论文部分内容阅读
目的 探讨硫酸镁对体外培养的神经细胞缺氧所致损伤的保护作用及其可能的机制。方法 将培养至 12d的乳鼠神经细胞 ,随机分为正常培养组、对照缺氧组和硫酸镁治疗组 ,加入氰化钾以阻断细胞氧化磷酸化反应 ,观察硫酸镁对缺氧神经细胞的影响 ,作用 12、2 4h后 ,在光、电镜下观察细胞形态变化 ,并以MTT法测定细胞活力。结果 氰化钾作用后 ,对照缺氧组细胞密度减小、突起萎缩、线粒体肿胀、嵴崩解、核浓缩 ;硫酸镁治疗组损伤程度明显较缺氧组轻 ;正常培养组与对照缺氧组MTT法测定A值 :12h为 0 2 87± 0 0 4 1、0 174± 0 0 2 1;2 4h为 0 2 93± 0 0 35、0 10 1± 0 0 2 9(P <0 0 1) ;硫酸镁治疗组A值 :12h为 0 2 14± 0 0 5 3、2 4h为 0 198± 0 0 2 6 ,与缺氧组比较差异有显著性(P <0 0 1)。分别比较各组 12h与 2 4h的A值 ,差异也有显著性 (P <0 0 1)。结论 硫酸镁用于缺氧早期 ,可减轻神经细胞的后续损伤 ,其机制可能为包括阻断兴奋性氨基酸受体在内的多种作用
Objective To investigate the protective effect of magnesium sulfate on the damage induced by hypoxia in cultured neurons and its possible mechanism. Methods The cultured neonatal rat neurons cultured for 12 days were randomly divided into normal culture group, control hypoxia group and magnesium sulfate treatment group. Potassium cyanide was added to block neuronal oxidative phosphorylation, and the effect of magnesium sulfate on hypoxic neurons After 12, 24 hours, the morphological changes of cells were observed under light and electron microscopy, and the cell viability was measured by MTT assay. Results After potassium cyanide treatment, the density of cells in the control hypoxia group decreased, the processes of atrophy, mitochondria swelling, cristae disintegration and nuclear condensation were observed. The damage degree in the magnesium sulfate treatment group was significantly lower than that in the hypoxia group. In the normal group and the control hypoxia group The value of A was determined by MTT method: 0 2 87 ± 0 0 4 1,0 174 ± 0 0 2 1 at 12h; 0 2 93 ± 0 0 35,0 10 1 ± 0 0 2 9 at 24 hours (P <0.01 ). The value of A in magnesium sulfate treatment group was 0 2 14 ± 0 053 at 12 hours and 0 198 ± 0 0 2 6 at 4 hours, which was significantly different from that in hypoxia group (P <0.01). The A values of 12h and 24h of each group were compared, the difference was also significant (P <0.01). Conclusion Magnesium sulphate can be used in the early stage of hypoxia to reduce the subsequent damage of nerve cells. Its mechanism may include various functions including blocking excitatory amino acid receptors