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目的 揭示脑在氧化应激状态下一氧化氮 (NO)产生增多对神经细胞的毒性作用和热休克减少NO的产生对神经细胞的保护作用机制。方法 对培养大鼠脑皮质神经元分别进行缺氧、H2 O2 、热休克 +缺氧和热休克+H2 O2 处理 ;检测丙二醛 (MDA)、超氧化物歧化酶 (SOD)、NO和乳酸脱氢酶 (LDH) ,并分析它们的变化和相互关系。结果 缺氧组和H2 O2 处理组MDA和NO产生明显增加 ,SOD活性降低 ,反映神经细胞受损指标LDH也明显增加 (P 均 <0 .0 1) ,对神经细胞在进行缺氧和H2 O2 作用前先进行热休克处理能明显降低NO含量 ,分别与缺氧组和H2 O2 组比较 ,差异非常显著 (P <0 .0 1) ,神经细胞受损程度也减轻。结论 在氧化应激条件下神经细胞NO产生增加并引起毒性作用 ,热休克能减少氧化应激时神经细胞NO的产生。
Objective To reveal the neuroprotective effects of increased nitric oxide (NO) on neurons and the protective effects of heat shock and NO on neurons under oxidative stress. Methods Hypoxia, H 2 O 2, heat shock + hypoxia and heat shock + H 2 O 2 treatment were performed on cultured cortical neurons. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), NO and lactate Dehydrogenase (LDH), and analyze their changes and correlations. Results The hypoxia group and H2O2 treatment group showed a significant increase in MDA and NO production and a decrease in SOD activity, indicating that LDH was also significantly increased (P <0.01) Heat shock treatment before treatment could significantly reduce NO content, compared with hypoxia group and H2O2 group, the difference was significant (P <0.01), and the degree of nerve cell damage was also reduced. CONCLUSIONS: Under oxidative stress, NO production in neurons increases and causes toxic effects. Heat shock can reduce NO production in neurons during oxidative stress.