| 秦彦昌,贾 栋,于庆伟,孙树凯,张百平.RUNX1对氧糖剥夺诱导PC12细胞凋亡的保护作用研究[J].,2017,17(10):1838-1842 |
| RUNX1对氧糖剥夺诱导PC12细胞凋亡的保护作用研究 |
| Protective Effects of RUNX1 on Oxygen-glucose Deprivation Induced Apoptosis in PC12 Cells |
| 投稿时间：2016-05-31 修订日期：2016-06-29 |
| DOI：10.13241/j.cnki.pmb.2017.10.009 |
| 中文关键词: RUNX1 氧糖剥夺 细胞凋亡 PI3K/Akt |
| 英文关键词: RUNX1 Oxygen-glucose deprivation Cell apoptosis PI3K/Akt |
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| 中文摘要: |
| 摘要 目的：研究RUNX1在PC12细胞氧糖剥夺模型中的表达及其对PC12细胞的保护作用，并探讨其相关机制。方法：体外培养PC12细胞并构建氧糖剥夺模型，将细胞分为对照组、氧糖剥夺组、RUNX1 siRNA处理组、siRNA对照处理组(sicontrol)、pcDNA3.1-RUNX1处理组(pcRUNX1)和pcDNA3.1对照处理组(pcDNA 3.1)。qRT-PCR和western blot检测RUNX1、磷酸化Akt(p-Akt)和总Akt(t-Akt)表达水平；MTT法检测细胞存活率；Annexin V-FITC/PI双染法检测细胞凋亡。结果：与对照组比较，RUNX1在PC12细胞氧糖剥夺模型中表达水平显著升高；沉默RUNX1可下调PC12细胞的存活率，促进细胞的凋亡，有效抑制p-Akt蛋白表达，而过表达RUNX1显著提高细胞存活率，抑制细胞凋亡，并上调p-Akt蛋白表达；此外，PI3K/Akt通路抑制剂LY294002明显抑制RUNX1过表达对细胞存活率的促进作用和对细胞凋亡的抑制作用。结论：RUNX1可通过PI3K/Akt信号通路保护OGD对PC12细胞的损伤作用。 |
| 英文摘要: |
| ABSTRACT Objective: To estimate the expression of RUNX1 in oxygen-glucose deprivation injured PC12 cells and investigate the protective effect and mechanisms of RUNX1 on apoptosis induced by oxygen-glucose deprivation in PC12 cells. Methods: The oxygen-glucose deprivation (OGD) model was built using PC12 cells, and cells were divided into control group, OGD group, RUNX1 siRNA group, control siRNA group, pcDNA3.1-RUNX1 group and pcDNA3.1 group. The expression of RUNX1, phosphorylated Akt (p-Akt) and total Akt (t-Akt) were measured using qRT-PCR and western blot assay. Cell viability was estimated using MTT assay and cell apoptosis was detected using Annexin V-FITC/PI assay. Results: Compared with control, RUNX1 expression was significantly higher in OGD model. Silence RUNX1 by RUNX1 siRNA remarkably inhibited cell viability, promoted apoptosis and down-regulated p-Akt protein expression, while RUNX1 overexpression showed a contrary effect. Besides, LY2904002, the inhibitor of PI3K/Akt, markedly impeded the the role of RUNX1 overexpression in promoting cell viability and inhibiting apoptosis. Conclusion: RUNX1 protected PC12 cells against oxygen-glucose deprivation injury through PI3K/Akt signaling pathway. |
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