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目的:探讨延迟性脑缺血后处理对大鼠海马CA1区神经元及超微病理改变的影响。方法:制作改良四动脉结扎全脑缺血模型,SPF级成年雄性SD大鼠随机分为:假手术组、缺血再灌注(I/R)组、延迟性脑缺血后处理(PostC)组。通过焦油紫染色方法观察神经元生存密度,透射电镜技术观察大鼠海马CA1区超微病理改变。结果:焦油紫染色显示I/R组海马CA1区神经元生存密度较低、电镜下病变最严重,可见神经元、微血管、星形胶质细胞、轴突的超微病理改变,并出现凋亡神经元;PostC组海马CA1区神经元生存密度明显高于I/R组(P<0.05),电镜下神经元及星形胶质细胞、微血管、轴突的超微病理改变显著减轻,未见明显凋亡神经元。假手术组海马CA1区神经元生存密度较高,细胞超微结构正常。结论:延迟性脑缺血后处理促进大鼠海马CA1区神经元的生存,抑制全脑缺血后大鼠海马CA1区神经元的凋亡样改变,大鼠CA1区超微病理变化明显得到改善。
Objective: To investigate the effects of delayed cerebral ischemic postconditioning on the neuronal and ultrastructural changes of hippocampal CA1 area in rats. Methods: The rats with SPF were randomly divided into four groups: sham operation group, I / R group, post-ischemic postconditioning group (PostC) . The viability of neurons was observed by the method of tar violet staining. The ultrastructural changes of hippocampal CA1 region were observed by transmission electron microscopy. Results: Tar staining showed that the density of neurons in hippocampal CA1 subfield of I / R group was lower than that of the control group, and the lesions were the most serious under electron microscopy. The ultrastructural changes of neurons, microvessels, astrocytes and axons were observed and apoptotic (P <0.05). The ultrastructural changes of neurons, astrocytes, microvessels and axons in PostC group were significantly lower than those in I / R group (P <0.05) Clearly apoptotic neurons. The hippocampal CA1 neurons in sham operation group had higher survival density and normal ultrastructure. CONCLUSION: Delayed ischemic postconditioning can promote the survival of neurons in CA1 area of hippocampus and inhibit the apoptosis of hippocampal CA1 neurons in rats after global cerebral ischemia. The ultrastructural changes of CA1 area in rats are obviously improved .