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目的 :应用原代培养胎鼠海马神经元 ,观察脱氢表雄酮唾液酸苷对 β 淀粉样蛋白 (Aβ2 5-3 5)损伤海马神经元的保护作用。方法 :海马神经元分别与Aβ2 5-3 5(0 .1μM )、脱氢表雄酮硫酸酯及脱氢表雄酮唾液酸苷孵育 2 4h后 ,检测细胞内漏出的乳酸脱氢酶 (LDH)、谷胱甘肽过氧化酶 (GSH Px)活性、脂质过氧化物 (MDA)含量及细胞存活率的变化。结果 :海马神经元与Aβ2 5-3 5共同孵育 2 4h后 ,细胞存活率显著下降、GSH Px活性降低、LDH和MDA含量升高 ;海马神经元与不同浓度脱氢表雄酮硫酸酯和脱氢表雄酮唾液酸苷共孵 2 4h后 ,能改变Aβ2 5-3 5引起的损伤 ,使细胞存活率显著升高、GSH Px活性升高、LDH活力和MDA含量降低。唾液酸苷衍生物在对部分指标的影响上 ,效价高于相应的硫酸酯。结论 :脱氢表雄酮唾液酸苷可对抗Aβ2 5-3 5所造成的神经元损伤 ,作用可能是通过清除氧自由基、抗脂质过氧化作用和提高神经元产生抗氧化能力实现的。
OBJECTIVE: To observe the protective effect of dehydroepiandrosterone on the hippocampal neurons damaged by β-amyloid protein (Aβ2 5-3 5) in primary cultured fetal rat hippocampal neurons. Methods: The neurons in hippocampus were respectively incubated with Aβ2 5-3 5 (0.1μM), DHEA and DHEA for 24 hours, and the intracellular leakage of lactate dehydrogenase (LDH ), Glutathione peroxidase (GSH Px) activity, lipid peroxidation (MDA) content and cell viability. Results: After incubated with Aβ2 5-3 5 for 24 h, the cell viability was significantly decreased, the activity of GSH Px was decreased and the contents of LDH and MDA were increased. Compared with different concentrations of dehydroepiandrosterone sulfate and Hydrogen eprosteninosalin incubated for 24 hours, can change Aβ2 5-3 5-induced damage, so that cell viability was significantly increased GSH Px activity, LDH activity and MDA content decreased. Sialic acid derivatives on the impact of some of the indicators, the titers higher than the corresponding sulfate. CONCLUSION: DHEA can antagonize the neuronal damage induced by Aβ2 5-3 5, which may be through the scavenging of oxygen free radicals, anti-lipid peroxidation and the anti-oxidative ability of neurons.