Granulocyte colony-stimulating factor treatment provides neuroprotection in surgically induced brain injured mice.
Granulocyte colony-stimulating factor treatment provides neuroprotection in surgically induced brain injured mice.
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DOI：
10.1007/978-3-7091-0693-8_44
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发表时间：
2011
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影响因子：
--
通讯作者：
Zhang, John H
中科院分区：
文献类型：
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作者：
Khatibi, Nikan H;Jadhav, Vikram;Saidi, Mehdi;Chen, Wanqiu;Martin, Robert;Stier, Gary;Tang, Jiping;Zhang, John H
手术诱导的脑损伤（SBI）是神经外科手术后常见的问题。目前旨在减少术后后遗症的治疗是有限的。粒细胞集落刺激因子（G-CSF）是一种参与炎症过程的造血生长因子，已在各种动物模型中显示出神经保护作用。因此，在这项研究中，我们研究了使用G-CSF作为治疗方式，以减少细胞死亡和脑水肿，同时改善小鼠SBI后的神经行为缺陷。将11周龄C57黑小鼠（n = 76）随机分为4组：假手术组（n = 19）、SBI组（n = 21）、SBI + G-CSF预处理组（n = 15）和SBI + G-CSF预/后处理组（n = 21）。给药组在术前24、12和1 h和/或术后6和12 h接受单剂量G-CSF腹腔内给药。术后评估在24小时进行，包括神经行为测试和细胞死亡和脑水肿的测量。结果表明，G-CSF预处理减少细胞死亡和脑水肿，而后处理减少神经行为缺陷。这项研究表明，大脑中的形态学变化受到预处理的影响;然而，为了激活和/或扩增恢复过程中涉及的靶点，可能需要更多的给药方案。
Surgically induced brain injury (SBI) is a common concern after a neurosurgical procedure. Current treatments aimed at reducing the postoperative sequela are limited. Granulocyte-colony stimulating factor (G-CSF), a hematopoietic growth factor involved in the inflammatory process, has been shown in various animal models to be neuroprotective. Consequently, in this study, we investigated the use of G-CSF as a treatment modality to reduce cell death and brain edema, while improving neurobehavioral deficits following an SBI in mice. Eleven-week-old C57 black mice (n = 76) were randomly placed into four groups: sham (n = 19), SBI (n = 21), SBI with G-CSF pre-treatment (n = 15) and SBI with G-CSF pre/post-treatment (n = 21). Treated groups received a single dose of G-CSF intraperitoneally at 24, 12 and 1 h pre-surgery and/or 6 and 12 h post-surgery. Postoperative assessment occurred at 24 h and included neurobehavioral testing and measurement for both cell death and brain edema. Results indicated that pre-treatment with G-CSF reduced both cell death and brain edema, while post-treatment reduced neurobehavioral deficits. This study implies that the morphological changes in the brain are effected by pre-treatment; however, in order to activate and/ or amplify targets involved in the recovery process, more dosing regimens may be needed.