CAJ | 학술논문

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1 d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15 min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PPARγ mRNA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 0 h,PPARγ表达与对照组相比无明显变化(P>0.05);复氧 6 h,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48 h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.
목적:관찰과양화물매체증식물격활수체γ(PPARγ)재신경원결양/복양손상불동시간적표체,이탐토PPARγ재신경원결혈재관주손상과정중적작용.방법:이신생1 d적SD대서위연구대상,채용해마신경원원대배양기술,급원대배양적신경원결양、결당15 min후재회복양화포도당공응,건입체외신경원류결혈재관주모형,JEM-200EX투사전자현미경관찰결양/복양후불동시간신경원결구변화,채용RT-PCR검측PPARγ mRNA표체,Western 인적방법검측PPARγ단백표체.결과:신경원결양/복양처리후불동시간,신경원정상결구출현손해.복양 0 h,PPARγ표체여대조조상비무명현변화(P>0.05);복양 6 h,PPARγ표체재mRNA화단백수평출현강저,여대조조상비차이유통계학의의(P<0.01),이차수착시간적연장표체축점강저,도48 h체도최저,불동시간점지간급여대조조지간차이유통계학의의(P<0.01).결론:PPARγ삼여신경원결혈재관주손상적병리과정,유망성위결혈성뇌혈관병치료적간예파점.
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.