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目的 探讨褪黑素 (Melatonin ,MT)在模拟缺血再灌注中对神经元的保护机制 ,从而为褪黑素的临床应用提供可靠的理论依据。方法 分离SD乳鼠的小脑颗粒细胞进行原代培养 ,待细胞发育成熟后建立体外模拟缺血再灌注模型。采用相差显微镜进行细胞的形态学观察 ;通过TBA荧光法和联苯三酚自氧化法来检测模拟缺血再灌注过程中细胞内丙二醛 (MDA)生成量、超氧化物歧化酶 (SOD)的活性变化以及褪黑素在模拟缺血再灌注过程中对二者的影响。结果 模拟缺血 (OGD)后再灌注 12h的细胞 ,胞内MDA的生成比在OGD后再灌注 6h明显增多 (P <0 .0 5 ) ,OGD后再灌注 12hMDA生成最多随后降低 ;经OGD处理后细胞内SOD的活性较正常组明显降低 (P <0 .0 5 ) ,OGD后再灌注 2 4h降到最低随后升高。MT能显著降低细胞内MDA的生成 (P <0 .0 5 ) ,并存在着一定的剂量依赖关系。SOD的活性在加入MT后也明显提高(P <0 .0 5 )。结论 MT可能通过其抗氧化作用在模拟缺血 (OGD)再灌注中起到神经保护作用。
Objective To investigate the protective mechanism of melatonin (MT) on neurons in simulated ischemia-reperfusion, and to provide a reliable theoretical basis for the clinical application of melatonin. Methods Primary cultured cerebellar granulosa cells of neonatal SD rats were isolated and cultured in vitro. After the cells were mature, the models of simulated ischemia-reperfusion were established. Morphological observation of the cells was carried out by phase-contrast microscopy. The content of malondialdehyde (MDA), the activity of superoxide dismutase (SOD) in the cells during simulated ischemia-reperfusion (I / R) And the effect of melatonin on them during simulated ischemia-reperfusion. RESULTS: After reperfusion for 12h, the generation of intracellular MDA was significantly increased (P <0.05) at 6h after reperfusion of OGD, and reached its peak at 12h after OGD reperfusion. After OGD treatment After intracellular SOD activity was significantly lower than the normal group (P <0. 05), OGD after 24 hours of reperfusion decreased to a minimum and then increased. MT can significantly reduce intracellular MDA (P <0.05), and there is a certain dose-dependent relationship. SOD activity was also significantly increased after addition of MT (P <0.05). Conclusion MT may play a neuroprotective role in the reperfusion of simulated ischemia (OGD) through its antioxidative effect.