MicroRNA‑634 alters nerve apoptosis via the PI3K/Akt pathway in cerebral infarction

In the present study, the role and mechanism of microRNA‑634 (miRNA‑634) in the adjustment of nerve inflammation and apoptosis in cerebral infarction were investigated. In a cerebral infarction rat model, the expression of miRNA‑634 was increased, compared with that in the normal control group. The upregulated expression of miRNA‑634 in an in vitro model of cerebral infarction increased cell apoptosis and the protein expression of capsase‑3/B‑cell lymphoma 2‑associated X protein (Bax) via inactivation of the phosphoinositide 3‑kinase (PI3K)/Akt pathway. The downregulation of miRNA‑634 enhanced cell growth and inhibited cell apoptosis in the in vitro model of cerebral infarction through induction of the PI3K/Akt pathway. Subsequently, a PI3K inhibitor was used to inhibit the expression of PI3K in the in vitro model of cerebral infarction via the downregulation of miRNA‑634, which showed that cell apoptosis and the protein expression of capsase‑3/Bax were also increased. A PI3K agonist reduced the effects of the upregulation of miRNA‑634 in the in vitro model of cerebral infarction. In conclusion, the data obtained demonstrated the possible future use of miRNA‑634 as a therapeutic target in cerebral infarction through the PI3K/Akt pathway.