Evaluation of the effects of herpes simplex glycoprotein B on complement system and cytokines in in vitro models of Alzheimer's disease.

Autor: Yirün A; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.; Department of Pharmaceutical Toxicology, Cukurova University Faculty of Pharmacy, Adana, Turkey., Çakır DA; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.; Department of Vaccine Technology, Hacettepe University Vaccine Institute, Ankara, Turkey., Sanajou S; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey., Erdemli Köse SB; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.; Department of Chemistry, Burdur Mehmet Akif Ersoy University Faculty of Arts and Sciences, Burdur, Turkey., Özyurt AB; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.; Department of Pharmaceutical Toxicology, Bahçeşehir University Faculty of Pharmacy, İstanbul, Turkey., Zeybek D; Department of Histology and Embryology, Hacettepe University Faulty of Medicine, Ankara, Turkey., Bozdemir Ö; Department of Histology and Embryology, Hacettepe University Faulty of Medicine, Ankara, Turkey., Baydar T; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey., Erkekoglu P; Department of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.; Department of Vaccine Technology, Hacettepe University Vaccine Institute, Ankara, Turkey.
Jazyk: angličtina
Zdroj: Journal of applied toxicology : JAT [J Appl Toxicol] 2023 Sep; Vol. 43 (9), pp. 1368-1378. Date of Electronic Publication: 2023 Apr 06.
DOI: 10.1002/jat.4471
Abstrakt: Alzheimer's disease (AD) is a neurodegenerative disorder that causes memory loss and dementia and is characterized by a decline in cognitive functions. Brain infections, especially induced by herpes simplex virus type-1 (HSV-1), are suggested to play a key role in the pathogenesis of AD. Within the scope of this study, two different AD models (Tau model and amyloid beta [Aβ]) were created in the SH-SY5Y cell line, and HSV glycoprotein B (gB) was applied to the cell line and on the generated AD models. Study groups (n = 3) were designed as (1) control, (2) HSV-gB group, (3) retinoic acid (RA) and brain derived neurotrophic factor (BDNF) induced Alzheimer's model (AD), (4) RA and BDNF induced Alzheimer's model + HSV-gB (ADH), (5) Aβ 1-42 peptide-induced Alzheimer's model (Aβ), and (6) