急性脑损伤后神经细胞凋亡机制的研究进展

李明, 殷玉华, 江基尧

李明, 殷玉华, 江基尧. 急性脑损伤后神经细胞凋亡机制的研究进展[J]. 实用临床医药杂志, 2013, (7): 156-159. DOI: 10.7619/jcmp.201307059
引用本文: 李明, 殷玉华, 江基尧. 急性脑损伤后神经细胞凋亡机制的研究进展[J]. 实用临床医药杂志, 2013, (7): 156-159. DOI: 10.7619/jcmp.201307059

急性脑损伤后神经细胞凋亡机制的研究进展

基金项目: 中国高校医学期刊临床专项资金
详细信息
  • 中图分类号: R742

  • 摘要: 1972年,Kerr等根据细胞的超微结构特征把细胞死亡分为坏死和凋亡2种方式.1973年,Schweichel等在此基础上又将溶酶体的作用纳入其中,把细胞死亡分为3种类型.然而早期对神经细胞凋亡的研究[1-2]大多集中在神经元正常发育过程中,或者是神经细胞的慢性变性的病变中,而对颅脑急性损伤中细胞凋亡的研究较少.Tominaga等(1993年)和MacManus等(1994年)相继证实缺血性脑损伤后存在神经细胞凋亡,而1995年Rink等[3]则首先证明了颅脑创伤后存在神经细胞的凋亡.神经细胞凋亡(apoptosis)或细胞的程序化死亡(PCD),是指在某些生理或病理性因素诱导下,激活膜信号系统,启动有关调控细胞凋亡的程序基因,最终导致细胞按一定程序控制自我破坏和死亡,其过程具有一定的可逆性.大量实验[4-6]表明,神经细胞的凋亡与脑损伤后细胞存活数量有直接的关系,并对脑损伤的预后产生重要影响,因此更进一步认识神经细胞的凋亡极具重要性.
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出版历程
  • 发布日期:  2013-06-12

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