Objective:To evaluate the relationship between microRNA-29a (miR-29a) and p53 up-regulated modulator of apoptosis (PUMA) in propofol-induced reduction of glucose deprivation (GD)-induced injury to human glioma cells.Methods:Human glioma U87 cells were cultured in vitro to the logarithmic growth phase. Cells were then divided into 6 groups ( n=24 each) by the random number table method: control group (group C), group GD, propofol + GD group (group P+ GD), miR-29a inhibitor group (group I), miR-29a inhibitor + GD group (group I+ GD) and miR-29a inhibitor+ propofol+ GD group (group I+ P+ GD). Cells were cultured in normal condition in group C. The culture medium was changed to glucose-free DMEM solution, and the cells were cultured for 12 h in group GD. In group P+ GD, cells were incubated with propofol 10 μmol/L for 12 h and then incubated in glucose-free DMEM solution for 12 h. In group I, group I+ GD and group I+ P+ GD, miR-29a inhibitor was transfected into cells using lipofectamine transfection kit, and then the cells were cultured for 48 h, and the other treatments were similar to those previously described in group P+ GD. The cell survival rate, mitochondrial membrane potential and level of reactive oxygen species (ROS) were determined. The expression of miR-29a was detected by quantitative real-time polymerase chain reaction, and the expression PUMA was detected by Western blot. Results:Compared with group C, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group GD and group I ( P<0.05). Compared with group GD, the cell survival rate and mitochondrial membrane potential were significantly increased, the level of ROS was decreased, the expression of miR-29a was up-regulated, and the expression of PUMA was down-regulated in group P+ GD, and the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ GD ( P<0.05). Compared with group P+ GD, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ P+ GD ( P<0.05). Conclusions:The mechanism by which propofol reduces glucose deprivation-induced injury to human glioma cells is related to up-regulation of miR-29a expression and down-regulation of PUMA expression.

Objective:To evaluate the relationship between microRNA-29a (miR-29a) and p53 up-regulated modulator of apoptosis (PUMA) in propofol-induced reduction of glucose deprivation (GD)-induced injury to human glioma cells.Methods:Human glioma U87 cells were cultured in vitro to the logarithmic growth phase. Cells were then divided into 6 groups ( n=24 each) by the random number table method: control group (group C), group GD, propofol + GD group (group P+ GD), miR-29a inhibitor group (group I), miR-29a inhibitor + GD group (group I+ GD) and miR-29a inhibitor+ propofol+ GD group (group I+ P+ GD). Cells were cultured in normal condition in group C. The culture medium was changed to glucose-free DMEM solution, and the cells were cultured for 12 h in group GD. In group P+ GD, cells were incubated with propofol 10 μmol/L for 12 h and then incubated in glucose-free DMEM solution for 12 h. In group I, group I+ GD and group I+ P+ GD, miR-29a inhibitor was transfected into cells using lipofectamine transfection kit, and then the cells were cultured for 48 h, and the other treatments were similar to those previously described in group P+ GD. The cell survival rate, mitochondrial membrane potential and level of reactive oxygen species (ROS) were determined. The expression of miR-29a was detected by quantitative real-time polymerase chain reaction, and the expression PUMA was detected by Western blot. Results:Compared with group C, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group GD and group I ( P<0.05). Compared with group GD, the cell survival rate and mitochondrial membrane potential were significantly increased, the level of ROS was decreased, the expression of miR-29a was up-regulated, and the expression of PUMA was down-regulated in group P+ GD, and the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ GD ( P<0.05). Compared with group P+ GD, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ P+ GD ( P<0.05). Conclusions:The mechanism by which propofol reduces glucose deprivation-induced injury to human glioma cells is related to up-regulation of miR-29a expression and down-regulation of PUMA expression.