miR-495-3p Attenuates Neuronal Apoptosis Through The Activation of Wnt/MAPK Pathways in Ischemic Stroke

The incidence of ischemic stroke, involving neuronal cell death and damaged blood vessels, is gradually increasing. In this study, we investigated the effects of a miR-495-3p-I on neuronal viability and recovery using both oxygen-glucose deprivation and recovery (OGD/R) and in transient middle cerebral artery occlusion (tMCAo) models of ischemic stroke. Cell viability increased with miR-495-3p-I treatment compared with the OGD/R group, and both early and late apoptosis decreased through by flow cytometry analysis. In the tMCAo model, tissues injected with miR-495-3p-I showed upregulation of canonical Wnt pathway genes (cyclin D1 and c-Myc) and neuronal marker (Tuj1), while non-canonical Wnt/MAPK pathway genes (caspase-3 and -7) were downregulated. Expression of the pro-apoptotic marker Bax was reduced, whereas the Bcl-2 family protein Mcl-1 increased. Behavioral tests revealed improved motor function compared to the sham group and treatment with miR-495-3p-I reduced brain infarct volume. This research explored the function of miR-495-3p-I in Wnt and MAPK pathways by using the miR-495-3p-I in a model of ischemic stroke, a neurological disease. Thus, we demonstrated that miR-495-3p-I reduced apoptosis and enhanced neuronal cell survival, suggesting it could be a potential therapeutic target.