N-乙酰半胱氨酸对过氧化氢诱导的骨髓间充质干细胞凋亡的保护及作用机制研究

被引:12
作者
谢荣辉 [1 ,2 ]
周师洁 [3 ,4 ]
殷明 [1 ]
殷嫦嫦 [3 ,4 ]
程细高 [1 ]
陈伟才 [1 ]
林思文 [1 ,2 ]
施剑明 [1 ,2 ]
耿书国 [1 ,2 ]
机构
[1] 南昌大学第二附属医院
[2] 南昌大学研究生院医学部
[3] 南昌大学
[4] 九江学院
关键词
N-乙酰半胱氨酸; 氧化应激; 过氧化氢; 骨髓间充质干细胞; 凋亡; PI3K-Akt途径; FOXO基因;
D O I
暂无
中图分类号
R329.2 [人体细胞学];
学科分类号
100107 [人体解剖与组织胚胎学(人体解剖学、组织与胚胎学)];
摘要
目的研究N-乙酰半胱氨酸(NAC)对过氧化氢(H2O2)诱导的骨髓间充质干细胞(BMSCs)凋亡的影响,并探讨其作用机制。方法采用全骨髓贴壁培养法培养SD大鼠BMSCs,随机分成5组:正常对照组、H2O2处理组、NAC组、NAC+H2O2组和LY294002干预组。流式细胞术检测各组的细胞凋亡率及细胞内活性氧水平;RT-PCR检测各组rBMSCs中FOXO1、FOXO3、FOXO4基因水平的表达;Western blot检测各组rBMSCs中Akt、p-Akt、Bcl-2的表达。结果与正常组相比,H2O2组诱导的rBMSCs凋亡数明显增高,细胞内ROS含量明显增高,FOXO1、FOXO3、FOXO4基因水平的表达量明显下降;NAC明显抑制了rBMSCs凋亡和ROS产生,上调了FOXO1、FOXO3、FOXO4基因水平的表达,增加了细胞内p-Akt和Bcl-2的表达,但LY294002抑制剂明显抑制了NAC对氧化应激后rBMSCs的上述功能。结论 N-乙酰半胱氨酸可通过激活PI3K-Akt信号途径抑制细胞内活性氧的产生、上调FOXO1、FOXO3、FOXO4基因水平及抗凋亡Bcl-2的表达来保护BMSCs免受氧化应激引起的凋亡。
引用
收藏
页码:54 / 59
页数:6
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