摘要
目的:观察腺苷A1受体拮抗剂DPCPX对低氧复氧(H/R)脑神经元乳酸脱氢酶(LDH)释放量、钙调神经磷酸酶(CaN)、乙酰胆碱酯酶(AChE)活性和细胞外液氨基酸水平的影响。方法:进行大鼠大脑皮层神经元的体外培养及H/R损伤模型的建立,在低氧同时加入不同浓度DPCPX(终浓度分别为:0、25、50和100nmol/L)培养8h、12h和24h后复氧24h,检测LDH释放量的变化,并观察了100nmol/L DPCPX对12h低氧的H/R神经元CaN、AChE活性和细胞外液氨基酸水平的影响。结果:与对照组比较,低氧暴露12h复氧后100nmol/L DPCPX组神经元LDH释放量明显增加,CaN和AChE活性显著升高,细胞外液γ-氨基丁酸水平显著降低。结论:DPCPX上调H/R神经元LDH释放量、CaN和AChE活性,降低细胞外液γ-氨基丁酸水平。
AIM： To investigate the effects of adenosine A1 receptor antagonist DPCPX on the release of cerebral neuronal lactate dehydrogenase （LDH）, the activity of calcineurin （CaN） and acetylcholinesterase （AChE）, and the level of extracellular amino acid after hypoxia and reoxygenation （H/R）.METHODS： Primary cultured rat cerebral cortical neurons were used to establish an H/R injury model. Different concentrations of DPCPX （the final concentrations were as follows： 0, 25, 50 and 100 nmol/L） were added at the same time of hypoxia treatment for 8 h, 12 h or 24 h,followed by reoxygenation for 24 h. The LDH release from the neurons was measured. The effects of DPCPX （100 nmol/L） on the activity of CaN and AChE, and the level of extracellular amino acid in neurons treated with hypoxia for 12 h followed by reoxygenation were observed. RESULTS： Compared to the cells in control groups, the neurons treated with 100 nmol/L DPCPX and exposed to hypoxia for 12 h followed by reoxygenation, showed significantly higher LDH release, higher activity of CaN and AChE, and lower level of extracellular γ-aminobutyric acid.CONCLUSION： These results suggest that DPCPX increases the LDH release and the activity of CaN and AChE, decreases the level of extracellular γ-aminobutyric acid in neurons with H/R.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2010年第11期2256-2258,2273,共4页
Chinese Journal of Pathophysiology
关键词
受体
腺苷A
低氧
神经元
脑
Receptors adenosine A1 Hypoxia Neurons Brain
