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The Potential Dual Effects of Anesthetic Isoflurane on A beta-Induced Apoptosis

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机构: [1]Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, Charlestown, MA 02129 USA [2]Harvard Univ, Sch Med, Charlestown, MA 02129 USA [3]China Med Univ, Fac Forens Med, Dept Forens Pathol, Shenyang 110001, Peoples R China [4]Fudan Univ, Dept Anesthesiol, Huashan Hosp, Shanghai 200041, Peoples R China [5]Capital Med Univ, Beijing Tongren Hosp, Dept Anesthesia, Beijing 100050, Peoples R China [6]Capital Med Univ, Beijing Chaoyang Hosp, Dept Anesthesia, Beijing 100020, Peoples R China
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关键词: Anesthesia Alzheimer's disease isoflurane apoptosis beta-Amyloid protein dual effects cytosolic calcium

摘要:
beta-amyloid protein (A beta)-induced neurotoxicity is the main component of Alzheimer's disease (AD) neuropathogenesis. Inhalation anesthetics have long been considered to protect against neurotoxicity. However, recent research studies have suggested that the inhalation anesthetic isoflurane may promote neurotoxicity by inducing apoptosis and increasing A beta levels. We therefore set out to determine whether isoflurane can induce dose-and time-dependent dual effects on A beta-induced apoptosis: protection versus promotion. H4 human neuroglioma cells, primary neurons from nave mice, and nave mice were treated with A beta and/or isoflurane, and levels of caspase-3 cleavage (activation), apoptosis, Bcl-2, Bax, and cytosolic calcium were determined. Here we show for the first time that the treatment with 2% isoflurane for six hours or 30 minutes potentiated, whereas the treatment with 0.5% isoflurane for six hours or 30 minutes attenuated, the A beta-induced caspase-3 activation and apoptosis in vitro. Moreover, anesthesia with 1.4% isoflurane for two hours potentiated, whereas the anesthesia with 0.7% isoflurane for 30 minutes attenuated, the A beta-induced caspase-3 activation in vivo. The high concentration isoflurane potentiated the A beta-induced reduction in Bcl-2/Bax ratio and caused a robust elevation of cytosolic calcium levels. The low concentration isoflurane attenuated the A beta-induced reduction in Bcl-2/Bax ratio and caused only a mild elevation of cytosolic calcium levels. These results suggest that isoflurane may have dual effects (protection or promotion) on A beta-induced toxicity, which potentially act through the Bcl-2 family proteins and cytosolic calcium. These findings would lead to more systematic studies to determine the potential dual effects of anesthetics on AD-associated neurotoxicity.

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出版当年[2010]版:
大类 | 2 区 医学
小类 | 2 区 神经科学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
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出版当年[2009]版:
Q1 NEUROSCIENCES
最新[2023]版:
Q3 CLINICAL NEUROLOGY Q4 NEUROSCIENCES

影响因子: 最新[2023版] 最新五年平均 出版当年[2009版] 出版当年五年平均 出版前一年[2008版] 出版后一年[2010版]

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第一作者机构: [1]Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, Charlestown, MA 02129 USA [2]Harvard Univ, Sch Med, Charlestown, MA 02129 USA
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通讯机构: [1]Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, Charlestown, MA 02129 USA [2]Harvard Univ, Sch Med, Charlestown, MA 02129 USA [*1]Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, 149 13th St,4310, Charlestown, MA 02129 USA
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