Neuroprotective and Therapeutic Effects of Tocovid and Twendee-X on Aβ Oligomer-Induced Damage in the SH-SY5Y Cell Line

Neurodegenerative Diseases

Hu X. · Yamashita T. · Yu H. · Bian Z. · Hu X. · Feng T. · Tadokoro K. · Morihara R. · Abe K.

Author affiliations

Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan

Log in to MyKarger to check if you already have access to this content.

Buy FullText & PDF Unlimited re-access via MyKarger Unrestricted printing, no saving restrictions for personal use
read more

CHF 38.00 *
EUR 35.00 *
USD 39.00 *

Select

KAB

Buy a Karger Article Bundle (KAB) and profit from a discount!

If you would like to redeem your KAB credit, please log in.

Save over 20% compared to the individual article price.

Learn more

Rent/Cloud Rent for 48h to view Buy Cloud Access for unlimited viewing via different devices Synchronizing in the ReadCube Cloud Printing and saving restrictions apply Rental: USD 8.50
Cloud: USD 20.00

Select

Subscribe Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use read more

Subcription rates

Select

* The final prices may differ from the prices shown due to specifics of VAT rules.

Article / Publication Details

First-Page Preview

Abstract of Research Article

Received: October 28, 2021
Accepted: March 06, 2022
Published online: March 10, 2022

Number of Print Pages: 9
Number of Figures: 5
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: https://www.karger.com/NDD

Abstract

Background: Alzheimer’s disease (AD) is the most frequent cause of dementia among the elderly. The accumulation of amyloid beta (Aβ) and its downstream pathological events such as oxidative stress play central roles in AD. Recent studies revealed that Aβ oligomer (AβO)-induced strong neurotoxicity in SH-SY5Y cells via the induction of oxidative stress. Objective: In the present study, we investigated the effect of two antioxidants, Tocovid and Twendee-X, on AβO-induced SH-SY5Y cell damage. Methods: AβOs (2.5 μM) were applied to induce cellular damage in the SH-SY5Y cell line. Cell viability following AβO toxicity, Tau protein phosphorylation, cell morphology, and intracellular reactive oxygen species were assayed with or without different concentrations of Tocovid or Twendee-X. Results: Tocovid (60 μg/mL) and Twendee-X (150 μg/mL) significantly recovered cell viability from AβO toxicity (**p < 0.01, vs. control), attenuated Tau protein phosphorylation (**p < 0.01, vs. AβOs), improved cell morphology (**p < 0.01, vs. AβOs), and suppressed intracellular ROS (**p < 0.01, vs. AβOs) in SH-SY5Y cells. Conclusion: These findings suggest the neuroprotective and therapeutic potential of Tocovid and Twendee-X for AD treatment.

