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

被引：11

作者：

Malar, Dicson Sheeja ^{[1
]}

Prasanth, Mani Iyer ^{[1
]}

Jeyakumar, Mahalingam ^{[1
]}

Balamurugan, Krishnaswamy ^{[1
]}

Devi, Kasi Pandima ^{[1
]}

机构：

[1] Alagappa Univ, Dept Biotechnol, Sci Campus, Karaikkudi 630003, Tamil Nadu, India

来源：

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY | 2021年 / 35卷 / 01期

关键词：

A beta; Alzheimer's disease; C; elegans; dnj-14; vitexin; AMYLOID PEPTIDE; GREWIA-TILIAEFOLIA; INDUCED TOXICITY; LIFE-SPAN; EXPRESSION; STRESS; CELLS; PROTEOSTASIS; MECHANISMS; ISOVITEXIN;

D O I：

10.1002/jbt.22632

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 transgenicCaenorhabditis elegansstrain (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 mu M) significantly extended the lifespan of the nematodes. Vitexin-treated nematodes showed a significant reduction in the expression ofA beta, ace-1, andace-2genes when compared to control. Further, vitexin significantly upregulated the expression ofacr-8anddnj-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, andxbp-1) and suppress the expression of A beta. Overall, the results show that vitexin acts as a neuroprotective agent and protects transgenicC. elegansstrains from A beta proteotoxicity.

引用

页数：6

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