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凋亡和坏死是癫痫持续状态后神经元损伤的两种形式。凋亡有内源性和外源性两种途径,其核心环节是线粒体膜通透性的改变和细胞色素C的释放,最终通过caspase-3的激活导致核内染色体DNA的阶段性降解。最新研究表明,神经元坏死的过程中也存在程序性细胞死亡机制的激活,其间涉及细胞色素C的释放和caspase-3的激活。兴奋毒性损伤的强度和线粒体的功能状态决定了癫痫持续状态后神经元的死亡形式。
Apoptosis and necrosis are two forms of neuronal damage after status epilepticus. Apoptosis has both endogenous and exogenous pathways, the core part of which is the change of mitochondrial membrane permeability and the release of cytochrome C, which leads to the phased degradation of nuclear DNA finally through the activation of caspase-3. Recent studies show that there is also a mechanism of apoptosis during neuronal necrosis, which involves the release of cytochrome C and the activation of caspase-3. The intensity of excitotoxic damage and the functional status of mitochondria determine the form of neuronal death after status epilepticus.