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目的为观察缺氧对大鼠海马神经元的影响及纳络酮的保护作用。方法采用细胞培养方法获取10～14d的海马神经元,将含药血清加入到培养液中,4h后建立95%N2+5%CO2混合气体急性缺氧模型,胎盘兰染色细胞计数并做流式细胞仪检测以及酶法测定抗氧化酶(超氧化物歧化酶)的抗氧化能力及丙二醛、NO的含量。结果离体条件下纳络酮可显著增强海马神经元的活性,降低其凋亡率及死亡率;提高细胞上清夜中超氧化物歧化酶的活性,降低丙二醛及NO的含量,且成量效比例关系。结论纳络酮在体外有抗缺氧损伤的作用。其作用机制可能是通过抑制细胞凋亡,提高抗氧化酶的活力,清除自由基,而发挥作用。
Objective To observe the effect of hypoxia on hippocampal neurons and the protective effect of naloxone in rats. Methods The hippocampal neurons of 10-14 days were obtained by cell culture method. The serum was added into the culture medium. After 4 hours, a acute hypoxia model of 95% N2 + 5% CO2 mixed gas was established. Cytometry and enzymatic determination of anti-oxidative enzyme (superoxide dismutase) antioxidant capacity and malondialdehyde, NO content. Results Naloxone could significantly enhance the activity of hippocampal neurons and reduce the apoptosis rate and mortality in vitro. The activity of superoxide dismutase in the supernatant of the cells and the content of malondialdehyde and nitric oxide were decreased, Quantitatively proportional relationship. Conclusion Naloxone has an anti-hypoxic injury in vitro. The mechanism may be through the inhibition of apoptosis, increase the antioxidant enzyme activity, scavenging free radicals, and play a role.