脑局部缺血大鼠大脑皮层神经元超微结构的变化

E. Bon', N. E. Maksimovich, S. Zimatkin, O. Ostrovskaya, Vitaliy Yur'evich Smirnov, M. A. Nosovich, K. A. Khrapovitskaya
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摘要

神经元细胞器的超微结构特征是缺血性脑损伤的重要指标,因此有必要对脑神经元超微结构的变化进行研究。本研究通过实验模型,在超微结构水平上观察脑局部缺血对神经元的影响。材料与方法。实验组为体重260±20 g的雄性大鼠12只,对照组为体重相同的假手术雄性大鼠6只。采用右颈总动脉结扎法建立脑局部缺血模型。术后1小时取材料。结果。研究表明,PCI大鼠顶叶皮质和海马神经元线粒体的大小和形状与对照组相比无显著差异(p>0.05),只是顶叶皮质神经元线粒体单位面积嵴数减少了18%,p<0.05)。高尔基复合体和溶酶体的大小和形状在两组之间也没有差异。而PCI大鼠顶叶皮质和海马神经元胞质中游离核糖体数量分别增加58%和54% (p<0.05)。对照组大鼠顶叶皮质固定核糖体与游离核糖体之比由3.4降至0.8 (p<0.05),海马区由2.33降至0.7 (p<0.05)。结论。总的来说,PCI大鼠的神经元超微结构与对照组相似,这可能与威利斯圈血流代偿有关。游离核糖体数量的增加是神经元中蛋白质生物合成紊乱的标志。顶叶皮层神经元线粒体嵴数量减少表明能量不足。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CHANGES IN THE CEREBRAL CORTEX NEURON ULTRASTRUCTURE IN RATS WITH PARTIAL CEREBRAL ISCHEMIA
The ultrastructural characteristics of neuronal organelles are significant indicators of brain damage under ischemic exposure, which necessitates the study of changes in the ultrastructure of brain neurons. The aim of the study was to examine the disorders of brain neurons under its partial ischemia at the ultrastructural level using an experimental model. Materials and Methods. The experimental group included 12 male rats weighing 260±20 g, the control group consisted of 6 falsely operated male rats of the same weight. Partial cerebral ischemia (PCI) was modeled by right common carotid artery ligation. The material was taken 1 hour after the operation. Results. The study showed that the size and shape of the mitochondria of neurons of the parietal cortex and the hippocampus in PCI rats did not differ from those of the control group (p>0.05), except for a smaller number of cristae per unit area in the mitochondria of parietal cortex neurons (by 18 %, p<0.05). The size and shape of the Golgi complex and lysosomes did not differ in the groups either. However, there was an increase in the number of free ribosomes in the cytoplasm of neurons in the parietal cortex and hippocampus of PCI rats, by 58 % and 54 %, respectively (p<0.05). The ratio of fixed and free ribosomes in control rats decreased from 3.4 to 0.8 in the parietal cortex (p<0.05) and from 2.33 to 0.7 in the hippocampus (p<0.05). Conclusions. In general, the neuron ultrastructure in PCI rats was similar to that in the control group, which might be due to blood flow compensation in the circle of Willis. An increase in the number of free ribosomes is a sign of deranged protein biosynthesis in neurons. A decrease in the number of mitochondrial cristae in neurons in the parietal cortex indicates energy deficiency.
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