CSNK1E:7.22 μM (EC50)|FATP2:5 μM|Nicastrin:6.03 μM (EC50)|FATP5:0.19 μM|NTCP:2.14 µM

方法：将原代大鼠肝细胞用100 μM Deoxycholic acid (DCA) 处理16小时或24小时，分别采用Real-Time RT-PCR、免疫印迹和H₂DCFDA荧光测定法检测相关指标。 结果：DCA短时间处理导致miR-21表达下调，伴随PIDD处理和caspase-2激活，从而促进肝损伤。[1]

方法：原代大鼠肝细胞经25–200 μM脱氧胆酸（DCA）处理24 h，采用Real-Time RT-PCR检测miR-21表达，荧光素酶报告基因检测NF-κB活性，Western blot检测PDCD4，Hoechst染色及caspase-3/7活性检测细胞凋亡。 结果：Deoxycholic acid以剂量依赖的方式抑制miR-21表达，降低NF-κB活性，并增加PDCD4表达及细胞凋亡。[1] 方法：采用C2C12成肌细胞，给予Deoxycholic acid（50 μM）处理5天诱导分化。通过免疫荧光检测MYH、RT-qPCR检测成肌分化及能量代谢标志物基因表达。 结果：Deoxycholic acid显著提高肌管分化指数及融合能力，上调Myh1/2、Pgc-1α等基因表达；该作用可被TGR5拮抗剂SBI-115阻断。[2]

Ethanol:56 mg/mL (142.65 mM);DMSO:145 mg/mL (369.36 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)