摘要/Abstract

摘要： 目的·探讨丙泊酚镇静对大鼠认知功能的影响及其可能的机制。方法· 48只SD大鼠被随机分为3组。10 mg/mL丙泊酚注射液以100 mg/kg或300 mg/kg腹腔注射45 min后，用定量PCR检测大鼠海马脑源性神经营养因子（brain derived neurotropic factor，BDNF） -TrkB/p75信号分子的mRNA水平；并用逃避性抑制（inhibitory avoidance，IA）试验评价丙泊酚作用后的大鼠学习记忆情况。结果·丙泊酚腹腔注射45 min后，100 mg/kg组和300 mg/kg组大鼠海马组织中BDNF的mRNA水平分别是对照组的（1.20±0.13）倍（P0.002）和（88±12）%（P0.044）；100 mg/kg组和300 mg/kg组大鼠海马组织中TrkB的mRNA水平分别是对照组的（1.01±0.11）倍（P0.982）和（86±11）%（P0.018）。另外，p75的mRNA水平分别是对照组的（1.02±0.10）倍（P0.778）和（1.59±0.18）倍（P0.000）。100 mg/kg组大鼠IA的潜伏期与对照组的差异无统计学意义（P0.875）；300 mg/kg组大鼠IA的潜伏期显著低于对照组（P0.028），亦显著低于100 mg/kg组（P0.020）。结论·丙泊酚呈剂量依赖性调节海马BDNF-TrkB/p75信号分子的表达，高剂量丙泊酚可能通过调节海马BDNF-TrkB/p75信号进而影响大鼠的认知功能。
关键词: 丙泊酚, 脑源性神经营养因子, 海马, 镇静
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


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