Jianhua Chang1, Xin Yan2, Yuan Zeng3. 1. Department of Anesthesiology, Shaanxi Provincial People's Hospital, Affiliated Hospital of Xi'an Medical University, Xi'an710068, China. 2. Department of Anesthesiology, Union Hospital, Huazhong University of Science and Technology, Wuhan430000, China. 3. Department of Anesthesiology, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University, Xi'an710018, China. Electronic address: zengyuan70zy@163.com.
Abstract
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.
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.