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目的:观察皮层神经元缺糖氧复氧后氧化-抗氧化分子的变化,并探讨其对凋亡的影响。方法:建立体外培养皮层神经元缺糖氧复氧损伤模型,实验分为正常对照组,缺糖氧复氧不同时间组(3、6、12及24h组),检测各组细胞上清液乳酸脱氢酶(LDH)、一氧化氮(NO)含量及一氧化氮合酶(NOS)活性;观察神经元谷胱甘肽(GSH)含量及谷胱甘肽过氧化物酶(GPx)活性变化;Hochest33258核染色观察皮层神经元凋亡情况。结果:与正常对照组相比,缺糖氧复氧后神经元LDH释放量及NO含量明显增多、GPx活性持续下降(P<0.05);于缺糖氧复氧3h及6h时,NOS活性增高、GSH含量减少(P<0.05),而于24h时二者变化无显著差异(P>0.05);神经元于缺糖氧复氧3h时出现凋亡,且随复氧时间的延长,凋亡持续增多(P<0.05)。结论:随着缺糖氧复氧时间的持续,氧化及抗氧化平衡的破坏,可能是致体外培养皮层神经元凋亡的原因之一。
OBJECTIVE: To observe the changes of oxidation-anti-oxidation molecules in cortical neurons after hypoglycemia and reoxygenation, and to explore their effects on apoptosis. Methods: Cortical neurons were cultured in vitro for hypoxia-reoxygenation injury model. The experiment was divided into normal control group, hypoxia-reoxygenation-free group (3, 6, 12 and 24 hours), and the levels of lactate The content of glutathione (GSH) and glutathione peroxidase (GPx) in neurons were observed. Hochest33258 nuclear staining was used to observe the apoptosis of cortical neurons. Results: Compared with the normal control group, the release of LDH and the content of NO in neurons after hypoxia / reoxygenation were significantly decreased and the activity of GPx decreased (P <0.05). The activity of NOS increased at 3h and 6h (P <0.05). However, there was no significant difference between the two groups at 24h (P> 0.05). Apoptosis of neurons occurred at 3h after hypoglycemic reoxygenation and apoptosis Continued to increase (P <0.05). CONCLUSION: With the continuous duration of hypoxia / reoxygenation, the destruction of oxidative and anti-oxidative balance may be one of the reasons for the apoptosis of cultured cortical neurons.