Yu Lu1, Minyu Jian1, Wei Xiong1, Ruquan Han2. 1. Department of Anesthesia, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China. 2. Department of Anesthesia, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China. Email: ruquan.han@gmail.com.
Abstract
OBJECTIVE: To explore the propofol regulation of Bcl-2 protein expression through miR-181a in glucose deprivation (GD) cultured astrocytes. METHODS: Primary cultured murine astrocytes were treated with 0, 1, 5, 10, 15, 20 µmol/L propofol for 12 h and then cultured with GD medium for 24 h. The cell survival rate was recorded with microscope. Reactive oxygen species (ROS) formation and mitochondrial membrane stabilization were observed. And the expression levels of miR-181a and Bcl-2 protein were recorded to analyze the protection effects of propofol on astrocytes. RESULTS: After the treatments of propofol and GD, the survival rates of 0, 1, 5, 10, 15, 20 µmol/L propofol groups were (0.51 ± 0.03)%, (0.52 ± 0.02) %, (0.52 ± 0.02) %, (0.73 ± 0.04) %, (0.31 ± 0.02) % and (0.21 ± 0.02)%. And there were statistical significance (F = 118.62, P < 0.001). Compared with 0 µmol/L propofol group, the survival rate was much higher in 10 µmol/L propofol group while much lower in 15 µmol/L and 20 µmol/L propofol groups. 10 µmol/L propofol could decrease ROS formation and stabilize mitochondrial membrane. And Bcl-2 protein expression was up-regulated while miR-181a expression inhibited by 10 µmol/L propofol. CONCLUSION: The protection of 10 µmol/L propofol against GD stress in astrocytes is correlated with inhibiting miR-181a and up-regulating Bcl-2 protein expression.
OBJECTIVE: To explore the propofol regulation of Bcl-2 protein expression through miR-181a in glucose deprivation (GD) cultured astrocytes. METHODS: Primary cultured murine astrocytes were treated with 0, 1, 5, 10, 15, 20 µmol/L propofol for 12 h and then cultured with GD medium for 24 h. The cell survival rate was recorded with microscope. Reactive oxygen species (ROS) formation and mitochondrial membrane stabilization were observed. And the expression levels of miR-181a and Bcl-2 protein were recorded to analyze the protection effects of propofol on astrocytes. RESULTS: After the treatments of propofol and GD, the survival rates of 0, 1, 5, 10, 15, 20 µmol/L propofol groups were (0.51 ± 0.03)%, (0.52 ± 0.02) %, (0.52 ± 0.02) %, (0.73 ± 0.04) %, (0.31 ± 0.02) % and (0.21 ± 0.02)%. And there were statistical significance (F = 118.62, P < 0.001). Compared with 0 µmol/L propofol group, the survival rate was much higher in 10 µmol/L propofol group while much lower in 15 µmol/L and 20 µmol/L propofol groups. 10 µmol/L propofol could decrease ROS formation and stabilize mitochondrial membrane. And Bcl-2 protein expression was up-regulated while miR-181a expression inhibited by 10 µmol/L propofol. CONCLUSION: The protection of 10 µmol/L propofol against GD stress in astrocytes is correlated with inhibiting miR-181a and up-regulating Bcl-2 protein expression.