Influence of dexamethasone on neurotoxicity caused by oxygen and glucose deprivation in vitro
Influence of dexamethasone on neurotoxicity caused by oxygen and glucose deprivation in vitro
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DOI：
10.1006/exnr.1996.0078
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发表时间：
1996-05-01
影响因子：
5.3
通讯作者：
Flavin, MP
中科院分区：
文献类型：
--
作者：
Flavin, MP
关于糖皮质激素暴露对缺氧缺血性脑损伤的影响，存在相互矛盾的证据。我们研究了地塞米松的时间、持续时间和浓度对体外氧葡萄糖剥夺（OGD）后神经元损伤的影响。分离的胚胎大鼠基底前脑细胞进行培养，并与地塞米松预孵育72小时或连续暴露之前，期间和之后OGD。在体外第13天，OGD后2天，通过形态学评级和胆碱乙酰转移酶（ChAT）活性评估损伤。与纳摩尔浓度的地塞米松预孵育导致损伤的剂量依赖性加重。联合应用谷氨酸受体拮抗剂消除了这种有害作用，表明地塞米松可能增加谷氨酸释放，减少摄取，或上调谷氨酸受体表达。在损伤之前、期间和之后连续应用窄浓度范围的地塞米松（100 nM和1 μ M）保护神经元。糖皮质激素给药的剂量、时间和持续时间可能是影响缺氧缺血性脑损伤结局的关键变量。(C)出版社：Academie Press，Inc.
There is conflicting evidence regarding the impact of glucocorticoid exposure on hypoxic ischemic brain injury We examined the effects of timing, duration, and concentration of dexamethasone on neuronal injury following in vitro oxygen glucose deprivation (OGD). Dissociated embryonic rat basal forebrain cells were cultured and either preincubated with dexamethasone for 72 h or continuously exposed prior to, during, and after OGD. Injury was assessed by morphology rating and cholineacetyltransferase (ChAT) activity at Day 13 in vitro, 2 days after OGD. Preincubation with nanomolar concentrations of dexamethasone resulted in a dose-dependent exaggeration of injury Combined glutamate receptor antagonist application negated this deleterious effect, suggesting that dexamethasone may increase glutamate release, decrease uptake, or upregulate glutamate receptor expression. Continuous application of a narrow concentration range of dexamethasone (100 nM and 1 mu M) prior to, during, and after insult protected neurons. Dose, timing, and duration of glucocorticoid administration may each be critical variables influencing outcome of hypoxic ischemic brain insult. (C) 1996 Academie Press, Inc.