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Peptides of corn oligopeptides improve Aβ1‐42‐injured SHSY5Y cells

寡肽 化学 食品科学 生物化学
作者
Han–Shuo Wu,Rui Liu,Xinxue Zhang,Hualei Wang,Ganlu Meng,Jie Ren,Wenying Liu,Shuguo Li
出处
期刊:Journal of the Science of Food and Agriculture [Wiley]
卷期号:105 (11): 5738-5750
标识
DOI:10.1002/jsfa.14307
摘要

Abstract BACKGROUND There are more and more Alzheimer's patients. The formation of plaques of A β 1‐42 in the brain is one of the main causes of Alzheimer's disease. Corn oligopeptides have natural antioxidant effects. It is aimed to develop functional corn oligopeptides to prevent Alzheimer's disease through antioxidation. METHODS According to previous laboratory studies, peptides of corn oligopeptides were screened by biological activity score and ADMET prediction, and molecular docking technology was used to screen the peptides that had high binding energy with A β 1‐42 . The protective effects of the selected peptides were evaluated against oxidative stress in A β 1‐42 ‐injured SHSY5Y cells, and the mechanism of the effects in the protein kinase A (PKA)/cAMP‐response element binding protein (CREB)/brain‐derived neurotrophic factor (BDNF)‐mediated signaling pathway was investigated, which is closely related to neurodegenerative and neurological diseases. RESULTS The results showed that three peptides (GL, FA and FQ) significantly increased the cell viability of A β 1‐42 ‐induced cells and mitochondrial intensity and decreased extracellular lactate dehydrogenase content. They also improved intracellular oxidative stress caused by A β 1‐42 , including reducing the overproduction of intracellular reactive oxygen species, and increasing the content of lipid oxidation, superoxide dismutase and glutathione peroxidase. In addition, western blot showed that treatment with GL, FA and FQ significantly increased the expression of PKA, CREB and BDNF, whereas cells injured with A β 1‐42 decreased the expression of these signaling proteins. CONCLUSION These results suggest that peptides of corn oligopeptides can effectively improve A β 1‐42 ‐induced Alzheimer's disease, and may improve oxidative stress response to protective nerve cells by up‐regulating the protein expression of the PKA/CREB/BDNF signaling pathway. © 2025 Society of Chemical Industry.

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