Deoxycholic acid

miR-21的表达在短时间接触去氧胆酸后下调，下游通路也是如此，伴随着PIDD的处理和caspase-2的激活，这对DCA诱导的肝损伤有所贡献[1]。

Deoxycholic acid i 以剂量依赖的方式抑制原代大鼠肝细胞中的miR-21表达，并增加miR-21促凋亡靶点程序性细胞死亡4（PDCD4）及凋亡。Deoxycholic acid i 降低NF-κB活性，这表明为调节miR-21/PDCD4途径的上游机制[1]。

DMSO:55 mg/mL (140.1 mM);Ethanol:56 mg/mL (142.6 mM);H2O:< 1 mg/mL (insoluble or slightly soluble)

Primary rat hepatocytes were isolated from male rats (100 to 150 g) by collagenase perfusion. After isolation, hepatocytes were resuspended in complete Williams E medium and plated on BD Primaria™ culture dishes at 5 × 104 cells/cm2. Cells are kept at 37 °C in a humidified atmosphere of 5% CO2 for 4-6 h to allow attachment. Plates are then washed with phosphate buffered saline (PBS) 1× in order to remove dead cells and incubated in Williams E medium supplemented with 25 to 200 μM DCA or no addition (control) for 24 h. Primary rat hepatocytes are processed for total RNA and protein isolation, cell viability, cytotoxicity and caspase activity assays and Hoechst staining. (Only for Reference)