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首页> 外文期刊>Neurochemical Research >Nerve Growth Factor Protects the Cortical Neurons from Chemical Hypoxia-induced Injury
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Nerve Growth Factor Protects the Cortical Neurons from Chemical Hypoxia-induced Injury

机译:神经生长因子保护皮质神经元免受化学性缺氧引起的损伤

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摘要

Previous studies showed that nerve growth factor (NGF) exerts protective effects on cultured neurons against various kinds of damage. However, a recent publication reported that exposure of NGF-treated PC12 cells to physical hypoxia resulted in a higher cell death rate when compared to the untreated controls. In the present study, we therefore investigated the effects of NGF on the hypoxic cortical neurons induced by potassium cyanide (KCN). We demonstrated that NGF at a higher concentration can significantly increase neuronal viability, decrease the release of lactate dehydrogenase and improve cellular morphology in the hypoxic cortical neurons. However, we also found that pretreatment of NGF was not able to completely revise the decreased cell viability and the increased leakage of lactate dehydrogenase (LDH) induced by KCN, although the indexes in the neurons treated with NGF and KCN were significantly higher than those in the neurons treated with KCN only. Analysis of the data showed that the incomplete revision of NGF should be not due to the dosage of NGF we used. It might be induced by the inability of NGF to inhibit all injury pathways induced by potassium cyanide.
机译:先前的研究表明,神经生长因子(NGF)对培养的神经元具有抵抗各种损害的保护作用。然而,最近的出版物报道,与未处理的对照组相比,NGF处理的PC12细胞暴露于身体缺氧会导致更高的细胞死亡率。因此,在本研究中,我们因此研究了NGF对氰化钾(KCN)诱导的缺氧皮质神经元的影响。我们证明了较高浓度的NGF可以显着增加神经元的活力,减少乳酸脱氢酶的释放并改善缺氧皮质神经元的细胞形态。然而,我们还发现,尽管用NGF和KCN处理的神经元的指数明显高于用NGF处理的神经元的指数,但NGF的预处理不能完全弥补KCN诱导的细胞活力下降和乳酸脱氢酶(LDH)泄漏增加。仅用KCN治疗的神经元。数据分析表明,NGF的不完全修订不应归因于我们使用的NGF剂量。 NGF不能抑制氰化钾诱导的所有损伤途径可能是导致这种情况的原因。

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