The expression levels of miR‑214 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) in dexamethasone (DEX)‑treated TC28 cells, and the femoral head cartilage tissues, serum and primary chondrocytes of patients with LCPD, and healthy individuals were determined via reverse transcription quantitative polymerase chain reaction and western blot analysis.
When compared with normal HCMs, the expressions of p53-upregulated modulator of apoptosis (PUMA), phosphatase and tensin homolog (PTEN), B-cell lymphoma-2-associated X protein (Bax) and caspase 7 proteins was decreased in HCMs overexpressing miRNA-214 following H<sub>2</sub>O<sub>2</sub> induction, and the rate of apoptosis decreased by 63.64, 21.95, 46.67 and 50.05%, respectively. miRNA-214 was highly expressed in the sera of elderly patients with AMI, which may inhibit myocardial cell apoptosis by inhibiting the expression of miR-214 target genes including <i>PUMA, PTEN, Bax and caspase 7</i>.
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.