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大鼠局灶性脑缺血后粒细胞集落刺激因子对神经发生和血管生成的增强作用

Potentiation of neurogenesis and angiogenesis by G-CSF after focal cerebral ischemia in rats.

作者信息

Sehara Yoshihide, Hayashi Takeshi, Deguchi Kentaro, Zhang Hanzhe, Tsuchiya Atsushi, Yamashita Toru, Lukic Violeta, Nagai Makiko, Kamiya Tatsushi, Abe Koji

机构信息

Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan.

出版信息

Brain Res. 2007 Jun 2;1151:142-9. doi: 10.1016/j.brainres.2007.01.149. Epub 2007 Mar 20.

Abstract

Recently, granulocyte colony-stimulating factor (G-CSF) is expected to demonstrate beneficial effects on cerebral ischemia. Here, we showed the potential benefit of G-CSF administration after transient middle cerebral artery occlusion (tMCAO). Adult male Wistar rats received vehicle or G-CSF (50 microg/kg) subcutaneously after reperfusion, and were treated with 5-bromodeoxyuridine (BrdU, 50 mg/kg) once daily by the intraperitoneal route for 3 days after tMCAO. Nissl-stained sections at 7 days after tMCAO showed significant reduction of the infarction area (31%, P<0.01). At 7 days after tMCAO, BrdU plus NeuN double-positive cells increased by 43.3% in the G-CSF-treated group (P<0.05), and BrdU-positive endothelial cells were increased 2.29 times in the G-CSF-treated group, to a level as high as that in the vehicle-treated group (P<0.01), in the periischemic area. Our results indicate that G-CSF caused potentiation of neuroprotection and neurogenesis and is expected to have practical therapeutic potential in treating individuals after ischemic brain injury.

摘要

最近,粒细胞集落刺激因子(G-CSF)有望对脑缺血显示出有益作用。在此,我们展示了短暂性大脑中动脉闭塞(tMCAO)后给予G-CSF的潜在益处。成年雄性Wistar大鼠在再灌注后皮下注射载体或G-CSF(50微克/千克),并在tMCAO后连续3天每天经腹腔途径给予5-溴脱氧尿苷(BrdU,50毫克/千克)。tMCAO后7天的尼氏染色切片显示梗死面积显著减小(31%,P<0.01)。tMCAO后7天,在缺血周边区域,G-CSF治疗组中BrdU加NeuN双阳性细胞增加了43.3%(P<0.05),G-CSF治疗组中BrdU阳性内皮细胞增加了2.29倍,达到与载体治疗组相同的高水平(P<0.01)。我们的结果表明,G-CSF可增强神经保护和神经发生作用,有望在治疗缺血性脑损伤患者方面具有实际治疗潜力。

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