| 胡霞,陈方方,孔陈苏.DJ-1保护多巴胺能神经元抵抗过氧化氢氧化应激损伤的研究[J].安徽医药,2018,22(12):2323-2326. |
| DJ-1保护多巴胺能神经元抵抗过氧化氢氧化应激损伤的研究 |
| The protective effect of DJ-1 on dopaminergic neurons oxidative stress damage induced by H2O2 |
| 投稿时间：2016-12-23 |
| DOI： |
| 中文关键词: DJ-1 过氧化氢 帕金森病 氧化损伤 |
| 英文关键词: DJ-1 H2O2 PD Oxidative stress damage |
| 基金项目: |
|
| 摘要点击次数: 2860 |
| 全文下载次数: 966 |
| 中文摘要: |
| 目的 探讨DJ-1保护多巴胺能神经元免受过氧化氢(H2O2)损伤的机制。 方法 使用神经生长因子(NGF)将大鼠嗜铬细胞瘤细胞(PC12细胞)诱导为多巴胺能神经元模型。H2O2处理引起细胞氧化应激损伤模型,CCK-8试剂盒检测细胞活性,DHE染色检测细胞内ROS水平。PI / Hoechst染色检测细胞凋亡,蛋白质免疫印迹法(Western blot)检测DJ-1和TH蛋白的表达。构建DJ-1过表达载体,检测DJ-1对H2O2中PC12细胞的保护作用及对细胞内活性氧(ROS)的影响。RT-qPCR检测α-synuclein,p53,Bax,Bcl-2的表达变化。 结果 H2O2处理可显着降低PC12细胞的活性,H2O2处理24 h以上可引起细胞凋亡。H2O2处理下调DJ-1蛋白和TH蛋白的表达,并且在RNA水平上α-突触核蛋白的表达增加。另外 p53, Bax和 caspase-3表达增加, Bcl-2表达减少。DJ-1的过表达可以抑制H2O2引起的ROS增加,DJ-1可以维持细胞活性,减少H2O2的凋亡。在RNA水平抑制α-突触核蛋白,p53,bax,bcl-2的凋亡和抗凋亡基因表达变化。 结论 DJ-1能够抑制H2O2引起的 ROS水平升高,减少α-synuclein积累,抑制 p53,凋亡基因如 bax的表达减弱了多巴胺能神经元中H2O2诱导的氧化应激损伤。 |
| 英文摘要: |
| Objective To investigate the mechanism of DJ-1 protective function against hydrogen peroxide (H2O2) damage of dopaminergic neurons. Methods The dopaminergic neurons model were established by PC12 cells stimulated by nerve growth factor (NGF).H2O2 treatment was used to create cell oxidative stress damage model.CCK-8 kit was used to detect cell activity and DHE dyeing was used to test ROS level of cells.PI/Hoechst staining was used to detect cell apoptosis.Western blot detection was used to detect the protein expression of DJ-1 and TH.The DJ-1 over expression vector was build,by which the protection of DJ-1 on cell activity and the influence of intracellular ROS was detected.RT-qPCR was used to detect the expression of α-synuclein,p53,Bax and Bcl-2. Results H2O2 can significantly reduce PC12 cell activity and induce high cell apoptosis ratio after 24 h.H2O2 treatment induced down-regulation of DJ-1 and TH protein.The expression of α-synuclein in RNA level was increased.The expression of p53,Bax and caspase-3 were increased,while the expression of Bcl-2 was decreased.Over expression of DJ-1 can inhibit ROS expression caused by H2O2and decrease cell apoptosis in H2O2.The changes of the RNA levels of α-synuclein,p53,Bax and Bcl-2 were weakened. Conclusions DJ-1 can inhibit H2O2 induced ROS production and cell apoptosis,the α-synuclein accumulation and the expression of p53,by which to protect dopaminergic neurons from H2O2 oxidative stress damage. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
