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用(56)铁粒子进行颅脑照射后的海马神经发生与神经炎症

Hippocampal neurogenesis and neuroinflammation after cranial irradiation with (56)Fe particles.

作者信息

Rola Radoslaw, Fishman Kelly, Baure Jennifer, Rosi Susanna, Lamborn Kathleen R, Obenaus Andre, Nelson Gregory A, Fike John R

机构信息

Department of Neurological Surgery, University of California San Francisco, San Francisco, CA 94110, USA.

出版信息

Radiat Res. 2008 Jun;169(6):626-32. doi: 10.1667/RR1263.1.

DOI:10.1667/RR1263.1
PMID:18494546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2583781/
Abstract

Exposure to heavy-ion radiation is considered a potential health risk in long-term space travel. In the central nervous system (CNS), loss of critical cellular components may lead to performance decrements that could ultimately compromise mission goals and long-term quality of life. Hippocampal-dependent cognitive impairments occur after exposure to ionizing radiation, and while the pathogenesis of this effect is not yet clear, it may involve the production of newly born neurons (neurogenesis) in the hippocampal dentate gyrus. We irradiated mice with 0.5-4 Gy of (56)Fe ions and 2 months later quantified neurogenesis and numbers of activated microglia as a measure of neuroinflammation in the dentate gyrus. Results showed that there were few changes after 0.5 Gy, but that there was a dose-related decrease in hippocampal neurogenesis and a dose-related increase in numbers of newly born activated microglia from 0.5-4.0 Gy. While those findings were similar to what was reported after X irradiation, there were also some differences, particularly in the response of newly born glia. Overall, this study showed that hippocampal neurogenesis was sensitive to relatively low doses of (56)Fe particles, and that those effects were associated with neuroinflammation. Whether these changes will result in functional impairments or if/how they can be managed are topics for further investigation.

摘要

在长期太空旅行中,暴露于重离子辐射被认为是一种潜在的健康风险。在中枢神经系统(CNS)中,关键细胞成分的丧失可能导致性能下降,最终可能危及任务目标和长期生活质量。暴露于电离辐射后会出现海马依赖性认知障碍,虽然这种效应的发病机制尚不清楚,但可能涉及海马齿状回中新生神经元(神经发生)的产生。我们用0.5-4 Gy的(56)Fe离子照射小鼠,2个月后量化神经发生以及活化小胶质细胞的数量,以此作为齿状回神经炎症的指标。结果显示,0.5 Gy照射后变化不大,但从0.5-4.0 Gy,海马神经发生呈剂量相关减少,新生活化小胶质细胞数量呈剂量相关增加。虽然这些发现与X射线照射后的报道相似,但也存在一些差异,特别是在新生胶质细胞的反应方面。总体而言,本研究表明海马神经发生对相对低剂量的(56)Fe粒子敏感,且这些效应与神经炎症有关。这些变化是否会导致功能障碍,或者能否以及如何进行控制,是有待进一步研究的课题。

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