640-79-9Glycochenodeoxycholic acid

产品属性：

Cas No.640-79-9

别名 N/A

化学名 N/A

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  For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition     Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述：
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.