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Glycochenodeoxycholic acid(Chenodeoxycholylglycine)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Glycochenodeoxycholic acid(Chenodeoxycholylglycine)图片
CAS NO:640-79-9
包装:10mg
规格:98%
市场价:445元
分子量:449.62

产品介绍
Glycochenodeoxycholicacid是从脱氧胆酸和甘氨酸在肝脏中形成的胆汁盐;科研中可用于诱导肝细胞凋亡。
CAS:640-79-9
分子式:C26H43NO5
分子量:449.62
纯度:98%
存储:Store at -20°C

Background:

Glycochenodeoxycholic acid is a bile salt formed in the liver from chenodeoxycholate and glycine; used to induce hepatocyte apoptosis in research.


Chenodeoxycholate is toxic to hepatocytes, and accumulation of chenodeoxycholate in the liver during cholestasis may potentiate hepatocellular injury. At a concentration of 250μM, glycochenodeoxycholate is more toxic than either chenodeoxycholate or taurochenodeoxycholate. Glycochenodeoxycholate cytotoxicity may result from ATP depletion followed by a subsequent rise in Ca2+. The rise in Ca2+ leads to an increase in calcium-dependent degradative proteolysis and, ultimately, cell death[1]. 4 h exposure of 50 μM GCDC induces apoptosis in 42% of hepatocytes. Intracellular PKC activity decreased to 44% of controls 2 h after exposure of hepatocytes to GCDC. GCDC-induced apoptosis is associated with decreases in total cellular PKC activity, which appear to be dependent on intracellular calpain-like protease activity[2].


GCDCA induces ER-related calcium release within about ten seconds. Significant increases in activities of calpain and caspase-12 are observed after 15 h of GCDCA treatment. Bip and Chop mRNA expressions are increased with the treated GCDCA dose and incubation time. Cytochrome c release from mitochondria peaks in about 2 h of incubation[3].


[1]. Spivey JR, et al. Glycochenodeoxycholate-induced lethal hepatocellular injury in rat hepatocytes. Role of ATP depletion and cytosolic free calcium. J Clin Invest. 1993 Jul;92(1):17-24. [2]. Gonzalez B, et al. Glycochenodeoxycholic acid (GCDC) induced hepatocyte apoptosis is associated with early modulation of intracellular PKC activity. Mol Cell Biochem. 2000 Apr;207(1-2):19-27. [3]. Tsuchiya S, et al. Involvement of endoplasmic reticulum in glycochenodeoxycholic acid-induced apoptosis in rathepatocytes. Toxicol Lett. 2006 Oct 10;166(2):140-9.