Downregulation of miR-23a-3p improves cognitive function in rats after subarachnoid hemorrhage by targeting VCAN.

Subarachnoid hemorrhage (SAH) is a complicated and deadly disorder. Dysregulation of miRNAs in SAH has been widely reported. This investigation elucidated the function of miR-23a-3p in the in vivo and in vitro models of SAH. The miR-23a-3p and VCAN levels in SAH rats and sham controls were detected by RT-qPCR. The SAH rats were intracerebrally administrated with miR-23a-3p antagomir. Morphological changes and brain function were assessed. The isolated brain microvascular endothelial cells (BMECs), identified by immunofluorescence staining, were used as the model of SAH in vitro. The viability and apoptosis of BMECs were evaluated using MTT, flow cytometry, and western blotting analyses. Targeted relationship between miR-23a-3p and VCAN was predicted in miRDB and validated by a luciferase reporter assay. We found that the miR-23a-3p level was upregulated in rats after SAH, while VCAN was downregulated. Silencing miR-23a-3p attenuated neurological deficits and neuronal apoptosis in rats after SAH. VCAN was verified to be targeted by miR-23a-3p. Functionally, miR-23a-3p downregulation or VCAN overexpression inhibited BMEC apoptosis and promoted cell activity. Moreover, knockdown of VCAN eliminated the influence of miR-23a-3p inhibition in BMECs. Overall, suppression of miR-23a-3p improves cognitive function after SAH by targeting VCAN.