Neuroprotective mechanisms of miR-124 activating PI3K/AKt signaling pathway in ischemic stroke

Abstract

The neuroprotective mechanisms of miR-124 activating phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in ischemic stroke were investigated. The oxygen-glucose deprivation model of nerve cells induced by PC12 cells was established in vitro, then miR-124 mimics or inhibitor was transfected and synthesized by liposome. Cells were divided into the blank control, model, mimics and inhibitor groups, and the apoptotic rate was determined using flow cytometry. Additionally, the expression levels of PI3K, Akt, Bax, Bcl-2, caspase-3 mRNA and protein were tested by quantitative PCR and western blot analysis at 0, 3, 6, 12 and 24 h, respectively. The apoptotic rate at each time-point in the blank control group was not significantly different. The apoptotic rate of the model and inhibitor groups increased over time, whereas the mimics group decreased (P<0.05). The apoptotic rate at each time-point in the mimics group was significantly lower than that of the model and inhibitor groups, and the rate of the inhibitor group was higher than that of the model group (P<0.05). PI3K, Akt and Bcl-2 mRNA and protein expression levels at the different time-points in the mimics group were significantly higher than those of the remaining groups (P<0.05). The expression levels of Bax and caspase-3 mRNA and protein in the inhibitor group were the highest, followed by the model and mimics groups, while that of the blank control group was the lowest (P<0.05). The results suggest that miR-124 participates in the neural protection of ischemic stroke by activating the PI3K/Akt signaling pathway.