丙泊酚对大鼠局灶性脑缺血后线粒体功能的影响

Effect of propofol on mitochondrial function in focal cerebral ischemia rats

目的通过观察丙泊酚对大鼠局灶性脑缺血后线粒体功能的影响，探讨其脑保护机制。方法24只健康雄性Wistar大鼠，体质量250—300g，采用线栓法制备大鼠局灶性大脑中动脉栓塞（MCAO）模型，随机分为三组（每组n=8），假手术组：仅暴露颈内动脉但不栓塞大脑中动脉；缺血组和丙泊酚组：栓塞大脑中动脉2h。提取各组大鼠缺血核心区皮质线粒体，丙泊酚组加入丙泊酚于37℃下孵育2min。流式细胞仪分析各组大鼠缺血核心区皮质线粒体膜电位及活性氧簇生成量。结果与缺血组比较，丙泊酚组脑皮质缺血核心区线粒体膜电位升高（P〈0．05），活性氧簇（ROS）生成量降低（P〈0．05）；与假手术组比较，丙泊酚组与缺血组脑皮质缺血核心区线粒体膜电位降低（P〈0．05），活性氧簇生成量升高（P〈0．05）。结论丙泊酚能够有效地改善大鼠局灶性脑缺血后线粒体的功能，这可能是丙泊酚脑保护作用的潜在机制之一。

Objective To observe the effects of propofol on mitochondrial function during focal cerebral ischemia in rats, and the mechanisms of propofol in brain protection. Methods Focal cerebral ischemia was induced by an intraluminal middle cerebral artery occlusion （MCAO） surgery. Twenty four male Wsitar rats （body weight 250 - 300 g） were divided into three groups randomly （n = 8）. Sham group： sham operation was performed; ischemia group and propofol group： middle cerebral artery was occluded for 2 h. Mitochondria from the cortical focal ischemia region were isolated in all groups, and the mitrochondria extraction was incubated with propofol for 2 min at 37 ℃ in propofol group. Flow cytometry was used to detect mitochondrial membrane potential and reactive oxygen species. Results Compared with ischemia group, mitochondria isolated from propofol group showed higher membrane potential and lower production of reactive oxygen species （ P 〈 0.05 ） ; compared with sham group, mitochondria isolated from propofol group and ischemic group showed lower membrane potential and higher production of reactive oxygen species （P 〈 0. 05 ）. Conclusion Propofol plays a protective role in mitochondrial function after focal cerebral ischemia in rats. This maybe involved in the mechanisms of brain protection of propofol.