Monascin from Monascus-Fermented Products Reduces Oxidative Stress and Amyloid-β Toxicity via DAF-16/FOXO in Caenorhabditis elegans
Journal
Journal of Agricultural and Food Chemistry
Journal Volume
64
Journal Issue
38
Pages
7114-7120
Date Issued
2016
Author(s)
Abstract
Amyloid-β (Aβ)-induced oxidative stress and toxicity are leading risk factors for Alzheimer's disease (AD). Monascin (MS) is a novel compound proposed for antioxidative stress applications and is derived from an edible fungus secondary metabolite. This study assessed the effects of MS on oxidative stress, paralysis, Aβ accumulation, and lifespan in the nematode Caenorhabditis elegans and investigated its underlying mechanisms of action. The results showed that MS increased the survival of C. elegans under juglone-induced oxidative stress and attenuated endogenous levels of reactive oxygen species. Furthermore, MS induced a decline in Aβ-induced paralysis phenotype and Aβ deposits in the transgenic strains CL4176 and CL2006 of C. elegans, which expresses human muscle-specific Aβ1-42 in the cytoplasm of body wall muscle cells. In addition, mRNA levels of strain CL4176 of several antioxidant genes (sod-1, sod-2, sod-3, hsp16.2) and daf-16 were up-regulated by MS treatment when compared to the nontreated controls. Further evidence showed that MS treatment in C. elegans strains lacking DAF-16/FOXO did not affect paralysis or lifespan phenotypes. The findings indicate that MS reduces oxidative stress and Aβ toxicity via DAF-16 in C. elegans, suggesting that MS can be used for the prevention of AD-associated oxidative stress complications. ? 2016 American Chemical Society.
Subjects
Alzheimer's disease (AD); amyloid-β; Caenorhabditis elegans; DAF-16; fungus secondary metabolite; monascin; oxidative stress
SDGs
Other Subjects
Antioxidants; Cells; Cytology; Glycoproteins; Metabolites; Muscle; Neurodegenerative diseases; Plants (botany); Strain; Toxicity; Alzheimer's disease; Caenorhabditis elegans; DAF-16; Monascin; Secondary metabolites; Oxidative stress; amyloid beta protein; amyloid beta-protein (1-42); antioxidant; Caenorhabditis elegans protein; daf-16 protein, C elegans; forkhead transcription factor; fused heterocyclic rings; heat shock protein; hsp-16.2 protein, C elegans; manganese superoxide dismutase; messenger RNA; monascin; peptide fragment; reactive oxygen metabolite; Sod-1 protein, C elegans; Sod-3 protein, C elegans; superoxide dismutase; Alzheimer disease; animal; Caenorhabditis elegans; cytoplasm; drug effects; fermentation; genetics; metabolism; Monascus; oxidative stress; risk factor; transgenic animal; upregulation; Alzheimer Disease; Amyloid beta-Peptides; Animals; Animals, Genetically Modified; Antioxidants; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Cytoplasm; Fermentation; Forkhead Transcription Factors; Heat-Shock Proteins; Heterocyclic Compounds, 3-Ring; Monascus; Oxidative Stress; Peptide Fragments; Reactive Oxygen Species; Risk Factors; RNA, Messenger; Superoxide Dismutase; Up-Regulation
Type
journal article