Anandamide and noladin ether prevent neurotoxicity of the human amyloid-β peptide
Anandamide and noladin ether prevent neurotoxicity of the human amyloid-β peptide
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DOI：
10.1016/s0304-3940(02)00936-9
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发表时间：
2002-10-31
影响因子：
2.5
通讯作者：
Milton, NGN
中科院分区：
文献类型：
--
作者：
Milton, NGN
大麻素受体激动剂包括阿南达胺和诺拉丁醚，最近被认为具有神经保护特性。淀粉样β蛋白(Abeta)被认为是与阿尔茨海默病病理相关的神经退行性变化的原因。本研究观察了安非他明和诺拉丁醚对Abeta对分化的人畸胎癌细胞株NTERA2/CL-D1神经元的神经毒性的影响。在纳摩尔浓度下，花青胺和诺拉丁醚对Abeta毒性有浓度依赖性的抑制作用。CB1大麻素受体拮抗剂AM251可阻止anandamide和诺拉丁醚的保护作用。丝裂原活化蛋白激酶(MAPK)途径抑制剂PD98059也可阻止大麻素和促肾上腺皮质激素释放激素的保护作用。这些结果表明，大麻素或促肾上腺皮质激素释放激素激活MAPK通路可用于预防Abeta多肽诱导的神经变性。(C)2002爱思唯尔科学爱尔兰有限公司。保留所有权利。
Cannabinoid receptor agonists including anandamide and noladin ether have recently been suggested to exhibit neuroprotective properties. The amyloid-beta (Abeta) peptide is thought to be responsible for the neurodegenerative changes associated with Alzheimer's disease pathology. This study characterizes the effects of anandamide and noladin ether on the neurotoxicity of Abeta in differentiated human teratocarcinoma cell line, Ntera 2/cl-D1 neurons. Anandamide and noladin ether, at nanomolar concentrations, showed concentration dependent inhibition of Abeta toxicity. A CB1 cannabinoid receptor antagonist, AM251, prevented the protective effects of anandamide and noladin ether. The mitogen activated protein kinase (MAPK) pathway inhibitor PD98059 also prevented the protective effects of cannabinoids and corticotrophin-releasing hormone. These results suggest that activation of the MAPK pathway by either cannabinoids or corticotrophin-releasing hormone could be used to prevent Abeta peptide induced neurodegeneration. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.