目的 探讨线粒体钙单向转运体在大鼠短暂性脑缺血再灌注损伤模型中对线粒体分裂的影响作用。 方法 将80只健康雄性Wistar大鼠随机分成4组（每组20只）：A组，假手术组；B组，脑缺血/再灌注+钌红处理组；C组，脑缺血/再灌注+精胺处理组；D组，脑缺血/再灌注组。采用线栓法建立大鼠大脑中动脉栓塞模型，缺血2小时再灌注24小时后对大鼠行神经行为学评分，取缺血侧脑组织测定其线粒体内钙含量、钙调神经磷酸酶（calcineurin, CN）活性、线粒体分裂相关蛋白Drp1的表达量，并观察线粒体形态。 结果 与D组比较，B组钌红预处理可以改善大鼠脑缺血/再灌注损伤引起的神经功能学障碍，降低脑缺血侧大鼠线粒体自由钙含量，降低钙调神经磷酸酶活性及Drp1的表达，并改善线粒体损伤；与D组比较，C组精胺预处理得到与钌红预处理相反地结果。 结论 线粒体钙单向转运体的开放状态可能影响大鼠脑缺血/再灌注损伤线粒体分裂，抑制线粒体钙单向转运体开放可以抑制线粒体分裂，从而减轻大鼠脑缺血/再灌注损伤，保护脑组织。
Objective To investigate whether mitochondrial calcium uniporter has effects on mitochondrial fission on the model of cerebral ischemia/reperfusion injury in rats. Methods The model was performed by thread occlusion of middle cerebral artery for 2 hours, and followed by reperfusion for 24hours. 6o rats were randomly divided into 4 groups: A: sham-operated; B: Ruthenium red +ischemia/reperfusion; C:spermine +ischemia/reperfusion; D: ischemia/reperfusion. After 24hours reperfusion, neuropsychological score, the mitochondrial free calcium content, the CN enzyme activities, Drp1 expression and mitochondrial ultrastructure were observed above all the groups. Results Compared with group D, Ruthenium red preconditioning in group B had better neuropsychological score, decreased the mitochondrial free calcium content, CN enzyme activities and Drp1 expression, and improved the mitochondrial ultrastructure. While group C got the opposite results. Conclusions The activity of mitochondrial calcium uniporter has effects on mitochondrial fission this relationship between MCU and mitochondrial fission may possibly provide protection against ischemia/reperfusion injury.
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