丙泊酚对缺氧原代胎鼠大脑神经元热休克蛋白70表达的影响  

Effects of propofol on expression of HSP70 in the anoxicprimary fetal rat neurons

作　　者：陈君[1] 王国林[2] 

机构地区：[1]天津环湖医院麻醉科,300060 [2]天津医科大学总医院麻醉科

出　　处：《临床麻醉学杂志》2009年第8期698-700,共3页Journal of Clinical Anesthesiology

摘　　要：目的探讨丙泊酚的脑保护机制。方法培养12d的胎鼠大脑神经元,随机分为丙泊酚组(n=12)、缺氧组(n=6)和对照组(n=6)。丙泊酚组于缺氧前1h换入含有14μmol/L和56μmol/L丙泊酚的培养液,随后缺氧30min。于缺氧后1、3、6、8、24、48h分别用原位杂交法和免疫组化法观察三组热休克蛋白70(HSP70)mRNA、热休克同源蛋白70(HSC70) mRNA及HSP70的表达。结果缺氧30min可诱导神经元HSP70 mRNA、HSC70 mRNA和HSP70表达,表达高峰分别为24、24和48h。14μmol/L和56μmol/L丙泊酚可诱导缺氧鼠脑神经元HSP70 mRNA和HSC70 mRNA表达高峰提前至8和6h;56μmol/L丙泊酚可使缺氧鼠脑神经元HSP70表达高峰提前至24h。结论丙泊酚可从转录和翻译两个水平促进缺氧鼠脑神经元HSP70的表达,产生延迟神经保护作用。Objective To investigate the neuroprotective mechanism of propofol. Methods The neurons cultured for 12 days were randomly divided into three groups of control, anoxic and propofol. Propofol 14 μmol/L and 56 μmol/L were added into cell culture medium 1 h before anoxia, respectively. The expressions of heat shock protein 70 （HSP70） mRNA and heat shock cognate protein70 （HSC 70） mRNA were detected by in situ hybridization technique and the expression of HSP70 was measured by immunohistochemical technique at 1 h （T1）, 3 h （T3）, 6 h （T6）, 8 h （T8）, 24 h （T24）,48 h （T48） after anoxia. Results Anoxia for 30 min could induce the synthesis of HSP70 mRNA, HSC70 mRNA and HSP70, the peaks of which were observed at 24,24 and 48 h after anoxia, respectively. Incubated with propofol 14 μmol/L and 56μmol/L before anoxia, the synthesis of HSP70 mRNA and HSC70 mRNA was significantly increased, and reached a maximum level at 8 h and 6 h after anoxia, respectively. Propofol 56 μmol/L could induce the synthesis of HSP70 and reached a maxium level at 24 h after anoxia. Conclusion Propofol could induce the synthesis of HSP70 at the level of both transcription and translation. The expression of HSP70 （HSP70 and HSC70） might participate in the delayed neuroprotection of propofol.

关 键 词：丙泊酚 神经元 缺氧损害 热休克蛋白70 热休克同源蛋白70 

分 类 号：R96[医药卫生—药理学]