Glycochenodeoxycholic Acid-d4 (Synonyms: GCDCA-d4) |
Catalog No.GC47408 |
El Ácido glicoquenodesoxicÓlico-d4 (Chenodeoxycholylglycine-d4) es el Ácido glicoquenodesoxicÓlico marcado con deuterio. El Ácido glicoquenodesoxicÓlico (quenodesoxicolilglicina) es un Ácido biliar formado en el hÍgado a partir de quenodesoxicolato y glicina. ActÚa como un detergente para solubilizar las grasas para su absorciÓn y se absorbe por sÍ mismo. El Ácido glicoquenodesoxicÓlico (Chenodeoxycholylglycine) induce la apoptosis de los hepatocitos.
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Cas No.: 1201918-16-2
Sample solution is provided at 25 µL, 10mM.
An internal standard for the quantification of glycochenodeoxycholic acid by GC- or LC-MS. 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 µM.2 GCDCA (50, 75, and 100 µM) reduces the number LC3 puncta, a marker of autophagy, and is cytotoxic to L-02 hepatocytes.1 GCDCA (50 µM) 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
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)
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