MicroRNA-214 suppresses propofol-induced neuroapoptosis through activation of phosphoinositide 3-kinase/protein kinase B signaling by targeting phosphatase and tensin homolog expression

The present study aimed to investigate the effects of microRNA (miR)-214 on neuroapoptosis induced by propofol and the possible mechanism of its anti-apoptotic effects. Initially, it was observed that miR-214 expression was upregulated in propofol-induced neuroapoptosis rats. Next, propofol-treated nerve cells were transfected with miR-214 mimics. The results revealed that miR-214 overexpression induced apoptosis, inhibited cell proliferation, inhibited cyclin D1 protein expression, promoted caspase-3 activity and B-cell lymphoma 2-associated X protein expression, and enhanced the levels of inflammation factors in nerve cells treated with propofol. In addition, miR-214 overexpression suppressed phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling by targeting the activation of phosphatase and tensin homolog (PTEN) and nuclear factor-B expression in nerve cells treated with propofol. Treatment with a PTEN inhibitor successfully suppressed the PTEN protein expression and decreased the apoptosis of propofol-treated nerve cells subsequent to miR-214 overexpression through PI3K/Akt signaling. In conclusion, the present study data revealed that miR-214 suppressed propofol-induced neuroapoptosis through the activation of PI3K/Akt signaling by targeting PTEN expression.