Abstract
To explore the effect of miR-199a-5p and AKT signal pathway on cognitive function and neuronal cells in rats with ischemic stroke. Sprague-Dawley rats were divided into 6 groups: Normal group (normal rats), Sham group (rats received sham operation), Model group (MCAO rats), miR-199a-5p inhibitor group (model rats treated with miR-199a-5p inhibitor), IGF-1 group (model rats treated with AKT signaling pathway activator), miR-199a-5p inhibitor + IGF-1 group (model rats treated by miR-199a-5p inhibitor and AKT signaling pathway activator). Rat behavior and cerebral infarction area were observed. TUNEL fluorescence staining was used to detect neuronal apoptosis in hippocampal CA1 region of rats. The dual luciferase reporter assay validated the targeting relationship between miR-199a-5p and AKT. qRT-PCR and WB were used to detect the expression level of miR-199a-5p, (p)-AKT and (p)-mTOR, apoptosis-related proteins Bax and Bcl-2. Compared with the normal group, the expression of miR-199a-5p was increased in the Model group, and the expression levels of AKT, mTOR, p-AKT, and p-mTOR were decreased (all P < 0.05); the cognitive function of the rats in the Model group was thereby significantly lower (P < 0.05). miR-199a-5p was targeted to inhibit AKT. Compared with the Model group, miR-199a-5p inhibition combined with IGF-1 showed more significant effects on improving cognitive function and protecting neuronal cells of rats. In conclusion, silencing miR-199a-5p can effectively improve cognitive function in ischemic stroke rats and decrease neuronal apoptosis in hippocampus by activating the AKT signaling pathway.