【摘要】 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。更多还原

【Abstract】 Objective To further address the neuron protective effect of MT and find some new treatment and target to prevent the secondary neuron injury in ischemia/reperfusion. Methods In our study, cerebellar granule cells dissected from eight-day-old Sprague-Dawley rats were cultured for 8 days and then exposed to oxygen-glucose deprivation to set up ischemia/reperfusion model. Morphologic structure changes were observed under microscope. The intracellular MDA and SOD activity were detected at various time intervals. Results In OGD exposed cultures, the production of MDA burst 12 hours after OGD, and the activity of SOD was sharply depressed 24 hours later. Mt could significantly decrease the generation of MDA, and it was time-dependent. Furthermore, MT could elevate the activity of SOD. Conclusions Melatonin can protect cerebellar granule cells exposed to OGD as an antioxidant and may have therapeutic potential in prevention and treatment of neuronal damage induced by ischemia/reperfusion更多还原