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粒细胞集落刺激因子可改善成年小鼠辐射诱导的海马神经发生抑制。

Granulocyte-colony stimulating factor ameliorates irradiation-induced suppression of hippocampal neurogenesis in adult mice.

机构信息

Department of Veterinary Anatomy, College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, South Korea.

出版信息

Neurosci Lett. 2010 Dec 3;486(1):43-6. doi: 10.1016/j.neulet.2010.09.041. Epub 2010 Sep 17.

Abstract

Granulocyte-colony stimulating factor (G-csf) is a member of the hematopoietic growth factor family and demonstrates neuroprotective functions in neurodegenerative diseases. This study evaluated the radioprotective effects of G-csf in the suppression of hippocampal neurogenesis in adult mice undergoing irradiation. The radioprotective effects were assessed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay and immunohistochemical markers of neurogenesis, including the proliferating cell marker Ki-67 and the immature progenitor neuron marker doublecortin (DCX). Acute exposure to cranial irradiation (5Gy γ-rays) induced neural apoptosis and inhibited neurogenesis in the dentate gyrus (DG) of the adult mouse hippocampus. Pretreatment with G-csf (100μg/kg every 12h subcutaneously on three consecutive days) attenuated neural apoptosis and decreased the number of Ki-67- and DCX-positive cells in the DG of the irradiated mouse hippocampus. Therefore, G-csf inhibited the detrimental effects of irradiation on hippocampal neurogenesis, suggesting that G-csf administration has potential therapeutic utility in brain irradiation.

摘要

粒细胞集落刺激因子(G-CSF)是造血生长因子家族的一员,在神经退行性疾病中具有神经保护功能。本研究评估了 G-CSF 在抑制照射后成年小鼠海马神经发生中的放射保护作用。使用末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记测定法和神经发生的免疫组织化学标志物,包括增殖细胞标志物 Ki-67 和未成熟祖细胞神经元标志物双皮质素(DCX),评估放射保护作用。急性颅脑照射(5Gyγ射线)诱导成年小鼠海马齿状回(DG)的神经凋亡并抑制神经发生。G-CSF(连续 3 天每天皮下注射 100μg/kg,每 12h 一次)预处理可减轻神经凋亡,并减少照射后小鼠海马 DG 中 Ki-67 和 DCX 阳性细胞的数量。因此,G-CSF 抑制了照射对海马神经发生的有害影响,表明 G-CSF 给药在脑照射中具有潜在的治疗效用。

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