Vitexin prevents Aβ proteotoxicity in transgenic Caenorhabditis elegans model of Alzheimer's disease by modulating unfolded protein response

• Published in: Journal of biochemical and molecular toxicology Vol. 35; no. 1; pp. e22632 - n/a
• Main Authors: Malar, Dicson Sheeja, Prasanth, Mani Iyer, Jeyakumar, Mahalingam, Balamurugan, Krishnaswamy, Devi, Kasi Pandima
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.01.2021
• Subjects: Alzheimer's disease; C. elegans; Caenorhabditis elegans; Dementia disorders; dnj‐14; Flavone glycosides; Genes; Life span; Nematodes; Neurodegenerative diseases; Neuroprotection; Paralysis; Physiological effects; Polymerase chain reaction; Protein folding; Proteins; vitexin; Western blotting; Worms; Aβ; C. elegans; dnj-14; Alzheimer's disease; vitexin
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.22632

Alzheimer's disease (AD) accounts for an estimated 60% to 80% of all dementia cases. The present study is aimed at evaluating the neuroprotective efficacy of vitexin, an apigenin flavone glycoside using transgenic Caenorhabditis elegans strain (CL2006) of AD. The neuroprotective effect of vitexin was determined using physiological assays, quantitative polymerase chain reaction, and Western blotting. The results of survival and paralysis assay indicate that vitexin (200 μM) significantly extended the lifespan of the nematodes. Vitexin‐treated nematodes showed a significant reduction in the expression of Aβ, ace‐1, and ace‐2 genes when compared to control. Further, vitexin significantly upregulated the expression of acr‐8 and dnj‐14, and increased the lifespan of the nematodes. Vitexin was also found to modulate the unfolded protein response genes (hsp‐4, pek‐1, ire‐1, and xbp‐1) and suppress the expression of Aβ. Overall, the results show that vitexin acts as a neuroprotective agent and protects transgenic C. elegans strains from Aβ proteotoxicity.