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

被引：12

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

共 39 条

[1] Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases [J].

Alexander, Adanna G. ;

Marfil, Vanessa ;

Li, Chris .

FRONTIERS IN GENETICS, 2014, 5

[2]

BRENNER S, 1974, GENETICS, V77, P71

[3] Antibody-free quantification of seven tau peptides in human CSF using targeted mass spectrometry [J].

Bros, Pauline ;

Vialaret, Jerome ;

Barthelemy, Nicolas ;

Delatour, Vincent ;

Gabelle, Audrey ;

Lehmann, Sylvain ;

Hirtz, Christophe .

FRONTIERS IN NEUROSCIENCE, 2015, 9

[4] The ER stress factor XBP1s prevents amyloid-β neurotoxicity [J].

Casas-Tinto, Sergio ;

Zhang, Yan ;

Sanchez-Garcia, Jonatan ;

Gomez-Velazquez, Melisa ;

Rincon-Limas, Diego E. ;

Fernandez-Funez, Pedro .

HUMAN MOLECULAR GENETICS, 2011, 20 (11) :2144-2160

[5] Vitexin and isovitexin from the Leaves of Ficus deltoidea with in-vivo α-glucosidase inhibition [J].

Choo, C. Y. ;

Sulong, N. Y. ;

Man, F. ;

Wong, T. W. .

JOURNAL OF ETHNOPHARMACOLOGY, 2012, 142 (03) :776-781

[6] Molecular mechanisms of neurodegeneration in Alzheimer's disease [J].

Crews, Leslie ;

Masliah, Eliezer .

HUMAN MOLECULAR GENETICS, 2010, 19 :R12-R20

[7] Oleuropein Aglycone Protects Transgenic C. elegans Strains Expressing Aβ42 by Reducing Plaque Load and Motor Deficit [J].

Diomede, Luisa ;

Rigacci, Stefania ;

Romeo, Margherita ;

Stefani, Massimo ;

Salmona, Mario .

PLOS ONE, 2013, 8 (03)

[8] Cardioprotection of Vitexin on Myocardial Ischemia/Reperfusion Injury in Rat via Regulating Inflammatory Cytokines and MAPK Pathway [J].

Dong, Liu-Yi ;

Li, Sheng ;

Zhen, Yi-Lan ;

Wang, Ya-Nan ;

Shao, Xu ;

Luo, Zhi-Gang .

AMERICAN JOURNAL OF CHINESE MEDICINE, 2013, 41 (06) :1251-1266

[9] Genetic Mechanisms of Coffee Extract Protection in a Caenorhabditis elegans Model of β-Amyloid Peptide Toxicity [J].

Dostal, Vishantie ;

Roberts, Christine M. ;

Link, Christopher D. .

GENETICS, 2010, 186 (03) :857-U163

[10] Free radical scavenging and antioxidant activities of flavonoids extracted from the radix of Scutellaria baicalensis Georgi [J].

Gao, ZH ;

Huang, KX ;

Yang, XL ;

Xu, HB .

BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 1999, 1472 (03) :643-650

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