miR-29家族在深低温停循环相关性神经元损伤中的作用 |
投稿时间:2017-09-04 修订日期:2017-09-06 点此下载全文 |
引用本文:李红梅,葛俊文,张儒舫,沈立.miR-29家族在深低温停循环相关性神经元损伤中的作用[J].医学研究杂志,2018,47(5):28-31,35 |
DOI:
10.11969/j.issn.1673-548X.2018.05.007 |
摘要点击次数: 1612 |
全文下载次数: 1199 |
|
基金项目:国家自然科学基金资助项目(81371449) |
|
中文摘要:目的 观察miR-29家族在低温糖氧剥夺/再灌注(oxygen-glucose deprivation/reoxygenation,OGD/R) HT22细胞中的表达,进而探究miR-29家族在深低温停循环(deep hypothermic circulatory arrest,DHCA)相关性神经元死亡中的特异性作用及其相关机制。方法 将HT22细胞随机分为对照组、低温OGD/R组、类似物组(agomir-NC组、agomir-29a组、agomir-29b组和agomir-29c组)和抑制剂组(antamir-NC组、antamir-29a组、antamir-29b组和antamir-29c组);运用一个密闭容器和一个厌氧产气袋建立OGD/R模型;定量PCR检测HT22细胞内miR-29家族的表达;CCK-8方法检测活细胞数目;Western blot法检测HT22细胞内Bax和PUMA蛋白含量;JC-1和H2DCFDA法分别测定HT22细胞内活性氧(reactive oxygen species,ROS)含量和线粒体膜电位(mitochondrial membrane potential,MMP)。结果 低温OGD/R模型中miR-29家族表达显著下降(P<0.01)。miR-29家族过表达显著抑制了低温OGD/R诱导的HT22细胞死亡,以及Bax和PUMA蛋白的表达(P均<0.01);同时减轻了ROS含量和MMP水平(P均<0.01)。结论 miR-29家族可以通过减轻氧化应激从而对DHCA介导的神经元损伤产生保护性作用。 |
中文关键词:深低温停循环 糖氧剥夺/再灌注 miR-29 氧化应激 |
|
Role of miR-29 Family in the DHCA-associated Neuron Injury |
|
|
Abstract:Objective To investigate the expression and role of miR-29 family in HT22 cells with low temperature OGD/R, and further explore the specific role and its related mechanism of miR-29 family in DHCA-related neuron death.Methods The HT22 cells were randomly divided into the control group, low temperature OGD/R group, analogue group (agomir-NC group, agomir-29a group, agomir-29b group and agomir-29c group), inhibitor group(antamir-NC group, antamir-29a group, antamir-29b group and antamir-29c group). The OGD/R model was established using an airtight container and an anaeropack. The expression of miR-29 family on HT22 cell was determined by quantitative PCR. CCK-8 kit was used to detect the number of living cells. Western blot was conducted for the quantification of Bax and PUMA proteins. JC-1 and H2DCFDA were used to measure reactive oxygen species (ROS) level and mitochondrial membrane potential (MMP) of HT22 cells, respectively.Results The expression of miR-29 family was significantly declined in low temperature OGD/R model (P<0.01). Overexpression of miR-29 family significantly alleviated the HT22 cell injury induced by low temperature OGD/R, and inhibited the expression of Bax and PUMA protein (P<0.05). In addition, the injection of miR-29 family analogues inhibited the increase of ROS and MMP in low temperature OGD/R model (P<0.05).Conclusion MiR-29 family could exert its protective effect against OGD/R-mediated HT22 cell injury by reducing oxidative stress. |
keywords:Deep hypothermic circulatory arrest Oxygen-glucose deprivation/reoxygenation miR-29 Ooxidative stress |
查看全文 查看/发表评论 下载PDF阅读器 |