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Abstract Title:

Ferulic acid delayed amyloidβ-induced pathological symptoms by autophagy pathway via a fasting-like effect in Caenorhabditis elegans.

Abstract Source:

Food Chem Toxicol. 2020 Oct 9:111808. Epub 2020 Oct 9. PMID: 33045309

Abstract Author(s):

Ningbo Wang, Yongtao Zhou, Longhe Zhao, Caiding Wang, Wuli Ma, Guangfei Ge, Yu Wang, Inam Ullah, Fahim Muhammad, Dhafer Alwayli, Dejuan Zhi, Hongyu Li

Article Affiliation:

Ningbo Wang

Abstract:

The amyloidβ (Aβ) generation or aggregation plays a crucial role in Alzheimer's disease (AD). Autophagy agonists, which function as the clearance of Aβ, could be the potential drug candidates against AD. In staple food crops, ferulic acid (FA) is an enormously copious and almost ubiquitous phenolic antioxidant. In the present study, FA significantly inhibited Aβ-induced pathological symptoms of paralysis and hypersensitivity to exogenous serotonin, meanwhile restrained Aβ monomers, oligomers, and deposits in AD C. elegans. FA increased the expression of autophagy reporter LGG-1 and enhanced autophagy flux. However, the autophagy inhibitors abolished the restrictive action of FA on the worm paralysis phenotype. According to these results, FA triggered autophagy and ameliorated Aβ-induced pathological symptoms by the autophagy pathway. Moreover, FA activated the HLH-30 transcription factor to nuclear localization, which acts upstream of autophagy in fasted animals, reduced the level of lipids, but affected nor the growth of E.coli OP50, neither animal food intake behavior. These suggest that FA induced a fasting-like effect to activate the autophagy pathway. Additionally, FA ameliorated poly Q aggregations in Huntington's disease worm. Thus, FA could not only affect AD, broadly but also neurodegenerative diseases characterized by misfolded or aggregated proteins.

Study Type : Animal Study

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