期刊
NEUROCHEMICAL RESEARCH
卷 41, 期 10, 页码 2627-2635出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-016-1975-0
关键词
MiR-93; Nrf2; HO-1; Oxidative stress; Ischemic stroke
资金
- National Natural Science Foundation of China (NSFC) [81501017]
- Innovation Foundation for the Unversity Students [201510160000013]
- President Foundation of Jinzhou Medical University [XZJJ20140105, XZJJ2015012]
The present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In vitro study demonstrated that miR-93 antagomir attenuated hydrogen peroxide (H2O2)-induced injury. Moreover, miR-93 antagomir suppressed oxidative stress in I/R brain and H2O2 treated cortical neurons. Furthermore, we founded that down-regulation of miR-93 increased the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) and the luciferase reporter assay confirmed that miR-93 directly binds to the predicted 3'-UTR target sites of the nrf2 gene. Finally, we found that knockdown of Nrf2 or HO-1 abolished miR-93 antagomir-induced neuroprotection against oxidative stress in H2O2 treated neuronal cultures. These results suggested that miR-93 antagomir alleviates ischemic injury through the Nrf2/HO-1 antioxidant pathway.
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