依达拉奉对原代海马神经元缺氧复氧损伤的保护作用
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Neuroprotective effects of edaravone against anoxia-reoxygenation injury in cultured hipp-ocampal cells
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    摘要:

    目的:研究依达拉奉对原代培养海马神经元缺氧复氧损伤的保护机制。方法:建立离体海马神经元缺氧复氧的细胞损伤模型,实验分组为正常对照组、缺氧复氧组、依达拉奉干预组,其中依达拉奉干预浓度分为1、10、100和300 μmol/L。观察海马细胞四甲基偶氮唑盐(MTT) 代谢率、丙二醛(MDA) 含量及一氧化氮合酶(NOS) 活性的变化,流式细胞仪观察细胞凋亡。结果:与缺氧复氧组相比,依达拉奉100 μmol/L组和300 μmol/L组的MTT 代谢率显著增高(P < 0.01) ,MDA 含量降低(P < 0.05),NOS活性降低(P < 0. 05),细胞凋亡率降低(P < 0. 01)。结论: 依达拉奉能够有效地抑制脂质过氧化作用,降低MDA及NOS活性,减少细胞凋亡率,对缺氧损伤的神经元具有显著的神经保护作用。

    Abstract:

    Objective:To demonstrate the protective effects of edaravone against neuronal anoxia-reoxygenation injury and to investigate the underlying mechanisms. Methods:Acute lucose-oxygen deprivation and subsequent reoxygenation were used to establish anoxia-reoxygenation injury model in cultured hippocampal cells. Cells were treated with different concentrations of edaravone upon reoxygenation. Metabolic rate of MTT, the content of malondialdehyde(MDA) and the activity of NOS were measured by assay kits. The rate of apoptosis was detected by flow cytometry. Results:Edaravone raised the metabolic rate of MTT and reduced malondialdehyde level and activity of NOS of anoxia-reoxygenation injury model in a dose-dependent manner compared with untreated group. The peak of neuroprotective effects occurred at the dose of 100 and 300 -滋mol/L. Cell apoptotic rate was significantly decreased following edaravone treatment(P < 0.01). There was no significant difference between 100 and 300 -滋mol/L group. Conclusion:Edaravone has protective effect on hippocampal neurons against anoxia-reoxygenation injury by increasing the metabolic rate of MTT, inhibiting lipid peroxidation,reducing the activity of NOS and decreasing apoptosis.

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王 蔚,丁新生,肖 杭,吴 婷,张 红.依达拉奉对原代海马神经元缺氧复氧损伤的保护作用[J].南京医科大学学报(自然科学版),2007,(4):389-393

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  • 收稿日期:2006-09-24
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