S1P通路在胆盐所致HL-7702细胞毒性损伤中的作用

摘要

目的：探讨S1P通路在胆盐所致HL-7702细胞毒性损伤中的作用。方法：应用甘氨鹅脱氧胆酸盐（GCDC）处理HL-7702细胞建立胆盐损伤肝细胞模型，应用CCK-8试剂盒-8检测细胞存活率，ELISA方法检测细胞培养上清液S1P的表达，Western blot法测定caspase-3蛋白的表达水平。结果：应用150μmol/L GCDC处理HL-7702细胞24 h可引起毒性损伤，10μmol/L VPC23019（S1PR1抑制剂）预处理30 min可对抗GCDC引起的损伤，使细胞存活率升高，凋亡细胞数目和cleaved caspase-3表达均减少。结论：GCDC可以引起HL-7702细胞毒性，S1P通路介导GCDC对HL-7702细胞的损伤作用。%Objective: To explore the role of S1P pathway in the bile salt-induced injury in HL-7702 cells.Method: HL-7702 cells were treated with glycochenodeoxycholate (GCDC) to establish a bile salt-induced cellular injury model, cell viability was detected by CCK-8 kit. The expression of S1P in the cell culture supernatant was detected by ELISA, and the expression level of caspase-3 protein was determined by Western blot assay.Result:Exposure of HL-7702 cells to 150 μmol/L GCDC for 24 h markedly enhanced cell apoptosis.Pretreatment of HL-7702 cells with 10 μmol/L VPC23019(a S1PR1 inhibitor) for 30 min before exposure to GCDC inhibited the cytotoxicity induced by GCDC, it made cell viability increase, the number of apoptotic cells and expression of cleaved caspase-3 decrease.Conclusion:GCDC can induced cytotoxicity in HL-7702 cells,S1P pathway mediates the GCDC-induced injury in HL-7702 cells.