期刊文献+

脑梗死后细胞骨架和暗神经元的变化 被引量:13

A study of the dark neurons and cytoskeleton changes of seven infarcted brains
原文传递
导出
摘要 目的 通过研究细胞骨架的变化 ,探讨脑梗死后神经元及暗神经元损伤的程度。方法7例尸检梗死脑做全脑大切片染色后 ,将梗死及其周围分成 4个区 (0~ 3区 ) ,各区取小块组织 ,用组织化学和免疫组织化学的方法观察梗死脑的暗神经元、微管相关蛋白 (MAP2 )、相对分子质量为2 0 0 0 0 0的神经丝 (NF2 0 0 )和星形细胞中的胶质纤维酸性蛋白 (GFAP) ,认识暗神经元、细胞骨架与梗死病理过程之间的关系 ,并进行病灶内外及其与对侧脑组织细胞骨架变化的对比。结果  1区暗神经元约为 90 % ;2区为 40 %~ 5 0 % ,有些暗细胞伴有细胞骨架的严重变化 ,有的细胞骨架显色正常 ,少数FAS染色阳性 ,末端脱氧核苷酸转移酶介导DUPT的缺口末端描记法 (TUNEL法 )全部阴性。 0区MAP2和NF2 0 0消失 ,1区MAP2和NF2 0 0显著异常 ,提示为不可逆的缺血损伤 ;2区MAP2和NF2 0 0有轻度改变 ,提示损伤可能为可逆性 ;3区细胞骨架正常而星形细胞增生明显 ,表明为损伤反应。结论暗神经元是脑缺血后的主要神经元变化形式之一 ,少数处于凋亡早期 ,多数则尚未凋亡。缺血细胞骨架损伤轻者 ,神经细胞功能有可能恢复 ;损伤重者 。 Objective By observing the cytoskeleton changes of seven infarcted human brains on autopsies,it was designed to find wheather the ischemic neurons and the dark neurons were reversible. Methods We selected 7 autopsy brains of the cerebral infarction patients. We devided each infarcted brain into four areas on the large section for each whole infarcted brain. We then examined the microtube associated protain 2 (MAP2) and 200 kd neurolfilaments(NF200) by immunohistochemistry. Results The area 0 with disappearance of MAP2 and NF200 represented a necrotic area. The area 1 with of NF200 and MAP2 dramatic abnormal changed of NF200, disclosed an irreversible area. The area 0 together with area 1 formed the central necrosis area. The area 2 with gently changes of MAP2 and NF200 and GFAP positive astrocyte hyperplasia, represented the possible penumbra in the reversible area. The area 3 with normal cytoskeleton and astrocyte hyperplasia disclosed the reflecting area and possible chronic penumbra. The dark neurons consisted of 80%~90% in the area 1,there were 40 %~50% in area 2, a few of them were positive with fuschin,alizerin and safracin staining ( FAS positive) and all of them were TUNEL negative. Conclusions The dark neurons might be considered one of the major neuronal changes following ischemia.A few of the irreversible dark neurons had FAS positive staining in the early apoptosis stage. Most of the dark neurons had no apoptosis. One part of the ischemic neuron with dramatic cytoskeleton changes was irreversible, whereas the other part of them with gentle changes of cytoskeleton was reversible.
出处 《中华神经科杂志》 CAS CSCD 2000年第1期39-41,共3页 Chinese Journal of Neurology
基金 九五国家重点科技项目攻关计划!(969060221)
关键词 脑梗塞 神经元 细胞支架 病理 治疗 Cerebral infarction Neurons Cytoskeleton
  • 相关文献

参考文献1

  • 1Posmantur R M,J Neuropathol Exp Neurol,1996年,55卷,68页

同被引文献88

  • 1孙莉,张昱,邹昕颖,金涛,吴江,姚丽芬.慢性前脑缺血致痴呆大鼠皮质及皮质下白质区病理学变化的对比研究[J].中风与神经疾病杂志,2004,21(5):403-405. 被引量:19
  • 2丁成赟,王致瑜,王凤梅.神经丝蛋白-200在大鼠脑内的分布[J].中国实验动物学杂志,1994,4(1):9-12. 被引量:5
  • 3张微微.心脑血管疾病危险因素与认知功能障碍[J].中华内科杂志,2005,44(10):797-798. 被引量:13
  • 4凌治萍.细胞生物学[M].北京:人民卫生出版社,2001.243-257.
  • 5Braun JS,Jander S,Schroeter M,et al.Spatiotemporal relationship of apoptotic cell death to lymphomonocytic infiltration in photochemically induced focal ischemia of the rat cerebral cortex.Acta Neuropathol,1996,92:255-263.
  • 6Mochizuki R,Takeda A,Sato N,et al.Induction of midkine expression in reactive astrocytes following rat transient forebrain ischemia.Exp Neurol,1998,149:73-88.
  • 7Heye N,Cervos-Navarro J.Microthromboemboli in acute infarcts analysis of 40 autopsy cases.Stroke,1996,27:431-434.
  • 8Schmidt-Kastner R,Ingvar M.Loss of immunoreactivity for GFAP in astrocytes as a marker for profound tissue damage in substantia nigra and basal cortical areas after status epilepticus induced by pilocarpine in rat.Glia,1994,12:165-172.
  • 9Cotrina ML,Kang J,Lin JH,et al.Astrocytic gap junctions remain open during ischemic conditions.J Neurosci,1998,18:2520-2537.
  • 10Catania A,Lipton JM.Peptide modulation of fever and inflammation within the brain.Ann N Y Acad Sci,1998,856:62-68.

引证文献13

二级引证文献78

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部