Zhu Li, Du Fang, Yang Lei, Wu Xiao Mei, Qian Zhong Ming
Institute for Nautical Medicine and Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, Jiangsu, PR China,
Neurochem Res. 2008 May;33(5):784-9. doi: 10.1007/s11064-007-9495-6. Epub 2007 Oct 17.
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.
先前的研究表明,神经生长因子(NGF)对培养的神经元免受各种损伤具有保护作用。然而,最近一篇发表的文章报道,与未处理的对照组相比,将经NGF处理的PC12细胞暴露于物理性缺氧环境中会导致更高的细胞死亡率。因此,在本研究中,我们调查了NGF对氰化钾(KCN)诱导的缺氧皮质神经元的影响。我们证明,较高浓度的NGF可显著提高缺氧皮质神经元的活力,降低乳酸脱氢酶的释放,并改善细胞形态。然而,我们还发现,NGF预处理不能完全纠正由KCN诱导的细胞活力下降和乳酸脱氢酶(LDH)泄漏增加,尽管用NGF和KCN处理的神经元中的指标明显高于仅用KCN处理的神经元。数据分析表明,NGF的不完全纠正不应归因于我们使用的NGF剂量。这可能是由于NGF无法抑制氰化钾诱导的所有损伤途径所致。