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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Insulin on activation of autophagy with integrins and syndecans against MPP+-induced alpha-synuclein neurotoxicity
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Insulin on activation of autophagy with integrins and syndecans against MPP+-induced alpha-synuclein neurotoxicity

机译:胰岛素对整联蛋白和二氯联苯的激活对α-突触核蛋白神经毒性的

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摘要

Parkinson's disease (PD) is the second most common neurodegenerative disease in the elderly caused by dopaminergic neuronal cell death. Human neuroblastoma SH-SY5Y cells differentiated by retinoic acid have been used to study the in vitro PD model induced by 1-methyl-4-phenyl pyridinium (MPP+). In this study, pretreatment of insulin inhibited MPP+-induced cell membrane damages, which also inhibited the Cox-2 and alpha-synuclein levels. In addition, MPP+ and/or insulin enhanced the autophagy LC3. Furthermore, MPP+-induced neurotoxicity diminished the integrins beta 3, alpha V and induced the syndecan-1 and -3. Insulin pretreatment enhanced the phosphorylation of integrin-linked kinase and further induced the integrin and syndecan molecules. These findings suggest that insulin prevents MPP+-induced alpha-synuclein apoptosis through the activation of integrin and syndecan pathways in SH-SY5Y + RA cells. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
机译:帕金森病(PD)是由多巴胺能神经元细胞死亡老年人造成的第二种最常见的神经变性疾病。 通过视黄酸分化的人神经母细胞瘤SH-SY5Y细胞已用于研究由1-甲基-4-苯基吡啶(MPP +)诱导的体外PD模型。 在这项研究中,胰岛素的预处理抑制了MPP +诱导的细胞膜损伤,这也抑制了COX-2和α-突触核蛋白水平。 此外,MPP +和/或胰岛素增强了自噬LC3。 此外,MPP +-诱导的神经毒性降低了整联蛋白β3,αv并诱导了Syndecan-1和-3。 胰岛素预处理增强了整联蛋白连接激酶的磷酸化,进一步诱导整联蛋白和同癸烷分子。 这些发现表明,胰岛素通过在SH-SY5Y + RA细胞中的整联蛋白和Syndecan途径的激活来阻止MPP +-unduclein凋亡。 (c)2016 Elsevier Ireland Ltd.保留所有权利。

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