Abstract

In the current study, we reported that overexpression of miR-152-3p effectively ameliorated neurological deficits and protected blood-brain barrier(BBB) integrity in middle cerebral artery occlusion (MCAO) rats. In an in vitro model, the level of miR-152-3p was significantly decreased in bEnd.3 cells after oxygen–glucose deprivation/reperfusion (OGD/R) insult. miR-152-3p overexpressing bEnd.3 cell monolayers were protected from OGD/R-induced microvascular hyperpermeability. The miR-152-3p-mediated protective effect was associated with lower apoptosis of endothelia by negatively modulating the MAP3K2/JNK/c-Jun pathway.