摘要
目的观察胞二磷胆碱对大鼠海马神经元缺糖缺氧再灌注损伤的保护作用。方法建立海马神经元缺糖缺氧再灌注损伤模型,随机分为正常对照组、缺糖缺氧再灌注组、胞二磷胆碱干预组(1、10、100μmol/L),观察再灌注6、24h还原型谷胱甘肽含量以及谷胱甘肽过氧化物酶(GPx)活性的改变;于再灌注24h检测海马神经元四甲基偶氮唑盐(MTT)代谢率,以及流式细胞术检测凋亡。结果与缺糖缺氧再灌注组相比,胞二磷胆碱于再灌注6h可明显提高谷胱甘肽(GSH)的含量及GPx的活性(P<0.05);于再灌注24h可增高MTT代谢率,提高GPx的活性及减少海马神经元凋亡(P<0.05)。结论胞二磷胆碱对海马神经元缺糖缺氧再灌注损伤有明显的保护作用,其机制可能与改善神经元GSH含量、GPx活性及减少凋亡有关。
Objective To demonstrate the protective effects of citicoline against neuronal oxygen- glucose deprivation and reperfusion injury and to investigate the underlying mechanisms. Methods The rat neurons cultivated as the object of study and then build the model of oxygen - glucose deprivation and reperfusion. They were randomly divided into 3 groups ： control group, oxygen - glucose deprivation group, citicoline treatment groups （ 1,10,100 μmol/L） , Metabolic rate of MTT at reperfusion 24 h, the content of reduced glutathione and the active of glutathion peroxidase were measured by assay kits at reperfusion 6 h and 24 h. Cells were dyed Annexin V - PI and the rate of apoptosis was detected by flow cytometry. Results Compared with OGD/reperfusion group, citicoline treatment after OGD obviously increased GSH level and activity GPx at reperfusion 6 h （ P 〈 0.05 ） ; citicoline increased cell survival rate, activity GPx and decreased cell apoptotic rate. Conclusion Citicoline has protective effect on hippocampal neurons against oxygen - glucose deprivation and reperfusion injury by increasing the metabolic rate of MTT, raising antioxidation, and decreasing apoptosis.
出处
《中国急救医学》
CAS
CSCD
北大核心
2007年第12期1094-1097,共4页
Chinese Journal of Critical Care Medicine
