[1]郭晓洁 毛善平 董慧敏等.缺血后处理对PC12细胞缺血再灌注损伤致细胞凋亡的作用及其机制研究[J].卒中与神经疾病杂志,2016,23(02):75-79.[doi:10.3969/j.issn.1007-0478.2016.02.001]
　Guo Xiaojie,Mao Shanping,Dong Huimin,et al.The effect and mechanism of ischemic postconditioning on PC12 cell apoptosis induced by ischemia/reperfusion injury[J].Stroke and Nervous Diseases,2016,23(02):75-79.[doi:10.3969/j.issn.1007-0478.2016.02.001]
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缺血后处理对PC12细胞缺血再灌注损伤致细胞凋亡的作用及其机制研究(/HTML)
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第23卷
期数:
2016年02期
页码:
75-79
栏目:
论 著
出版日期:
2016-04-26

文章信息/Info

Title:
The effect and mechanism of ischemic postconditioning on PC12 cell apoptosis induced by ischemia/reperfusion injury
作者:
郭晓洁 毛善平 董慧敏等
作者单位:430060 武汉大学人民医院神经内科[郭晓洁 毛善平(通信作者)董慧敏 腊琼 王舜 方聪聪],神经外科[刘宝辉]
Author(s):
Guo Xiaojie;  Mao Shanping;  Dong Huimin;  et al.
Department of Neurology, Renmin Hospital, Wuhan University, Wuhan 430060
关键词:
缺血后处理 PC12细胞 NF-κB/p65 凋亡
Keywords:
Ischemic postconditioning PC12 cells NF-κB/p65 Apoptosis
分类号:
R743
DOI:
10.3969/j.issn.1007-0478.2016.02.001
文献标志码:
A
摘要:
目的 探讨缺血后处理对PC12细胞缺血再灌注损伤引起的细胞凋亡的作用及其作用机制。方法 将PC12细胞分为3组:正常组、缺血再灌注组、缺血后处理组。缺血再灌注组予以糖氧剥夺12 h后正常培养,缺血后处理组经糖氧剥夺12 h后予以3个循环的正常培养(10 min)→糖氧剥夺(10 min),再正常培养12 h后通过Hoechst染色检测各组细胞的凋亡情况,应用Westernblot 检测各组细胞Caspase-3活化蛋白及磷酸化NF-κB/p65蛋白表达水平,采用RT-PCR检测各组细胞NF-κB及Caspase-3 mRNA表达水平。结果 Hoechst染色显示缺血后处理可降低缺血再灌注引起的细胞凋亡; 与对照组相比, 缺血再灌注组磷酸化NF-κB/p65和Cleaved caspase-3的蛋白表达水平高; 缺血后处理组磷酸化NF-κB/p65和Cleaved caspase-3的蛋白表达水平明显低于缺血再灌注组; NF-κB和Caspase-3的mRNA表达趋势与蛋白表达基本一致。结论 缺血后处理可以减轻缺血再灌注损伤引起的PC12细胞凋亡,这可能与NF-κB/p65信号通路有关。
Abstract:
ObjectiveTo investigate the effect and the probable mechanism of ischemic postconditioning on PC12 cell apoptosis induced by ischemia/reperfusion injury.Methods The PC12 cells were divided into 3 groups: the control group, the ischemia/reperfusion group, and the ischemic postconditioning group. The ischemia/reperfusion group was subjected to a 12-hour oxygenglucose deprivation. The ischemic postconditioning group was given three cycles of 10 minutes of normal cultivation after a 12-hour oxygenglucose deprivation, and then 10 minutes of oxygenglucose deprivation. The PC12 cells were cultivated normally. Afterward the apoptosis of PC12 cells were evaluated by fluorescence microscope. Western blot was used to detect the protein level of cleaved caspase-3 and phosphorylated p65. Reverse transcription-PCR(RT-PCR)was used to observe the mRNA level of NF-κB and Caspase-3.Results Hoechst staining showed ischemic postconditioning can reduce cell apoptosis caused by ischemia and reperfusion injury. Compared with the control group, the expression of Caspase-3 and NF-κB/p65 increased in the PC12 cells treated with ischemia/reperfusion procedure. The level of NF-κB/p65 and Caspase-3 significantly reduced in ischemia postconditioning group.Conclusion NF-κB/p65 signal pathway may be involved in the protection of ischemic postconditioning against apoptosis of PC12 cells induced by ischemia/reperfusion injury.

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备注/Memo

备注/Memo:
(2015-12-11收稿)
更新日期/Last Update: 2016-05-04