Propofol weakens hypoxia-aroused apoptosis and autophagy via elevating microRNA-137 in neurocytes.

BACKGROUND

Hypoxia was proven to cause brain cell apoptosis and autophagy. Herein, we tested the influences of propofol, a commonly used intravenous sedative hypnotic drug, on apoptosis and autophagy aroused by hypoxia stimulation in PC-12 and HT-22 cells.

METHODS

Followed by hypoxia and/or propofol treatment, cell viability of PC-12 and HT-22 cells, apoptosis and autophagy, along with microRNA-137 (miR-137) expression were measured, respectively. Then, miR-137 inhibitor was transfected to silence miR-137. Whether miR-137 took part in the impacts of propofol on hypoxia-exposed cells was explored. Finally, the activities of PI3K/AKT/mTOR and ERK pathways were measured.

RESULTS

Hypoxia stimulation aroused cell apoptosis and elevated cell autophagy in PC-12 and HT-22 cells. Propofol weakened the apoptosis and autophagy of PC-12 and HT-22 cells aroused by hypoxia. Moreover, propofol elevated the miR-137 level in PC-12 and HT-22 cells. Silencing miR-137 declined the influences of propofol on hypoxia-induced injuries. Besides, propofol promoted PI3K/AKT/mTOR and ERK pathways activation in hypoxia-exposed cells through raising miR-137.

CONCLUSION

Propofol weakened hypoxia-aroused apoptosis and autophagy of PC-12 and HT-22 cells might be through raising miR-137 level and thereby promoting PI3K/AKT/mTOR and ERK pathways activation.