产品
编 号：F298610
分子式：C24H39NaO4
分子量：414.55
分子式：C24H39NaO4
分子量：414.55
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CAS No: 2646-38-0
产品详情
生物活性：
Chenodeoxycholic acid sodium is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.
体外研究：
Chenodeoxycholic acid sodium (CDCA) and Deoxycholic acid (DCA) both inhibit 11 beta HSD2 with IC50 values of 22 mM and 38 mM, respectively and causes cortisol-dependent nuclear translocation and increases transcriptionalactivity of mineralocorticoid receptor (MR). Chenodeoxycholic acid sodium is able to stimulate Ishikawa cell growth by inducing a significant increase in Cyclin D1 protein and mRNA expression through the activation of the membrane G protein-coupled receptor (TGR5)-dependent pathway. Chenodeoxycholic acid sodium (CDCA) induces LDL receptor mRNA levels approximately 4 fold and mRNA levels for HMG-CoA reductase and HMG-CoA synthase two fold in a cultured human hepatoblastoma cell line, Hep G2. Chenodeoxycholic acid sodium-induced Isc is inhibited (≥67%) by Bumetanide, BaCl2, and the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTRinh-172. Chenodeoxycholic acid sodium-stimulated Isc is decreased 43% by the adenylate cyclase inhibitor MDL12330A and Chenodeoxycholic acid sodium increases intracellular cAMP concentration. Chenodeoxycholic acid sodium treatment activates C/EBPβ, as shown by increases in its phosphorylation, nuclear accumulation, and expression in HepG2 cells. Chenodeoxycholic acid sodium enhances luciferase gene transcription from the construct containing -1.65-kb GSTA2 promoter, which contains C/EBP response element (pGL-1651). Chenodeoxycholic acid sodium treatment activates AMP-activated protein kinase (AMPK), which leads to extracellular signal-regulated kinase 1/2 (ERK1/2) activation, as evidenced by the results of experiments using a dominant-negative mutant of AMPKα and chemical inhibitor.
Chenodeoxycholic acid sodium is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.
体外研究：
Chenodeoxycholic acid sodium (CDCA) and Deoxycholic acid (DCA) both inhibit 11 beta HSD2 with IC50 values of 22 mM and 38 mM, respectively and causes cortisol-dependent nuclear translocation and increases transcriptionalactivity of mineralocorticoid receptor (MR). Chenodeoxycholic acid sodium is able to stimulate Ishikawa cell growth by inducing a significant increase in Cyclin D1 protein and mRNA expression through the activation of the membrane G protein-coupled receptor (TGR5)-dependent pathway. Chenodeoxycholic acid sodium (CDCA) induces LDL receptor mRNA levels approximately 4 fold and mRNA levels for HMG-CoA reductase and HMG-CoA synthase two fold in a cultured human hepatoblastoma cell line, Hep G2. Chenodeoxycholic acid sodium-induced Isc is inhibited (≥67%) by Bumetanide, BaCl2, and the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTRinh-172. Chenodeoxycholic acid sodium-stimulated Isc is decreased 43% by the adenylate cyclase inhibitor MDL12330A and Chenodeoxycholic acid sodium increases intracellular cAMP concentration. Chenodeoxycholic acid sodium treatment activates C/EBPβ, as shown by increases in its phosphorylation, nuclear accumulation, and expression in HepG2 cells. Chenodeoxycholic acid sodium enhances luciferase gene transcription from the construct containing -1.65-kb GSTA2 promoter, which contains C/EBP response element (pGL-1651). Chenodeoxycholic acid sodium treatment activates AMP-activated protein kinase (AMPK), which leads to extracellular signal-regulated kinase 1/2 (ERK1/2) activation, as evidenced by the results of experiments using a dominant-negative mutant of AMPKα and chemical inhibitor.
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