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目的动态观察缺血预处理后大鼠大脑皮层和海马CA1区神经元凋亡与Fas蛋白表达变化情况,初步探讨缺血预处理后Fas蛋白表达与迟发性神经元凋亡的关系。方法四血管阻断法复制全脑缺血模型,动物随机分为非缺血对照组、预处理对照组、缺血预处理组和缺血组。采用尼氏和TUNEL染色法观察皮层及海马CA1区神经元存活数和凋亡细胞数,免疫组化方法检测Fas蛋白在缺血预处理后表达变化情况。结果缺血组缺血6h在皮质及海马CA1区Fas阳性表达细胞计数升高,12h达高峰;缺血预处理组缺血12h阳性细胞计数升高,24h达高峰。缺血组缺血6h出现凋亡细胞,48h凋亡细胞数达到高峰;缺血预处理组凋亡细胞数较缺血组明显减少。缺血组缺血7d神经元数明显减少,12周时神经元大量减少;缺血预处理组缺血7d时神经元数无明显变化,但12周时神经元同样大量减少。结论全脑缺血可能通过诱导Fas蛋白的表达增多,启动细胞凋亡,导致缺血后神经元凋亡的发生;缺血预处理虽可延缓缺血后神经元的凋亡,但无法提供真正的长时期的神经元保护作用,其有限的保护作用可能是通过延缓Fas蛋白的表达而减缓了神经元凋亡的进程。
Objective To observe the changes of neuronal apoptosis and Fas protein expression in rat cerebral cortex and hippocampus CA1 after ischemic preconditioning and to explore the relationship between the expression of Fas protein and the apoptosis of delayed neurons after ischemic preconditioning. Method 4: The model of global cerebral ischemia was reproduced by vascular occlusion. Animals were randomly divided into non-ischemic control group, pretreatment control group, ischemic preconditioning group and ischemia group. Nissl and TUNEL staining was used to observe the number of neurons and the number of apoptotic cells in cortex and hippocampal CA1 area. The expression of Fas protein in ischemic preconditioning was detected by immunohistochemistry. Results The number of Fas-positive cells in cortex and hippocampal CA1 area of ischemic group increased 6 hours after ischemia and peaked at 12 hours. The number of positive cells increased 12 hours after ischemia in ischemic preconditioning group and peaked at 24 hours. Apoptotic cells appeared in ischemic group 6h after ischemia, and the number of apoptotic cells peaked at 48h. The number of apoptotic cells in ischemic preconditioning group was significantly lower than that in ischemia group. The number of neurons in ischemic group decreased significantly at 7th day and decreased significantly at 12th week. Neurons in ischemic preconditioning group had no obvious change at 7th day, but also decreased significantly at 12th week. Conclusion Ischemia preconditioning may induce neuronal apoptosis by inducing the increase of Fas protein expression, leading to the apoptosis of neurons after ischemia. Although ischemic preconditioning can delay the apoptosis of neurons after ischemia, it can not provide true Of the long-term neuronal protection, its limited protective effect may be slowed down the process of neuronal apoptosis by delaying the expression of Fas protein.