Abstract
Dysfunction of the microRNA (miR) network has been indicated as a major regulator in neurological diseases. However, there is limited understanding regarding the functional significance of miRs in ischemic brain injury. In the present study, miR-196a expression was significantly increased in rat brains and neurons following transient middle cerebral artery occlusion (MCAO) or oxygen-glucose deprivation, respectively. In addition, repression of miR-196a significantly decreased neuron cell apoptosis and the infarct size in rats subjected to MCAO (P<0.05). Furthermore, miR-196a was indicated to directly target and inhibit high mobility group A1 expression, which indicated a potential role for miR-196a in ischemic brain injury. These findings suggested that miR-196a may be involved in regulating neuronal cell death, thus offering a novel target for the development of therapeutic agents against ischemic brain injury.
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