Glycocholic acid
(Synonyms: 甘氨胆酸) 目录号 : GC34134
A glycine-conjugated form of cholic acid
Cas No.:475-31-0
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
Glycocholic acid is a glycine-conjugated form of the primary bile acid cholic acid and has roles in the emulsification of fats.1,2 It reduces expression of the gene encoding the farnesoid X receptor (FXR) and increases expression of the genes encoding the bile acid receptors TGR5 and S1PR2 in SNU-245 cells when used at a concentration of 1.6 μmol/ml.3 Glycocholic acid (250 μM) increases the intracellular accumulation and cytotoxicity of epirubicin in Caco-2 cells, as well as decreases expression of the genes encoding multidrug resistance protein 1 (MDR1), MDR-associated protein 1 (MRP1), and MRP2 when used alone or in combination with epirubicin.4 It increases absorption of epirubicin into everted sacs of rat ileum and jejunum when used at a concentration of 250 μM. The bile acid composition ratio of glycocholic acid is elevated in bile of patients with cholangiocarcinoma compared with patients with pancreatic cancer or benign biliary diseases.3 Serum levels of glycocholic acid are elevated in patients with hepatocellular carcinoma compared with healthy individuals.2
1.Lefebvre, P., Cariou, B., Lien, F., et al.Role of bile acids and bile acid receptors in metabolic regulationPhysiol. Rev.89(1)147-191(2009) 2.Guo, C., Xie, C., Ding, P., et al.Quantification of glycocholic acid in human serum by stable isotope dilution ultra performance liquid chromatography electrospray ionization tandem mass spectrometryJ. Chromatogr. B. Analyt. Technol. Biomed. Life Sci.1072315-319(2018) 3.Song, W.-S., Park, H.-M., Ha, J.M., et al.Discovery of glycocholic acid and taurochenodeoxycholic acid as phenotypic biomarkers in cholangiocarcinomaSci. Rep.8(1)11088(2018) 4.Lo, Y.L., Ho, C.T., and Tsai, F.L.Inhibit multidrug resistance and induce apoptosis by using glycocholic acid and epirubicinEur. J. Pharm. Sci.35(1-2)52-67(2008)
| Cas No. | 475-31-0 | SDF | |
| 别名 | 甘氨胆酸 | ||
| Canonical SMILES | O=C(O)CNC(CC[C@@H](C)[C@H]1CC[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@]12C)=O | ||
| 分子式 | C26H43NO6 | 分子量 | 465.62 |
| 溶解度 | DMSO : ≥ 100 mg/mL (214.77 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 | 2.1477 mL | 10.7384 mL | 21.4767 mL |
| 5 mM | 0.4295 mL | 2.1477 mL | 4.2953 mL |
| 10 mM | 0.2148 mL | 1.0738 mL | 2.1477 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。
Glycocholic acid and glycodeoxycholic acid but not glycoursocholic acid inhibit bile acid synthesis in the rabbit
Gastroenterology 1992 May;102(5):1717-23.PMID:1568582DOI:10.1016/0016-5085(92)91735-m.
Feedback regulation of derepressed hepatic bile acid biosynthesis was studied individually with glycocholic, glycodeoxycholic, and glycoursocholic acids by infusion into bile acid-depleted rabbits. Construction of a bile fistula drained the endogenous bile acid pool (90% glycodeoxycholic acid, 10% Glycocholic acid) within 24 hours and elicited maximal bile acid synthesis after about 72 hours, at which time Glycocholic acid became the only biliary bile acid (greater than 98%). Replacement of the bile acid pool with Glycocholic acid or glycodeoxycholic acid at a rate equivalent to the hepatic endogenous bile acid flux inhibited endogenous biosynthesis by 40%. In contrast, glycoursocholic acid, the 7 beta-hydroxy epimer of Glycocholic acid, failed to suppress synthesis. Hepatic bile acid depletion increased hydroxymethyglutary coenzyme A (HMG-CoA) reductase activity fourfold and cholesterol 7 alpha-hydroxylase activity threefold, which were reduced 48% and 51%, respectively, from their maximum levels during replacement with Glycocholic acid. Glycodeoxycholic acid infusion depressed cholesterol 7 alpha-hydroxylase activity by 59% without reducing HMG-CoA reductase activity significantly. There was no significant change in the activity of either enzyme during glycoursocholic acid infusion. Biliary cholesterol and cholestanol secretion declined 13% and 53%, respectively, during Glycocholic acid infusion, were not affected by glycodeoxycholic acid infusion, but increased 19% and 43%, respectively, during glycoursocholic acid infusion. These results show that in rabbits the feedback regulation of hepatic bile acid synthesis depends on the hepatic flux of the normally present endogenous bile acids Glycocholic acid and glycodeoxycholic acid but does not respond to the 7 beta-hydroxy glycoursocholic acid. Glycocholic acid inhibits both HMG-CoA reductase and cholesterol 7 alpha-hydroxylase while glycodeoxycholic acid affects primarily cholesterol 7 alpha-hydroxylase. Thus, the regulation of bile acid synthesis may be mediated by both the availability of cholesterol substrate and the activity of the rate-determining enzyme for bile acid synthesis.
Glycocholic acid aggravates liver fibrosis by promoting the up-regulation of connective tissue growth factor in hepatocytes
Cell Signal 2023 Jan;101:110508.PMID:36341984DOI:10.1016/j.cellsig.2022.110508.
