S1P通路在胆盐所致HL-7702细胞毒性损伤中的作用  

Role of S1P Pathway in Bile Salt-induced Injury in HL-7702 Cells

作　　者：梁君铭 曾宽[2] 邹堂斌[3] 

机构地区：[1]广东省佛山市顺德区第一人民医院附属杏坛医院,广东佛山528325 [2]中山大学附属孙逸仙纪念医院 [3]广东医学院公共卫生学院

出　　处：《中国医学创新》2015年第20期15-17,共3页Medical Innovation of China

基　　金：广东省科技计划项目(2013B031800016);东莞市科技计划项目(2014108101053)

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 S1 P 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 S1 P 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,S1 P pathway mediates the GCDC-induced injury in HL-7702 cells.

关 键 词：甘氨鹅脱氧胆酸盐 凋亡 S1P SphK1激酶 HL-7702细胞 

分 类 号：R363[医药卫生—病理学]