugs
ChemMedChem 2009 Mar;4(3):466-72.PMID:19173214DOI:10.1002/cmdc.200800383.
One of the most common mechanisms of hepatotoxicity is drug-induced cholestasis. Hence, new approaches for screening the cholestatic potential of drug candidates are desirable. In this context, we describe herein the use of synthetic 4-nitrobenzo-2-oxa-1,3-diazole (NBD) fluorescent conjugates of Cholic acid (ChA) at positions 3alpha, 3beta, 7alpha, and 7beta for in vitro assessment of bile acid uptake. All the conjugates show a strong absorption band between 400 and 550 nm and have a fluorescence quantum yield of approximately 0.45, with an emission maximum centered at approximately 530 nm. After their photophysical characterization, 3alpha-, 3beta-, 7alpha-, and 7beta-NBD-ChA were used to monitor uptake in freshly isolated rat hepatocytes by means of a previously optimized flow cytometry technique. Transport of the Cholic acid derivatives inside the cell was detected and quantified by measuring the increase of NBD green fluorescence within cells over time. The effect of troglitazone, a well-known inhibitor of bile acid uptake by the sodium taurocholate co-transporting polypeptide, supports the specificity of fluorescent NBD-ChA transport. According to the final intracellular fluorescence level attained and the uptake rate, 3alpha-NBD-ChA was found to be the most efficient derivative. Furthermore, sodium valproate, cyclosporin A, and chlorpromazine decreased the uptake of 3alpha-NBD-ChA, in agreement with their relative in vivo potency as cholestatic compounds; in contrast, sodium citrate (the negative control) had no effect. These results support the suitability of the in vitro flow cytometric assay with NBD-ChA to detect compounds that affect bile acid uptake.
Enterobacteria modulate intestinal bile acid transport and homeostasis through apical sodium-dependent bile acid transporter (SLC10A2) expression
J Pharmacol Exp Ther 2011 Jan;336(1):188-96.PMID:20884752DOI:10.1124/jpet.110.171736.
In our study, ampicillin (AMP)-mediated decrease of enterobacteria caused increases in hepatic bile acid concentration through (at least in part) elevation of bile acid synthesis in C57BL/6N mice. We investigated the involvement of enterobacteria on intestinal bile acid absorption in AMP-treated mice in the present study. Fecal enterobacterial levels and fecal bile acid excretion rates were markedly decreased in mice treated with AMP (100 mg/kg) for 3 days, whereas bile acid concentrations in portal blood were significantly increased compared with those in mice treated with a vehicle. Ileal apical sodium-dependent bile acid transporter (SLC10A2) mRNA levels and ileal SLC10A2 protein levels in brush-border membranes were significantly increased compared with those in mice treated with the vehicle. In AMP-treated mice, total bile acid levels were increased, whereas levels of enterobacteria-biotransformed bile acid, taurodeoxycholic acid, and Cholic acid were decreased in intestinal lumen. These phenomena were also observed in farnesoid X receptor-null mice treated with AMP for 3 days. Discontinuation of AMP administration after 3 days (vehicle administration for 4 days) increased levels of fecal enterobacteria, fecal bile acid excretion, and taurodeoxycholic acid and Cholic acid in the intestinal lumen, whereas the discontinuation decreased ileal SLC10A2 expression and bile acid concentrations in the portal blood. Coadministration of taurodeoxycholic acid or Cholic acid decreased ileal SLC10A2 expression in mice treated with AMP. These results suggest that enterobacteria-mediated bile acid biotransformation modulates intestinal bile acid transport and homeostasis through down-regulation of ileal SLC10A2 expression.