Glycochenodeoxycholic acid (Chenodeoxycholylglycine)
(Synonyms: 甘氨鹅脱氧胆酸; Chenodeoxycholylglycine) 目录号 : GC34092
A quantitative analytical standard guaranteed to meet MaxSpec? identity, purity, stability, and concentration specifications
Cas No.:640-79-9
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
Animal experiment: | Rats: The freshly isolated hepatocytes are preincubated for 2 h at a density of 1× 106 cells/mL in a mixture of William’s E medium supplement with 10% FBS. Isolated rat hepatocytes are incubated in William’s E medium with or without (used as a control) GCDCA (50, 100 and 300 μM), or TG (1, 2 and 5 μM) for 1-24 h[3]. |
References: [1]. Liang S, et al. Effect of quercetin 7-rhamnoside on glycochenodeoxycholic acid-induced L-02 human normal livercell apoptosis. Int J Mol Med. 2013 Aug;32(2):323-30. | |
Glycochenodeoxycholic acid (GCDCA) is a glycine-conjugated form of the primary bile acid chenodeoxycholic acid .1 It reduces formation of cholic acid in primary human hepatocytes when used at a concentration of 100 ?M.2 GCDCA (50, 75, and 100 ?M) reduces the number of LC3 puncta, a marker of autophagy, and is cytotoxic to L-02 hepatocytes.1 GCDCA (50 ?M) induces apoptosis in isolated rat hepatocytes, an effect that can be blocked by the protein kinase C (PKC) inhibitor chelerythrine .3 Fecal levels of GCDCA are decreased in a rat model of high-fat diet-induced obesity compared with rats fed a normal diet.4
Glycochenodeoxycholic acid MaxSpec? standard is a quantitative grade standard of glycochenodeoxycholic acid 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 Glycochenodeoxycholic acid 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.
1.Lan, W., Chen, Z., Chen, Y., et al.Glycochenodeoxycholic acid impairs transcription factor E3-dependent autophagy-lysosome machinery by disrupting reactive oxygen species homeostasis in L02 cellsToxicol. Lett.33111-21(2020) 2.Ellis, E., Axelson, M., Abrahamsson, A., et al.Feedback regulation of bile acid synthesis in primary human hepatocytes: Evidence that CDCA is the strongest inhibitorHepatology38(4)930-938(2003) 3.Gonzalez, B., Fisher, C., and Rosser, B.G.Glycochenodeoxycholic acid (GCDC) induced hepatocyte apoptosis is associated with early modulation of intracellular PKC activityMol. Cell. Biochem.207(1-2)19-27(2000) 4.Lin, H., An, Y., Tang, H., et al.Alterations of bile acids and gut microbiota in obesity induced by high fat diet in rat modelJ. Agric. Food Chem.67(13)3624-3632(2019)
| Cas No. | 640-79-9 | SDF | |
| 别名 | 甘氨鹅脱氧胆酸; Chenodeoxycholylglycine | ||
| Canonical SMILES | C[C@@]12[C@](CC[C@]2([H])[C@H](C)CCC(NCC(O)=O)=O)([H])[C@@]3([H])[C@]([C@@]4([C@](C[C@H](O)CC4)([H])C[C@H]3O)C)([H])CC1 | ||
| 分子式 | C26H43NO5 | 分子量 | 449.62 |
| 溶解度 | DMSO : ≥ 29 mg/mL (64.50 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 | 2.2241 mL | 11.1205 mL | 22.241 mL |
| 5 mM | 0.4448 mL | 2.2241 mL | 4.4482 mL |
| 10 mM | 0.2224 mL | 1.1121 mL | 2.2241 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。
Glycochenodeoxycholic acid induces stemness and chemoresistance via the STAT3 signaling pathway in hepatocellular carcinoma cells
Aging (Albany NY) 2020 Aug 3;12(15):15546-15555.PMID:32756004DOI:10.18632/aging.103751.
The poor prognosis of hepatocellular carcinoma (HCC) is primarily attributed to its high frequency of recurrence and resistance to chemotherapy. Epithelial-to-mesenchymal transition (EMT) and the acquisition of cancer stem cells (CSCs) are the fundamental drivers of chemoresistance in HCC. Glycochenodeoxycholic acid (GCDC), a component of bile acid (BA), has been reported to induce necrosis in primary human hepatocytes. In the present work, we investigated the function of GCDC in HCC chemoresistance. We found that GCDC promoted chemoresistance in HCC cells by down-regulating and up-regulating the expression of apoptotic and anti-apoptotic genes, respectively. Furthermore, GCDC induced the EMT phenotype and stemness in HCC cells and activated the STAT3 signaling pathway. These findings reveal that GCDC promotes chemoresistance in HCC by inducing stemness via the STAT3 pathway and could be a potential target in HCC chemotherapy.
Glycochenodeoxycholic acid inhibits calcium phosphate precipitation in vitro by preventing the transformation of amorphous calcium phosphate to calcium hydroxyapatite
J Clin Invest 1991 Oct;88(4):1265-71.PMID:1655828DOI:10.1172/JCI115430.
