Saturation of neuroprotective effects of adenosine in cortical culture.
Saturation of neuroprotective effects of adenosine in cortical culture.
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皮质培养物中腺苷神经保护作用的饱和。
DOI：
10.1097/00001756-200211150-00017
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发表时间：
2002
期刊：
影响因子：
1.7
通讯作者：
Lobner,Doug
中科院分区：
文献类型：
--
作者：
Lobner,Doug
腺苷和腺苷A1受体激动剂通常但不总是对代谢损伤具有保护作用。在皮层细胞培养中测定A1激动剂和拮抗剂对神经元死亡的影响。A1激动剂环己基腺苷没有减弱由氧-葡萄糖剥夺引起的神经元死亡，但确实减弱了由葡萄糖剥夺或NMDA引起的死亡。细胞外腺苷水平在氧-葡萄糖剥夺显着高于在葡萄糖剥夺或NMDA暴露。A1拮抗剂8-环戊基茶碱增加氧-葡萄糖剥夺诱导的死亡，但不增加葡萄糖剥夺或NMDA暴露引起的死亡。因此，虽然A1受体的激活可以提供神经保护，但在氧-葡萄糖剥夺期间，这种保护作用似乎因高水平的内源性细胞外腺苷而变得饱和。
Adenosine and adenosine A1 receptor agonists are often, but not always, protective against metabolic insults. The effects of an A1 agonist and antagonist on neuronal death were determined in cortical cell cultures. The A1 agonist cyclohexyladenosine did not attenuate neuronal death induced by oxygen–glucose deprivation, but did attenuate death caused by glucose deprivation or NMDA. Extracellular adenosine levels during oxygen–glucose deprivation were significantly higher than those during glucose deprivation or NMDA exposure. The A1 antagonist 8-cyclopentyltheophylline increased death induced by oxygen–glucose deprivation, but not that caused by glucose deprivation or NMDA exposure. Thus, while activation of A1 receptors can provide neuroprotection, the protective effect appears to become saturated by high levels of endogenous extracellular adenosine during oxygen–glucose deprivation.