摘要
目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)在神经元缺氧/复氧损伤不同时间的表达,以探讨PPARγ在神经元缺血再灌注损伤过程中的作用。方法:以新生1d的SD大鼠为研究对象,采用海马神经元原代培养技术,给原代培养的神经元缺氧、缺糖15min后再恢复氧和葡萄糖供应,建立体外神经元类缺血再灌注模型,JEM-200EX透射电子显微镜观察缺氧/复氧后不同时间神经元结构变化,采用RT-PCR检测PPARγmRNA表达,Western印迹方法检测PPARγ蛋白表达。结果:神经元缺氧/复氧处理后不同时间,神经元正常结构出现损害。复氧0h,PPARγ表达与对照组相比无明显变化(P>0.05);复氧6h,PPARγ表达在mRNA和蛋白水平出现降低,与对照组相比差异有统计学意义(P<0.01),而且随着时间的延长表达逐渐降低,到48h达到最低,不同时间点之间及与对照组之间差异有统计学意义(P<0.01)。结论:PPARγ参与神经元缺血再灌注损伤的病理过程,有望成为缺血性脑血管病治疗的干预靶点。
Objective To observe the expression of peroxisome proliferator-activated receptor γ（PPARγ）in hippocampus neurons in rats after different time of neuron oxygen deprivation/oxygen supply,and to investigate the role of PPARγ in neuron ischemia reperfusion injury.Methods One day old newborn SD rats were chosen.Primary cultured hippocampus neurons were used to establish neuron ischemic reperfusion model in vitro by oxygen and glucose depriving 15 minutes and supplying again,and then the neuron structure was observed by transmission electron microscope of JEM-200EX.The expression of PPARγ mRNA and protein were detected by RT-PCR and Western blot,respectively.Results Neuron structure was damaged after neuron oxygen deprivation/oxygen supply.There was no significant difference between 0 h oxygen supply group and the control group.The expression of PPARγ was decreased both at mRNA and protein level after 6 h of oxygen supply.The difference between 6 h oxygen supply group and the control group was significant（P〈0.01）,which decreased with the length of reperfusion and the lowest was at 48 h after the reperfusion.The difference among the different reperfusion groups and the control group was significant（P〈0.01）.Conclusion PPARγ may participate in the pathological damage course of neuron ischemical reperfusion injury,and may become a new intervention target of treatment for ischemic cerebrovascular disease.
出处
《中南大学学报（医学版）》
CAS
CSCD
北大核心
2009年第12期1238-1242,共5页
Journal of Central South University ：Medical Science
基金
陕西省科技攻关项目(2006K15-G3)
陕西省卫生厅科研基金(06D16)
西安市科技攻关项目(GG05129)~~
关键词
过氧化物酶体增殖物激活受体Γ
原代神经元培养
缺氧/复氧
缺血再灌
peroxisome proliferator-activated receptor γ
primary neurons culture
oxygen deprivation/oxygen supply
ischemia reperfusion
