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γ 射线辐照比 D-半乳糖/亚硝酸钠更能耗尽海马神经发生。

Gamma-irradiation is more efficient at depleting hippocampal neurogenesis than D-galactose/NaNO₂.

机构信息

Radiation Biotechnology Research Division, Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, 1266 Sinjeong-dong, Jeongeup-si, Jeonbuk 580-185, Republic of Korea.

出版信息

Neurosci Lett. 2011 Jul 1;498(1):47-51. doi: 10.1016/j.neulet.2011.04.059. Epub 2011 May 6.

DOI:10.1016/j.neulet.2011.04.059
PMID:21571038
Abstract

This study was performed to compare the fractionated irradiation with the chronic d-galactose/NaNO(2) administration as models for hippocampal neurogenesis suppression. Eight-week-old C57BL/6 mice were exposed to γ-rays at 0.5 Gy semiweekly for 10 weeks or injected with d-galactose/NaNO(2) mixture (1250 mg/kg of d-galactose and 90 mg/kg of NaNO(2), i.p) 5 times per week for 10 weeks. To evaluate the suppression of hippocampal neurogenesis, we examined the numbers of the doublecortin (DCX; an immature progenitor cell marker) and Ki-67 (a proliferating cell marker) expressing cells by immunohistochemistry in the dentate gyrus (DG) region of the hippocampus in each treated group in comparison with those of age-matched control and 24-month-old mice as the positive control. The number of DCX-positive cells in the DG area was significantly decreased in both the irradiation and d-galactose/NaNO(2) groups (96% and 50%) compared with the control. Also Ki-67-positive cells were significantly decreased in both groups (91% and 41%) compared with the control. Especially, both DCX and Ki-67-positive cells of irradiation group was much more significantly changed than those of the d-galactose/NaNO(2) group. The positive control group of 24-momth-old mice showed dramatic decreases as similar irradiation group in DCX (99%) and Ki-67 (98%) - positive cells compared to the control group. In conclusion, this fractionated irradiation was a more effective method for depleting hippocampal neurogenesis than chronic d-galactose/NaNO(2) exposure.

摘要

本研究旨在比较分次照射与慢性 D-半乳糖/NaNO2 给药作为海马神经发生抑制模型。将 8 周龄 C57BL/6 小鼠暴露于 0.5 Gy γ射线,每周半次,共 10 周;或每周腹腔注射 D-半乳糖/NaNO2 混合物(1250 mg/kg D-半乳糖和 90 mg/kg NaNO2)5 次,共 10 周。为了评估海马神经发生的抑制作用,我们通过免疫组织化学方法检测了每个处理组的海马齿状回(DG)区中双皮质素(DCX;一种未成熟祖细胞标志物)和 Ki-67(增殖细胞标志物)表达细胞的数量,并与年龄匹配的对照组和 24 月龄的小鼠(阳性对照)进行了比较。与对照组相比,照射组和 D-半乳糖/NaNO2 组 DG 区的 DCX 阳性细胞数量均显著减少(分别为 96%和 50%)。此外,两组的 Ki-67 阳性细胞数量均显著减少(分别为 91%和 41%)。特别是,照射组的 DCX 和 Ki-67 阳性细胞数量变化均明显大于 D-半乳糖/NaNO2 组。24 月龄的阳性对照组与对照组相比,DCX(99%)和 Ki-67(98%)阳性细胞明显减少,与照射组相似。综上所述,与慢性 D-半乳糖/NaNO2 暴露相比,分次照射是一种更有效的耗尽海马神经发生的方法。

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