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首页> 外文期刊>Brain research >IGF-1 protects oligodendrocyte progenitor cells and improves neurological functions following cerebral hypoxia-ischemia in the neonatal rat.
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IGF-1 protects oligodendrocyte progenitor cells and improves neurological functions following cerebral hypoxia-ischemia in the neonatal rat.

机译:IGF-1保护新生鼠脑缺氧缺血后的少突胶质祖细胞并改善神经功能。

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To investigate if insulin-like growth factor-1 (IGF-1) provides neuroprotection to oligodendrocyte progenitor cells (OPCs) following cerebral hypoxia-ischemia, a previously developed neonatal rat model of white matter damage was used in this study. Postnatal day 4 (P4) SD rat pups were subjected to bilateral common carotid artery ligation, followed by exposure to 8% oxygen for 10 min. IGF-1 (0.5 microg) or vehicle was injected into the left ventricle after artery ligation and before the hypoxic exposure. Cerebral hypoxia-ischemia caused death of O4+ late OPCs in the P5 rat brain and impaired myelination in the P9 and P21 rat brain. Caspase-3 activation was involved in the death of OPCs. Moreover, cerebral hypoxia-ischemia impaired neurobehavioral performance in juvenile rats. IGF-1 treatment attenuated damages to OPCs and improved neurological functions after cerebral hypoxia-ischemia. It reduced death of O4+ OPCs by 39% on P5 and enhanced myelination on P9 and P21. Bromodeoxyuridine uptake assay showed that cerebral hypoxia-ischemia inhibited proliferation of stem/progenitor cells in the subventricular zone and NG2+ early OPCs in the white matter area. IGF-1 treatment increased cell proliferation in the subventricular zone by 31% 1 day following hypoxic-ischemic insult. Proliferation of early and late OPCs in the IGF-1-treated group was 1.5- and 2.4-fold of that in the vehicle-treated group, respectively. In conclusion, IGF-1 provided potent neuroprotection to OPCs and improved neurological functions following cerebral hypoxia-ischemia in the neonatal rat. The neuroprotection of IGF-1 was associated with its antiapoptotic and mitogenic effects.
机译:为了研究胰岛素样生长因子-1(IGF-1)是否在脑缺氧缺血后为少突胶质祖细胞(OPC)提供神经保护,本研究使用了先前开发的新生大鼠白质损伤模型。出生后第4天(P4),对SD大鼠幼崽进行双侧颈总动脉结扎,然后在8%的氧气中暴露10分钟。在动脉结扎后和低氧暴露之前,将IGF-1(0.5微克)或媒介物注入左心室。脑缺氧缺血导致P5大鼠脑中O4 +晚期OPC死亡,并损害P9和P21大鼠脑中的髓鞘形成。 Caspase-3激活与OPC的死亡有关。此外,脑缺氧缺血会损害幼年大鼠的神经行为表现。 IGF-1治疗可减轻脑缺氧缺血后对OPC的损害并改善神经功能。它使P5上O4 + OPC的死亡减少了39%,并增强了P9和P21的髓鞘形成。溴脱氧尿嘧啶核苷摄取分析表明,脑缺氧缺血抑制了脑室下区干细胞/祖细胞的增殖,并抑制了白质区域中NG2 +早期OPC的增殖。缺氧缺血性损伤后1天,IGF-1处理可使脑室下区域的细胞增殖增加31%。在IGF-1治疗组中,早期和晚期OPCs的增殖分别是载体治疗组的1.5倍和2.4倍。总之,在新生大鼠脑缺氧缺血后,IGF-1为OPC提供了有效的神经保护,并改善了其神经功能。 IGF-1的神经保护作用与其抗凋亡和促有丝分裂作用有关。

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