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Paraquat Treatment Compromises the Clearance of β-Amyloid and Tau Proteins and Induces Primary Hippocampal Neuronal Cell Death through HSP70, P20S, and TFEB Disruption
Chemical Research in Toxicology ( IF 3.7 ) Pub Date : 2020-11-06 , DOI: 10.1021/acs.chemrestox.0c00370
Paula Moyano 1 , Javier Sanjuna 1 , José Manuel Garcia 1 , Jimena Garcia 2 , María Teresa Frejo 1 , María Victoria Naval 3 , Javier Del Pino 1
Affiliation  

The herbicide paraquat (PQ) induces hippocampal neuronal cell loss and cognitive dysfunction after one and repeated treatment. All the mechanisms involved in these effects are not well understood. Single and repeated PQ treatment increased Aβ and tau protein levels, through HSP70 and TFEB downregulation and proteasome 20S inhibition, producing cell death in primary hippocampal neurons associated with cognitive decline. Our results reveal the mechanisms through which PQ could induce the accumulation of abnormal proteins and neurodegeneration that could originate the cognitive decline produced by it and could help managing its degenerative effects.

中文翻译:

百草枯治疗会影响 β-淀粉样蛋白和 Tau 蛋白的清除,并通过 HSP70、P20S 和 TFEB 破坏诱导原发性海马神经元细胞死亡

除草剂百草枯 (PQ) 在一次和重复治疗后会导致海马神经元细胞丢失和认知功能障碍。这些影响所涉及的所有机制尚不清楚。通过 HSP70 和 TFEB 下调以及蛋白酶体 20S 抑制,单次和重复 PQ 治疗增加了 Aβ 和 tau 蛋白水平,导致与认知能力下降相关的原代海马神经元细胞死亡。我们的研究结果揭示了 PQ 诱导异常蛋白质积累和神经退行性变的机制,这可能导致其产生的认知能力下降,并有助于管理其退行性影响。
更新日期:2020-11-06
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