© 2022 S. Karger AG, Basel

References Briggs R, Kennelly SP, O’Neill D. Drug treatments in Alzheimer’s disease. Clin Med. 2016 Jun;16(3):247–53. Hishikawa N, Fukui Y, Sato K, Kono S, Yamashita T, Ohta Y, et al. Characteristic features of cognitive, affective and daily living functions of late-elderly dementia. Geriatr Gerontol Int. 2016 Apr;16(4):458–65. Jiao SS, Yao XQ, Liu YH, Wang QH, Zeng F, Lu JJ, et al. Edaravone alleviates Alzheimer’s disease-type pathologies and cognitive deficits. Proc Natl Acad Sci USA. 2015 Apr;112(16):5225–30. Cheignon C, Tomas M, Bonnefont-Rousselot D, Faller P, Hureau C, Collin F. Oxidative stress and the amyloid beta peptide in Alzheimer’s disease. Redox Biol. 2018 Apr;14:450–64. Zhang L, Guo Y, Wang H, Zhao LL, Ma ZL, Li T, et al. Edaravone reduces Aβ-induced oxidative damage in SH-SY5Y cells by activating the Nrf2/ARE signaling pathway. Life Sci. 2019 Mar 15;221:259–66. De Medeiros LM, De Bastiani MA, Rico EP, Schonhofen P, Pfaffenseller B, Wollenhaupt-Aguiar B, et al. Cholinergic differentiation of human neuroblastoma SH-SY5Y cell line and its potential use as an in vitro model for Alzheimer’s disease studies. Mol Neurobiol. 2019 Nov;56(11):7355–67. Reiss AB, Arain HA, Stecker MM, Siegart NM, Kasselman LJ. Amyloid toxicity in Alzheimer’s disease. Rev Neurosci. 2018 Aug;29(6):613–27. Yasumoto T, Takamura Y, Tsuji M, Watanabe-Nakayama T, Imamura K, Inoue H, et al. High molecular weight amyloid β1-42 oligomers induce neurotoxicity via plasma membrane damage. FASEB J. 2019 Aug;33(8):9220–34. Liu Z, Li T, Li P, Wei NN, Zhao ZQ, Liang HM, et al. The ambiguous relationship of oxidative stress, Tau hyperphosphorylation, and autophagy dysfunction in Alzheimer’s disease. Oxid Med Cell Longev. 2015;2015:352723. Tönnies E, Trushina E. Oxidative stress, synaptic dysfunction, and Alzheimer’s disease. J Alzheimers Dis. 2017;57(4):1105–21. Kusaki M, Ohta Y, Inufusa H, Yamashita T, Morihara R, Nakano Y, et al. Neuroprotective effects of a novel anti-oxidant mixture Twendee X in mouse stroke model. J Stroke Cerebrovasc Dis. 2017 Jun;26(6):1191–6. Shang J, Yan H, Jiao Y, Ohta Y, Liu X, Li XH, et al. Therapeutic effects of pretreatment with Tocovid on oxidative stress in postischemic mice brain. J Stroke Cerebrovasc Dis. 2018 Aug;27(8):2096–105. Jiao Y, Shang J, Ohta Y, Yan HJ, Liu X, Li XH, et al. Neuroprotective effects of Tocovid pretreatment in a mouse stroke model. J Stroke Cerebrovasc Dis. 2018 Aug;27(8):2166–74. Liu X, Yamashita T, Shang J, Shi XW, Morihara R, Huang Y, et al. Twendee X ameliorates phosphorylated Tau, α-Synuclein and neurovascular dysfunction in Alzheimer’s disease transgenic mice with chronic cerebral hypoperfusion. J Stroke Cerebrovasc Dis. 2019 Oct;28(10):104310. Herzer S, Meldner S, Rehder K, Gröne HJ, Nordström V. Lipid microdomain modification sustains neuronal viability in models of Alzheimer’s disease. Acta Neuropathol Commun. 2016 Sep 17;4(1):103. Wen J, Fang F, Guo SH, Zhang Y, Peng XL, Sun WM, et al. Amyloid β-derived diffusible ligands (ADDLs) induce abnormal autophagy associated with Aβ aggregation degree. J Mol Neurosci. 2018 Feb;64(2):162–74. Coullery RP, Ferrari ME, Rosso SB. Neuronal development and axon growth are altered by glyphosate through a WNT non-canonical signaling pathway. Neurotoxicology. 2016 Jan;52:150–61. Kamat PK, Kalani A, Rai S, Swarnkar S, Tota S, Nath C, et al. Mechanism of oxidative stress and synapse dysfunction in the pathogenesis of Alzheimer’s disease: understanding the therapeutics strategies. Mol Neurobiol. 2016 Jan;53(1):648–61. Martínez MA, Rodríguez JL, Lopez-Torres B, Martínez M, Martínez-Larrañaga MR, Maximiliano JE, et al. Use of human neuroblastoma SH-SY5Y cells to evaluate glyphosate-induced effects on oxidative stress, neuronal development and cell death signaling pathways. Environ Int. 2020 Feb;135:105414. Feng T, Yamashita T, Tsunoda K, Matsumoto N, Tadokoro K, Sasaki R, et al. In vitro free radical scavenging activities of dietary supplements by electron spin resonance. Brain Supplement. 2020;2:1–12. Abe K, Kogure K, Arai H, Nakano M. Ascorbate induced lipid peroxidation results in loss of receptor binding in tris, but not in phosphate, buffer. Implications for the involvement of metal ions. Biochem Int. 1985 Sep;11(3):341–8. Chakraborty A, Jana NR. Vitamin C-conjugated nanoparticle protects cells from oxidative stress at low doses but induces oxidative stress and cell death at high doses. ACS Appl Mater Interfaces. 2017 Dec;9(48):41807–17. Kaźmierczak-Barańska J, Boguszewska K, Adamus-Grabicka A, Karwowski BT. Two faces of vitamin C-antioxidative and pro-oxidative agent. Nutrients. 2020 May;12(5):1501. Neddens J, Temmel M, Flunkert S, Kerschbaumer B, Hoeller C, Loeffler T, et al. Phosphorylation of different tau sites during progression of Alzheimer’s disease. Acta Neuropathol Commun. 2018 Jun;6(1):52. Barthélemy NR, Bateman RJ, Hirtz C, Marin P, Becher F, Sato C, et al. Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer’s disease and PET amyloid-positive patient identification. Alzheimers Res Ther. 2020 Mar;12(1):26. Article / Publication Details

First-Page Preview

Abstract of Research Article

Received: October 28, 2021
Accepted: March 06, 2022
Published online: March 10, 2022

Number of Print Pages: 9
Number of Figures: 5
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: https://www.karger.com/NDD

Copyright / Drug Dosage / Disclaimer Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

留言 (0)

沒有登入
gif