Neuroprotection induced by post-conditioning following ischemia/reperfusion in mice is associated with altered microRNA expression

被引:22
|
作者
Miao, Wei [1 ]
Bao, Tian-Hao [2 ]
Han, Jian-Hong [1 ]
Yin, Mei [1 ]
Zhang, Jie [1 ]
Yan, Yong [1 ]
Zhu, Yu-Hong [1 ]
机构
[1] Kunming Med Univ, Dept Neurol, Affiliated Hosp 2, 374 Dianmian Rd, Kunming 650031, Yunnan, Peoples R China
[2] Psychiat Hosp Yunnan Kunming, Dept Geratol, Kunming 650224, Yunnan, Peoples R China
关键词
ischemia-reperfusion; ischemic postconditioning; miRNA; cognitive functions; ISCHEMIC POSTCONDITIONING PROTECTS; TRANSIENT FOCAL ISCHEMIA; CEREBRAL-ISCHEMIA; BRAIN-INJURY; RATS; STROKE; MODEL; REPERFUSION; ACTIVATION; MIR-17-92;
D O I
10.3892/mmr.2016.5576
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ischemic preconditioning and ischemic postconditioning (IPostC) represent promising strategies to reduce ischemia-reperfusion (I/R) injury and attenuate the lethal ischemic damage following stroke. However, the mechanism underlying this attenuation remains to be elucidated. It was hypothesized that alterations in microRNA (miRNA) expression in the cerebral cortex and hippocampus of mice following I/R is associated with the functional improvement induced by IPostC. Behavioral changes were assessed in a mouse model of I/R in the absence or presence of IPostC, followed by microarray analyses to investigate the expressional alterations of miRNAs in the cerebral cortex and hippocampus of mice. The results of the present study revealed that IPostC abrogated the neurological impairment and hippocampus-associated cognitive deficits induced by I/R, and upregulated or downregulated the expression levels of numerous miRNAs. Furthermore, the upregulation of miR-19a, and the downregulation of miR-1, let-7f and miR-124 expression levels following IPostC was confirmed utilizing reverse transcription-quantitative polymerase chain reaction. The results of the present study demonstrated that alterations in miRNA expression in the cerebral cortex and hippocampus of mice following I/R was associated with the neuroprotection induced by IPostC.
引用
收藏
页码:2582 / 2588
页数:7
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