Trehalose Inhibits A53T Mutant α-Synuclein Overexpression and Neurotoxicity in Transduced PC12 Cells.

Trehalose Inhibits A53T Mutant α-Synuclein Overexpression and Neurotoxicity in Transduced PC12 Cells.
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海藻糖抑制 A53T 突变体 α-突触核蛋白过度表达和转导 PC12 细胞的神经毒性

DOI:
10.3390/molecules22081293
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发表时间:
2017-08-08
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
Zhou P
Zhou P
中科院分区:
其他
文献类型:
--
作者:
Zhao J;Zhi X;Pan L;Zhou P

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A53T突变型α-突变体A53T-AS在路易小体内纤维聚集是帕金森氏症的症状之一。在体内抑制α-突触核蛋白(AS)的过度表达和纤维聚集可能是治疗帕金森病(PD)的一种有前途的策略。在本研究中,在低于1 mM的浓度下,海藻糖降低了转导PC12细胞中A53T-AS的表达水平。虽然过氧化氢和铝离子增加了A53T-AS在细胞中的表达水平和神经毒性,但适当的海藻糖浓度抑制了这一事件。这些研究充分证明,适当剂量的海藻糖可能对帕金森病的治疗有用。
Fibrillar accumulation of A53T mutant α-synuclein (A53T-AS) in Lewy bodies is a symptom of Parkinsonism. Inhibitions of the overexpression and fibrillar aggregation of α-synuclein (AS) in vivo could be a promising strategy for treating Parkinson’s disease (PD). In this study, at concentrations lower than 1 mM, trehalose decreased the A53T-AS expression level in transduced PC12 cells. Although H2O2 and aluminum ions increased the expression level and neurotoxicity of A53T-AS in cells, proper trehalose concentrations inhibited the event. These studies adequately prove that trehalose at an appropriate dose would be potentially useful for PD treatment.
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