Silencing lncRNA SIX3OS1 mitigates inflammation and apoptosis in post-stroke cognitive impairment via miR-511-3p.

Abstract

The present study aimed to explore the expression and molecular mechanisms of lncRNA SIX3OS1 in post-stroke cognitive impairment (PSCI). Middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) were applied to establish an in vitro and in vivo model of PSCI. RT-qPCR was conducted to examine the mRNA levels of SIX3OS1, miR-511-3p, and RBP4. Morris water maze test was used to evaluate spatial learning and memory ability. Cell viability and apoptosis were examined by CCK-8 and flow cytometry. The secretion level of inflammatory factors was analyzed by ELISA. DLR and RIP assay were performed to validate the target relationship. In MCAO rats and OGD/R-induced cells, SIX3OS1 and RBP4 levels were significantly elevated, while miR-511-3p was reduced. miR-511-3p targets SIX3OS1 and RBP4. Compared with the sham, the spatial learning and memory ability of MCAO rats were decreased, but the silencing of SIX3OS1 could restore them, but this restoration was partially impaired by lowing of miR-511-3p. Silencing of SIX3OS1 enhanced OGD/R-induced SH-SY5Y cell viability and inhibited apoptosis and inflammatory factor secretion, but they were both attenuated by the lowing of miR-511-3p. Silencing of SIX3OS1 can protect PSCI via targeting miR-511-3p to promote cell viability and inhibit apoptosis and inflammation.