An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model
An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model
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幼鼠急性辐射认知功能障碍的实验研究
DOI：
10.3174/ajnr.a1801
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发表时间：
2010-02-01
影响因子：
3.5
通讯作者：
Suo, W. Z.
中科院分区：
文献类型：
--
作者：
Liu, Y.;Xiao, S.;Suo, W. Z.
背景和目的：放射引起的认知功能障碍是脑肿瘤放射治疗后常见且严重的临床并发症，但对其机制的了解却很少。本研究的目的是建立急性辐射引起的认知功能障碍和相关血脑屏障损伤以及组织病理学变化的幼年大鼠模型。 材料与方法：幼年雄性大鼠随机分为4组，接受300 cGy/min的辐照治疗，剂量分别为0（假）、10、20和40 Gy。每个治疗组被进一步随机分为 4 个亚组，以在第 0、7、20 和 60 天时进行认知测试并评估其 BBB 完整性和潜在的组织病理学变化。 结果：我们发现 10 Gy 的照射未能产生任何显着效果。 20 Gy 的照射导致第 7 天和第 20 天认知功能出现短暂损害，并在第 60 天恢复正常。 40 Gy 的辐射造成最严重的认知障碍，在 7 天时达到峰值，并持续至少 60 天。 20-Gy和40-Gy照射大鼠的认知受损或多或少伴随着脑含水量增加和血脑屏障功能恶化，尽管40-Gy照射大鼠仅在20天时观察到轻微的组织病理学改变。 结论：20至40 Gy的单剂量暴露足以在年轻雄性大鼠的认知和病理水平上诱发急性脑损伤。此外，形态学结果可能不够敏感，无法揭示所有病理变化，而血脑屏障破坏可能是急性 RE 的早期且更敏感的指标。因此，本模型对于急性 RE 的基础和治疗研究很有用。
BACKGROUND AND PURPOSE: Radiation-induced cognitive dysfunction is a common and serious clinical complication after radiation therapy for a brain tumor, but the knowledge of its mechanism is poorly understood. The purpose of this study was to establish a young rat model for acute radiation-induced cognitive dysfunction and associated BBB damage, as well as histopathologic changes.MATERIALS AND METHODS: Young male rats were randomized into 4 groups to receive irradiation treatments at 300 cGy/min with doses of 0 (sham), 10, 20, and 40 Gy, respectively. Each treatment group was further randomized into 4 subgroups for following up cognitive tests and assessment of their BBB integrity and potential histopathologic changes at 0, 7, 20, and 60 days.RESULTS: We found that irradiation at 10 Gy failed to induce any significant effects. Irradiation at 20 Gy resulted in a transient impairment of the cognitive functions at 7 and 20 days and returned to normal at 60 days. Irradiation at 40 Gy caused the severest cognitive impairment, which peaked at 7 days, and lasted for at least 60 days. The impaired cognition in both the 20-Gy and 40-Gy-irradiated rats was more or less accompanied with increased brain water content and deteriorated BBB function, though mild histopathologic alternations were only noticed in the 40-Gy-irradiated rats at 20 days.CONCLUSION: A single-dose exposure at 20 to 40 Gy is sufficient to induce acute brain injury at both cognitive and pathologic levels in young male rats. In addition, morphologic outcomes may not be sensitive enough to reveal all of the pathologic changes, whereas BBB disruption may be an earlier and more sensitive index for acute RE. Therefore, the present model is useful for basic and therapeutic studies of acute RE.