突触蛋白I
突触可塑性
长时程增强
突触素
细胞生物学
生物
脑源性神经营养因子
SIRT3
化学
神经营养因子
神经科学
生物化学
突触小泡
锡尔图因
乙酰化
免疫学
小泡
受体
免疫组织化学
基因
膜
作者
Hongyan Lu,Fang Li,Ji Wang,Fanrui Zhao,Chunlei Liu,Yawen Gao,Jingsheng Liu,Weihong Min
出处
期刊:Food & Function
[Royal Society of Chemistry]
日期:2021-01-01
卷期号:12 (17): 8026-8036
被引量:43
摘要
-induced PC12 cell model, treatment with mitochondrial sirtuin 3 (SIRT3) inhibitor and inducer molecules confirmed that the <3 kDa fraction and WYPGK activated SIRT3, leading to the decrease in Ace-SOD2 acetylation and increasing the expression of SYP, SYN-1, SNAP25, and PSD95, thus enhancing synaptic plasticity. The <3 kDa fraction and WYPGK also activated the ERK/CREB pathway and upregulated the expression of brain-derived neurotrophic factor. Our results show that fraction <3 kDa and WYPGK improve learning and memory ability through SIRT3-induced synaptic plasticity in vitro and in vivo.
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