Calcium hydroxyapatite can be a significant component of black pigment gallstones. Diverse molecules that bind calcium phosphate inhibit hydroxyapatite precipitation. Because glycine-conjugated bile acids, but not their taurine counterparts, bind calcium phosphate, we studied whether Glycochenodeoxycholic acid inhibits calcium hydroxyapatite formation. Glycochenodeoxycholic acid (2 mM) totally inhibited transformation of amorphous calcium phosphate microprecipitates to macroscopic crystalline calcium hydroxyapatite. This inhibition was not mediated by decreased Ca2+ activity. Taurocholic acid (2-12 mM) did not affect hydroxyapatite formation, but antagonized Glycochenodeoxycholic acid. Both amorphous and crystalline precipitates contained a surface fraction relatively rich in phosphate. The surface phosphate content was diminish by increasing Glycochenodeoxycholic acid concentrations, and this relationship was interpreted as competition between bile acid and HPO4(-4) for binding sites on the calcium phosphate surface. A phosphate-rich crystal surface was associated with rapid transition from amorphous to crystalline states. These results indicate that Glycochenodeoxycholic acid prevents transformation of amorphous calcium phosphate to crystalline hydroxyapatite by competitively inhibiting the accumulation of phosphate on the crystal embryo surface.
Glycochenodeoxycholic acid Does Not Increase Transforming Growth Factor-Beta Expression in Bile Duct Epithelial Cells or Collagen Synthesis in Myofibroblasts
J Clin Exp Hepatol 2017 Dec;7(4):316-320.PMID:29234196DOI:10.1016/j.jceh.2017.04.002.
Background/aims: Primary sclerosing cholangitis (PSC) is a chronic, progressive hepatobiliary disorder characterized by extensive fibrosis and stricturing of the intra- and/or extra-hepatic bile ducts: Previous studies have documented low phosphatylcholine (PC) concentrations in PSC bile. The aim of this study was to determine whether low PC levels in bile facilitate toxic bile acid induced injury of biliary tract epithelial cells resulting in enhanced transforming growth factor-beta (TGF-β) expression and increased collagen synthesis by myofibroblasts. Methods: TGF-β mRNA expression was documented in bile duct epithelial cells exposed to varying concentrations of the toxic bile acid; Glycochenodeoxycholic acid (GCDCA) ± PC. Results: In these experiments, as well as in co-culture experiments where bile duct epithelial cells were cultured with peripheral blood mononuclear cells and myofibroblasts, TGF-β mRNA expression remained unaltered in the presence or absence of PC. Moreover, collagen type Iα1 mRNA expression by myofibroblasts also remained unaltered. Conclusion: The results of this study do not support the hypothesis that PC deficiency contributes to toxic bile acid-induced bile duct injury and/or myofibroblast activation.
Glycochenodeoxycholic acid impairs transcription factor E3 -dependent autophagy-lysosome machinery by disrupting reactive oxygen species homeostasis in L02 cells
Toxicol Lett 2020 Oct 1;331:11-21.PMID:32439580DOI:10.1016/j.toxlet.2020.05.017.
Cholestasis represents pathophysiologic syndromes defined as impaired bile flow from the liver. As an outcome, bile acids accumulate and promote hepatocyte injury, followed by liver cirrhosis and liver failure. Glycochenodeoxycholic acid (GCDCA) is relatively toxic and highly concentrated in bile and serum after cholestasis. However, the mechanism underlying GCDCA-induced hepatotoxicity remains unclear. In this study, we found that GCDCA inhibits autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH, contributing to defects in autophagic clearance and subsequently leading to the death of L02 human hepatocyte cells. Notably, through tandem mass tag (TMT)-based quantitative proteomic analysis and database searches, 313 differentially expressed proteins were identified, of which 71 were increased and 242 were decreased in the GCDCA group compared with those in the control group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that GCDCA suppressed the signaling pathway of transcription factor E3 (TFE3), which was the most closely associated with autophagic flux impairment. In contrast, GCDCA-inhibited lysosomal function and autophagic flux were efficiently attenuated by TFE3 overexpression. Specifically, the decreased expression of TFE3 was closely related to the disruption of reactive oxygen species (ROS) homeostasis, which could be prevented by inhibiting intracellular ROS with N-acetyl cysteine (NAC). In summary, our study is the first to demonstrate that manipulation of ROS/TFE3 signaling may be a therapeutic approach for antagonizing GCDCA-induced hepatotoxicity.
Enzymatic sulfation of Glycochenodeoxycholic acid by tissue fractions from adult hamsters
J Lipid Res 1979 Nov;20(8):952-9.PMID:533830doi
Using a radiometric assay with Glycochenodeoxycholic acid as substrate, bile acid:3'-phosphoadenosine-5'-phosphosulfate sulfotransferase activity was found in 105,000 g supernatant fractions of liver, proximal intestine, and adrenal gland homogenates from adult hamsters. Optimum conditions for measurement of the hepatic enzyme were determined. In both male and female animals sulfation only occurred at the 7 alpha-position. Saturation analysis with glycohenodeoxycholic acid revealed that the higher activity observed in fractions from female compared to male hamsters was due to a 4-fold lower apparent Km (79 muM vs. 317 muM) for this bile acid in the females. The sulfation of glycohenodeoxycholic acid was competitively inhibited by glycolithocholic acid, chenodeoxycholic acid, and ursodeoxycholic acid. The data are consistent with the concept that sulfation of many, if not all, bile acids can occur in vivo.