摘要
目的建立H2O2诱导氧化的L02人肝细胞模型,从细胞凋亡调控因子FAS、具有死亡功能区的Fas相关蛋白（fas associateddeath domain protein,FADD）和Caspase-8的表达变化来研究五味子乙素（Sch B）对L02细胞的可能作用机制。方法用实时荧光定量PCR法检测FAS、FADD和Caspase-8 mRNA的变化,流式细胞术检测细胞凋亡率,ELISA法检测FAS蛋白含量,Westernblotting检测FADD蛋白变化和分光光度法检测Caspase-8活性。结果在5~15μmol/L剂量范围内,Sch B可剂量依赖性抑制H2O2引起的FAS、FADD的表达和Caspase-8的活化。结论 Sch B可部分抑制H2O2诱导的L02细胞凋亡,其作用机制可能是通过影响了FAS-FADD-Caspase-8通路。
Objective To investigate the role of Fas pathway in H2O2-induced apoptosis of L02 human hepatocytes and the effect of schisandrin B on Fas pathway.Methods Real-time quantitative PCR was used to detect the expressions of FAS,fas associated death domain protein（FADD） and caspase-8 mRNA in L02 cells exposed to H2O2.Flow cytometry was employed to assess the cell apoptosis.ELISA,Western blotting and spectrophotometric assay were performed to determine the expressions of FAS protein,FADD protein and caspase-8 activity.Results Within the dose range of 5-15 mol/L,schisandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation.Conclusion Schisandrin B can partially inhibit H2O2-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2012年第4期583-585,592,共4页
Journal of Southern Medical University
基金
广东省高等学校科技创新团队(06CXTD003)
