摘要
目的 :研究环孢霉素A对短暂缺氧血清剥夺再灌流后PC1 2细胞的保护作用和可能的作用机制。方法 :将PC1 2细胞随机分为对照组、缺氧组和干预组 ,缺氧组于缺氧血清剥夺 1 5min后复氧复注血清 1h ,干预组自缺氧前 4h即给予环孢霉素A ,并同样于缺氧血清剥夺 1 5min后复氧复注血清 1h ,测定各组ATP含量 (生化发光法 )、线粒体膜电位 (Rhodamine1 2 3标记 ,流式细胞仪测定 )、细胞活性 (MTT法 )。结果 :与对照组相比 ,缺氧组ATP含量、线粒体膜电位、细胞活性显著降低 ,差异具有统计学意义 (P <0 .0 1 ) ;干预组与缺氧组的ATP含量、线粒体膜电位、细胞活性的差异有统计学意义 (P <0 .0 1 )。干预组与对照组间差异无统计学意义 (P >0 .0 5 )。结论 :环孢霉素A是线粒体膜渗透性转换孔抑制剂 ,在短暂缺氧血清剥夺再灌流后对维持PC1 2细胞线粒体的完整和功能起着非常重要的作用 。
Aim: To investigate the neuroprotective effect of cyclosporin A on the PC12 cells after transient anoxia serium deprivation / reperfusion and its probable mechanism. Methods: The PC12 cells were randomly divided into control group, anoxia group, and treatment group. The anoxia group was reperfused 1h after 15 min anoxia serium deprivation. The treatment group had been given cyclosporin A before experiment and was also reperfused 1h after 15 min anoxia serium deprivation. The content of ATP ( firefly luciferase ), mitochondria membrane potential ( Rhodamine 123 labeling ) and cell activity ( MTT assay ) were determined.Results: Compared with control group, the content of ATP, mitochondria membrane potential and cell activity in the anoxia group were significantly lower than those of control( P < 0.01),and there was significant difference between treatment group and anoxia group ( P < 0.01 ). Conclusions: Cyclosporin A is mito chondrial permeability transition pore inhibitor and plays an important role in keeping shape and function of mitochondria after transient anoxia serium deprivation / reperfusion , it also has obvious protective effect on neuron.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2004年第4期575-577,共3页
Journal of Zhengzhou University(Medical Sciences)
基金
国家自然科学基金资助项目 3 0 0 70 82 5
关键词
环孢霉素A
缺氧
血清剥夺
再灌流
cyclosporin A
anoxia
serium deprivation
reperfusion