脑缺血大鼠脑组织中发动蛋白相关蛋白1和线粒体融合基因2的动态表达

The dynamic change of dynamin-related protein 1 and mito fusion-2 in ischemia rat cells

目的:探讨脑缺血后线粒体分裂蛋白及融合蛋白表达水平的变化。方法:72只大鼠随机分为脑缺血后组及假手术组,每组18只。采用线栓法经左侧颈外-颈内动脉插线栓塞大脑中动脉建立脑缺血模型。应用苏木精-伊红染色(HE染色)观察大脑皮质神经元形态结构,蛋白免疫印迹法检测脑组织Drp1及Mfn2的蛋白含量,rt-PCR检测Drp1及Mfn2的mRNA基因的表达情况。结果:脑缺血组的Drp1蛋白及其mRNA基因的表达明显高于假手术组,且随着时间的延长表达逐渐增加(P<0.01);脑缺血组Mfn2蛋白及其表达mRNA基因的表达低于假手术组,且随着时间的延长表达逐渐减少(P<0.01)。结论:线粒体分裂和融合蛋白表达异常可能是脑缺血后脑组织损伤的重要机制。

Objective： Investigate the mitochondrial division protein Drpl after cerebral ischemia and the change of Mfn2 fusion protein expression. Methods： 72 rats were randomly divided into ischemia group and sham group, 18 rats in each group. Line switch method is used to plug wire via external carotid - left internal carotid artery embolism MCAO models. Application of hematoxylin eosin staining （ HE staining） observe the cerebral cortex neurons morphology, protein immunoblot method （western-blot） testing Drpl and the protein content of Mfn2, rt-PCR detects the content of gene mRNA of Drpl and Mfn2. Results： Cerebral iscbemia group of Drpl protein and mRNA gene expression were significantly higher than the control group, and gradually increase with the extension of time expression （P 〈 0. 01） ; Cerebral ischemia group Mfn2 protein and mRNA expression gene expression were lower than control group, and gradually reduce over time expression （P 〈 0.01 ）. Conclusion： Mitochondrial fission and fusion energy metabolism disorder caused by abnormal apoptosis, may be cerebral isehemia afterbrain tissue damage and reshape one of the important mechanisms.