Sodium glycocholate hydrate, 98%

Sodium glycocholate hydrate, 98% is a bile acid derivative. Sodium glycocholate hydrate, 98% downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Sodium glycocholate hydrate, 98% inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Sodium glycocholate hydrate, 98% modulates related bile acid receptor signaling. Sodium glycocholate hydrate, 98% suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Sodium glycocholate hydrate, 98% can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA)^[1][2][3]. In Vitro:Glycocholic acid (0-500 μM; 0, 24, 48, 72 h) hydrate reduces the viability of human colon adenocarcinoma Caco-2 cells in a time- and concentration-dependent manner^[1].
Glycocholic acid (250 μM; 72 h) hydrate at 250 μM significantly increases the chemosensitivity of human colon adenocarcinoma Caco-2 cells to Epirubicin (HY-13624)^[1].
Glycocholic acid (250 μM; 72 h) hydrate alters the expression of multidrug resistance and apoptosis-related genes in human colon adenocarcinoma Caco-2 cells, downregulating MDR1, MRP1, MRP2, and Bcl-2 while upregulating Bax, caspase-3, caspase-9, and p53, and increasing the Bax-to-Bcl-2 ratio^[1].
Glycocholic acid (250 μM; 72 h) hydrate reduces hMDR1 promoter activity in human colon adenocarcinoma Caco-2 cells^[1].
Glycocholic acid (250 μM; 72 h) hydrate induces chromatin condensation, a marker of apoptosis, in human colon adenocarcinoma Caco-2 cells^[1].
Glycocholic acid (250 μM; 72 h) hydrate increases the sub-G1 DNA content population, indicating apoptosis, in human colon adenocarcinoma Caco-2 cells^[1].
Glycocholic acid (GCA) (1.6 μM; 48 h) hydrate modulates bile acid receptor gene expression in SNU-245 cholangiocarcinoma cells, reducing FXR expression and increasing TGR5 and S1PR2 expression^[2].
Glycocholic acid hydrate inhibits late logarithmic phase growth of E. coli K1037, clinical UTI E. coli, Klebsiella pneumoniae, Klebsiella oxytoca, Salmonella Typhimurium, Raoultella ornithinolytica, and Citrobacter freundii in liquid LB culture, but not on solid LB agar medium^[3].
Glycocholic acid hydrate reduces the MIC of ampicillin for E. coli K1037 by 2-fold and the MIC of chloramphenicol for Raoultella ornithinolytica and Citrobacter freundii by 2-fold, resulting in additive antimicrobial interactions (FIC index 0.625-0.75)^[3].
Glycocholic acid (0.125-2%; 6 h) hydrate reduces conjugation frequency of multiple Enterobacteriaceae conjugative plasmids by 70 to 97% in a dose-dependent manner, with no prominent reduction in donor strain viability^[3].
Glycocholic acid (0.2-2%; 16 h) hydrate significantly reduces E. coli K1037 motility on soft LB agar by downregulating fliC gene expression^[3].
Glycocholic acid (0.125-2%) hydrate increases membrane permeability and compromises membrane integrity of E. coli K1037, as shown by increased NPN/EtBr uptake and cytoplasmic DnaK leakage^[3].