论文部分内容阅读
目的探讨氧化苦参碱(oxymatrine,OM)对亚砷酸钠致人胎肝(L-02)细胞株损伤的拮抗作用。方法将处于对数生长期的L-02细胞分别培养于0μmol/L亚砷酸钠(对照)、OM(200μg/ml)、亚砷酸钠(100μmol/L)及亚砷酸钠(100μmol/L)+OM(50、100、200μg/ml)的培养基中暴露18 h。检测细胞培养液中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)的水平和细胞葡萄糖调节蛋白78(glucose regulated protein 78,GRP78)、CCAAT/增强子结合蛋白同源蛋白(CCAAT/enhancer-binding protein homologous protein,CHOP)蛋白的表达水平及细胞凋亡率。结果OM组与对照组各项指标差异均无统计学意义(P>0.05)。与对照组及OM处理组比较,亚砷酸钠组细胞培养上清液中AST、ALT水平、细胞凋亡率、GRP78及CHOP蛋白表达水平显著升高(P<0.05);而不同浓度OM干预后,上述指标均有不同程度下降(P<0.05)。且随着OM干预浓度的升高,上述指标均呈下降趋势。结论砷可致L-02细胞损伤,OM可通过抑制L-02细胞内质网应激及减少肝细胞凋亡,从而发挥对肝细胞的保护作用。
Objective To investigate the antagonistic effect of oxymatrine (OM) on injury induced by sodium arsenite in human fetal liver (L-02) cell line. Methods L-02 cells at logarithmic growth phase were cultured in 0μmol / L sodium arsenite (control), OM (200μg / ml), sodium arsenite (100μmol / L) and sodium arsenite (100μmol / L) + OM (50, 100, 200 μg / ml) for 18 h. The levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in cell culture medium were measured and the levels of glucose regulated protein 78 (GRP78), CCAAT / enhancer binding protein (CCAAT / enhancer-binding protein homologous protein, CHOP) protein expression and apoptosis rate. Results There was no significant difference between OM group and control group (P> 0.05). Compared with control group and OM group, AST, ALT level, apoptosis rate, GRP78 and CHOP protein expression in the arsenite group were significantly increased (P <0.05); while OM intervention with different concentrations After the above indicators have decreased to varying degrees (P <0.05). And with the increase of OM intervention concentration, the above indicators showed a downward trend. Conclusion Arsenic can cause injury of L-02 cells. OM can exert protective effect on hepatocytes by inhibiting endoplasmic reticulum stress and reducing apoptosis of L-02 cells.