摘要
目的:观察不同浓度外源性锌对神经元细胞内游离钙([Ca2+]i)的影响,探讨低浓度外源性锌对于缺氧神经元保护作用的可能机制。方法:原代培养大鼠皮层神经元,加入不同浓度的外源性锌,激光扫描共聚焦显微镜检测神经元[Ca2+]i的变化;建立细胞缺氧模型,检测10μmol/L外源性锌对于缺氧神经元[Ca2+]i和[Zn2+]i的影响。结果:神经元的[Ca2+]i,10μmol/L锌组与对照相比无明显变化;100μmol/L锌组一过性升高,后降至对照水平;500μmol/L锌组,明显高于对照水平。除正常加锌组外,其余各组神经元[Zn2+]i和[Ca2+]i均较正常对照组增高;但正常加锌组、缺氧加锌组神经元[Zn2+]i和[Ca2+]i均较缺氧组降低。结论:外源性锌对于神经元的作用随浓度而不同;10μmol/L外源性锌维持了神经元的钙稳态,它对于缺氧神经元的保护作用,可能通过抑制钙超载实现。
Objective.. To investigate the effects of exogenous zinc on intracellular free calcium of cortical neurons, and to explore the possible mechanisms of low-dose exogenous zinc in protecting hypoxia-injured neurons. Methods: Cultured primary cortical neurons of rats were treated with various concentrations of exogenous zinc in vitro, and the changes of their intracel- lular free calcium were detected by laser scanning confocal microscopy. The hypoxic cell model was established and the effects of 10 μmol/L exogenous zinc on intracellular free calcium and zinc were observed. Results: Compared with the control, the change of intracellular free calcium was unremarkable in 10 μmol/L zinc group, but it increased transiently in 100 μmol/L zinc group and became remarkable in 500 μmol/L zinc group. Intracellular free calcium and zinc increased in all groups except in the zinc group when compared with the control; however, they decreased in the zinc group and zinc & anoxia group compared with the anoxia group. Conclusion: The effects of exogenous zinc on neurons alter with its concentrations. Low'dose (10 μmol/L) exogenous zinc may keep the calcium homeostasis of the neurons, and its mechanisms in protecting hypoxia-injured neurons may be fulfilled by inhibiting calcium overload.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2008年第5期684-686,705,共4页
Chinese Journal of Anatomy