Aims: The precise role of bile acid in the progression of liver fibrosis has yet to be elucidated. In this study, common bile duct ligation was used as an in vivo mouse model for the evaluation of bile acids that promote liver connective tissue growth factor expression. Main methods: Primary rat and mice hepatocytes, as well as primary rat hepatic stellate and HepaRG cells were evaluated as in vitro models for promoting the expression of connective tissue growth factor by bile acids. Key findings: Compared with taurochenodeoxycholic acid, glycochenodeoxycholic acid, and taurocholic acid, Glycocholic acid (GCA) most strongly promoted the secretion of connective tissue growth factor in mouse primary hepatocytes, rat primary hepatocytes and HepaRGs. GCA did not directly promote the activation of hepatic stellate cells. The administration of GCA in mice with ligated bile ducts promotes the progression of liver fibrosis, which may promote the yes-associated protein of hepatocytes into the nucleus, resulting in the hepatocytes secreting more connective tissue growth factor for hepatic stellate cell activation. In conclusion, our data showed that GCA can induce the expression of connective tissue growth factor in hepatocytes by promoting the nuclear translocation of yes-associated protein, thereby activating hepatic stellate cells. Significance: Our findings help to elucidate the contribution of GCA to the progression of hepatic fibrosis in cholestatic disease and aid the clinical monitoring of cholestatic liver fibrosis development.
Discovery of Glycocholic acid and taurochenodeoxycholic acid as phenotypic biomarkers in cholangiocarcinoma
Sci Rep 2018 Jul 23;8(1):11088.PMID:30038332DOI:10.1038/s41598-018-29445-z.
Although several biomarkers can be used to distinguish cholangiocarcinoma (CCA) from healthy controls, differentiating the disease from benign biliary disease (BBD) or pancreatic cancer (PC) is a challenge. CCA biomarkers are associated with low specificity or have not been validated in relation to the biological effects of CCA. In this study, we quantitatively analyzed 15 biliary bile acids in CCA (n = 30), BBD (n = 57) and PC (n = 17) patients and discovered Glycocholic acid (GCA) and taurochenodeoxycholic acid (TCDCA) as specific CCA biomarkers. Firstly, we showed that the average concentration of total biliary bile acids in CCA patients was quantitatively less than in other patient groups. In addition, the average composition ratio of primary bile acids and conjugated bile acids in CCA patients was the highest in all patient groups. The average composition ratio of GCA (35.6%) in CCA patients was significantly higher than in other patient groups. Conversely, the average composition ratio of TCDCA (13.8%) in CCA patients was significantly lower in all patient groups. To verify the biological effects of GCA and TCDCA, we analyzed the gene expression of bile acid receptors associated with the development of CCA in a CCA cell line. The gene expression of transmembrane G protein coupled receptor (TGR5) and sphingosine 1-phosphate receptor 2 (S1PR2) in CCA cells treated with GCA was 8.6-fold and 3.4-fold higher compared with control (untreated with bile acids), respectively. Gene expression of TGR5 and S1PR2 in TCDCA-treated cells was not significantly different from the control. Taken together, our study identified GCA and TCDCA as phenotype-specific biomarkers for CCA.
Glycocholic acid in chronic active hepatitis and mild liver diseases
Clin Investig 1993 Dec;72(1):36-9.PMID:8136614DOI:10.1007/BF00231114.
Serum levels of fasting Glycocholic acid were measured in various noncirrhotic liver diseases. Forty-five patients were evaluated, 15 with chronic active hepatitis and 30 with mild liver diseases including chronic persistent hepatitis, steatosis, and minimal changes. There were increased levels of Glycocholic acid in 53.3% of chronic active hepatitis cases and in 10% of mile liver disease cases (P = 0.003), and the levels reached by patients with chronic active hepatitis were higher than those in patients with mild liver disease (P < 0.0001). The latter did not show significant differences in their serum levels or in the percentage of abnormal results with respect to control group. There were weak, although significant, correlations between Glycocholic acid and transaminases, alkaline phosphatase, gamma-glutamyltranspeptidase, albumin, and gammaglobulin. In the present study, the specificity of Glycocholic acid was high in the detection of chronic active hepatitis patients at different cut-off levels. Glycocholic acid appeared to reflect histological severity in this group of noncirrhotic liver diseases and might have practical applications in the management of these patients.
Taurocholic Acid and Glycocholic acid Inhibit Inflammation and Activate Farnesoid X Receptor Expression in LPS-Stimulated Zebrafish and Macrophages
Molecules 2023 Feb 21;28(5):2005.PMID:36903252DOI:10.3390/molecules28052005.
A hyperactive immune response can be observed in patients with bacterial or viral infection, which may lead to the overproduction of proinflammatory cytokines, or "cytokine storm", and a poor clinical outcome. Extensive research efforts have been devoted to the discovery of effective immune modulators, yet the therapeutic options are still very limited. Here, we focused on the clinically indicated anti-inflammatory natural product Calculus bovis and its related patent drug Babaodan to investigate the major active molecules in the medicinal mixture. Combined with high-resolution mass spectrometry, transgenic zebrafish-based phenotypic screening, and mouse macrophage models, taurochiolic acid (TCA) and glycoholic acid (GCA) were identified as two naturally derived anti-inflammatory agents with high efficacy and safety. Both bile acids significantly inhibited the lipopolysaccharide-induced macrophage recruitment and the secretion of proinflammatory cytokines/chemokines in in vivo and in vitro models. Further studies identified strongly increased expression of the farnesoid X receptor at both the mRNA and protein levels upon the administration of TCA or GCA, which may be essential for mediating the anti-inflammatory effects of the two bile acids. In conclusion, we identified TCA and GCA as two major anti-inflammatory compounds in Calculus bovis and Babaodan, which could be important quality markers for the future development of Calculus bovis, as well as promising lead compounds in the treatment of overactive immune responses.