脑缺氧损伤后细胞色素C、Bcl-2表达的实验研究

发布时间：2018-04-29 20:42

本文选题：脑缺氧 + 神经元缺失　；参考：《四川大学》2004年硕士论文

【摘要】：研究背景缺氧脑损伤(Hypoxic Brain Injury,HBI)是临床常见的病理现象,也是法医实践中各种原因所致窒息情况下最常发生的病变以及主要的死亡原因之一。中枢神经系统对缺氧敏感,脑组织耗氧量大、代谢率高,组织氧和ATP储备少;脑以有氧代谢为主,几乎没有无氧代谢能力,对缺氧耐受差,缺氧对其结构和功能影响最早且严重。脑缺氧时相继发生神经元能量供求失衡,膜内外离子梯度消失,无氧去极化和细胞死亡。缺氧所致的神经元损害机制一般认为有坏死和凋亡两种细胞死亡形式。坏死对缺氧损伤反应迅速,在损伤后很快出现;凋亡是由基因控制的细胞主动死亡过程,需要新的蛋白质合成,以DNA的早期降解为特征,表现为迟发性的神经元死亡。缺氧后线粒体损伤,细胞发生能量缺失和代谢功能障碍;并介导凋亡调节信号传递,是缺氧后神经元损害的一个中心环节。线粒体膜通透性改变,释放细胞色素C(cytochrome c,Cyt C)活化特定的Caspase蛋白酶,导致细胞凋亡或使呼吸链电子传递中断促使细胞发生坏死。Bcl-2蛋白定位于线粒体膜上,对正常细胞的自身稳定性起重要作用,调控细胞色素C释放,抑制神经元凋亡。 Cyt C、Bcl-2在外伤性、缺血—缺氧性、中毒性脑损伤后均会出现神经元中表达变化,在不同模型中,由于存在许多非缺氧影响因素,表达变化的规律也不尽相同。缺氧后,脑的不同部位神经元CytC、Bcl-2表达随损伤后不同时间亦呈现一定的变化规律。目前单纯窒息缺氧所致神
[Abstract]:Research background Hypoxic Brain injury (HBI) is a common pathological phenomenon in clinical practice. It is also one of the most common pathological changes and one of the main causes of death in cases of asphyxia caused by various reasons in forensic practice. The central nervous system is sensitive to hypoxia, the brain has high oxygen consumption, high metabolic rate and little oxygen and ATP reserves. Hypoxia had the earliest and severe effect on its structure and function. During cerebral anoxia, neuronal energy supply and demand imbalance occurred, ion gradient disappeared, anoxic depolarization and cell death occurred. Anoxia-induced neuronal damage mechanisms are generally considered to be necrosis and apoptosis of two forms of cell death. Apoptosis is a process of active cell death controlled by gene, which needs new protein synthesis and characterized by early degradation of DNA, which is characterized by delayed neuronal death. Mitochondria damage, cell energy loss and metabolic dysfunction after hypoxia, and mediated apoptosis regulation signal transmission, is a central link of neuronal damage after hypoxia. Mitochondrial membrane permeability was changed, cytochrome C(cytochrome ct C) was released to activate specific Caspase protease, which led to cell apoptosis or disruption of electron transfer in respiratory chain, resulting in necrosis of the cell. Bcl-2 protein was located on the mitochondrial membrane. It plays an important role in the self-stability of normal cells, regulates the release of cytochrome C and inhibits neuronal apoptosis. After traumatic, ischemia-hypoxia and toxic brain injury, the expression of Cyt Bcl-2 in neurons would change. In different models, the expression of Bcl-2 was different due to the existence of many non-hypoxic factors. After hypoxia, the expression of CytCon Bcl-2 in different parts of brain also showed a certain change with different time after injury. At present, asphyxia is the cause of anoxia.
【学位授予单位】：四川大学
【学位级别】：硕士
【学位授予年份】：2004
【分类号】：D919.1

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