摘要
目的:研究黄芪甲甙是否通过Nrf2-Keap1/ARE信号通路发挥抗氧化作用来抑制骨髓间充质细胞的凋亡。方法:培养Wistar大鼠BMSCs,设立正常组和黄芪甲甙干预组。采用实时荧光定量RT-PCR方法测定Nrf-2以及GSH的基因表达,Westem blot检测其蛋白表达。结果:TUNEL和流式结果表明黄芪甲甙有抑制BMSCs凋亡的作用,50μg/L组作用较强,与ADR组比较差异有显著性。增加浓度抑制凋亡的作用增加不明显,ADR+AST(100μg/L、50μg/L)两组,细胞凋亡率差异无显著性。黄芪甲甙作用后明显降低Nrf2 mRNA的表达,与ADR模型组比较差异有统计学意义。各组分别与阿霉素模型组比较差异均有统计学意义。结论:黄芪甲甙可以通过Nrf-2表达调控细胞凋亡,可能是其抑制神经细胞氧化应激、发挥保护作用的机制之一。
Objective:To study the effect of astragaloside on the apoptosis of mesenchymal stem cells ( BMSCs)by regulating N / / - K eapl/A R Esignal pathway. Methods: From Balb/c mouse femur bone marrowextracted and identifiedBMSCs,established the normal group and the astragaloside treatment group. The GSH genes were determined by real - time fluorescence quantitative RT - PCR method, and TUNEL and flow cytometry showed that astragaloside can inhibit the apoptosis of BMSCs,5 0 jg /L group was stronger,there was significant difference compared with ADR group, to increase the concentration of apoptosis was not obviouslyincreased, ADR + AST ( ( 0 0 j g / L ,50|jLg/L) of two groups, there was no significant difference in apoptosis rate. Theastragaloside significantly reduced expression of Nrf/ mRNA, compared with the ADR model group with statistical significantdifference. The GSH group compared with model group showed significant differences. Conclusion : Astragaluscan regulate the expression of apoptosis by N r - 2 , may be the inhibition of oxidative stress mechanism of nerve cells.【Key wor ds ] Nrf - 2 , bone marrowmesenchymal cells, tragaloside
作者
袁鹤立
欧阳文献
谭艳芳
李双杰
Yuan Heli,;Ouyang Wenxian;Tan Yanfang;Li Shuangie(Liver Disease Center o f Hunan Children's Hospital, Hunan Changsha 4 1 / 0 0 7,China)
出处
《现代肿瘤医学》
CAS
2016年第14期2183-2186,共4页
Journal of Modern Oncology