二硫卡钠对原代培养皮层神经元缺氧损伤的保护作用

取体外原代培养14 d左右的大鼠皮层神经元，换上无血清除氧培养基并置通95％ N₂+5% CO₂的缺氧罐中造成神经元缺氧. 以研究缺氧对皮层神经元的损伤及二硫卡钠(DTC)的保护作用. 用存活神经元数目及神经元线粒体活性来评价神经元活力. 乳酸脱氢酶(LDH)活性及脂质过氧化产物丙二醛(MDA)含量分别用紫外分光光度法和硫代巴比酸法测定，作为评价损伤的指标. 原代培养皮层神经元分别缺氧4, 5和6 h后，活细胞数显著减少，线粒体活性明显降低；LDH释放及MDA产生显著增加；而缺氧2 h 后，仅活细胞数无明显变化. 超氧阴离子清除剂超氧化物歧化酶(SOD)可逆转上述变化，抑制缺氧对神经元的损伤， 表明培养神经元缺氧损伤可能与自由基产生有关. 类似SOD作用，DTC可显著对抗缺氧对神经元的损伤，剂量依赖地抑制缺氧引起的LDH释放和MDA形成的增加. 结果表明：DTC对神经元缺氧损伤具保护作用，其作用可能与清除自由基有关.

Protective effects of ditiocarb sodium against anoxic damage of primary cortical neurons in culture

Anoxia- induced damage of primary cortical neurons in culture and the protective effects of ditiocarb sodium (DTC) against it were studied. Anoxia was produced by exchanging media with serum-free oxygen-depleted media and placing the cultures in an anoxia chamber. Anoxia could induce damage of neuron reflected by the decrease in both the viable neuron number and the mitochondrial activity, and induce the increase in LDH release and MDA production. Superoxide dismutase (SOD) reversed the effects of anoxia. DTC, as well as SOD, protected the viability of neuron against anoxic damage and dose-dependently inhibited LDH release and MDA production. The results suggested that the formation of oxygen free radicals be implicated in anoxic damage of cortical neuron. DTC could protect the cultured neuron against anoxic damage, that might be mediated by scavenging oxygen free radicals.