Abstract: Objective · To detect the effects of propofol sedation on cognitive function in rats and its mechanism. Methods · Forty-eight SD rats were randomly divided into three groups, i.e. control group, 100 mg/kg group and 300 mg/kg group. Rats were administrated intraperitoneally with propofol (10 mg/mL, 100 mg/kg or 300 mg/kg). The mRNA levels of brain derived neurotropic factor (BDNF)-TrkB/p75 signal molecules in rat hippocampus were evaluatedreal time PCR 45 min after propofol treatment. Learning and memory ability was examinedinhibitory avoidance (IA) test after propofol treatment. Results · The mRNA levels of BDNF in the hippocampal tissue were (1.20±0.13) fold (P0.002) and (88±12) % (P0.044) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group after injection of propofol. The mRNA levels of TrkB were (1.01±0.11) fold (P0.982) and (86±11) % (P0.018) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group. The mRNA levels of p75 were (1.02±0.10) fold (P0.778) and (1.59±0.18) fold (P0.000) of that in control group, respectively, in 100 mg/kg group and 300 mg/kg group. There was no significant difference of the 24 h IA memory retention latency between 100 mg/kg group and control group. The 24 h IA memory retention latency in 300 mg/kg group was significantly decreased compared with control group (P0.028) and 100 mg/kg group (P0.020). Conclusion · Propofol dose-dependently regulates the of BDNF-TrkB/p75 signal molecules, and high dose propofol may reduce cognitive function via BDNF-TrkB/p75 signal.

Key words: propofol, brain derived neurotropic factor, hippocampus, sedation