Apoptosis and necrosis in developing cerebellum and brainstem induced after focal cerebral hypoxic-ischemic injury
Apoptosis and necrosis in developing cerebellum and brainstem induced after focal cerebral hypoxic-ischemic injury
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DOI：
10.1016/j.devbrainres.2005.02.002
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发表时间：
2005-04-21
期刊：
影响因子：
--
通讯作者：
Parker, JC
中科院分区：
文献类型：
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作者：
Peng, JHF;Feng, YZ;Parker, JC
众所周知，孤立性血管功能不全引起的局灶性脑缺氧-缺血可引起同侧而不是对侧的脑细胞凋亡。在这样的模型中，小脑和脑干的缺氧缺血性损伤尚未建立。这项实验性啮齿动物研究通过脱氧核糖核酸断裂和末端脱氧核苷酸转移酶介导的脱氧尿苷5‘-三磷酸-地高辛缺口末端标记分析表明，新生大鼠局灶性脑缺氧缺血性损伤后，这些幕下区域的神经细胞也遭受轻微的凋亡和坏死。这些数据为进一步了解局灶性脑缺氧缺血性损伤导致小脑和脑干区神经损伤的机制提供了新的见解，并表明未来对缺氧缺血性脑病系统的治疗干预应涉及整个中枢神经系统。(C)2005 Elsevier B.V.保留所有权利。
Focal cerebral hypoxia-ischemia due to isolated vascular insufficiency is well known to cause ipsilateral, but not contralateral, cerebral apoptosis. Hypoxic-ischemic damage to the cerebellum and brainstem in such a model has riot been established. This experimental rodent Study demonstrates, through deoxyribonucleic acid fragmentation and terminal deoxynucleotidyl transferase-mediated deoxyuridine 5'-triphosphate-digoxigenin nick end labeling analysis, that neuronal cells in these infratentorial regions also suffer mild apeptosis and necrosis after focal cerebral hypoxic-ischemic injury in the newborn rat.These data provide additional insight into the mechanisms of neurological injury in the cerebellum and brainstem areas resulting from a focal cerebral hypoxic-ischemic insult and demonstrate that future therapeutic interventions for hypoxic-ischemic encephalopathy system should deal with the entire central nervous system. (c) 2005 Elsevier B.V. All rights reserved.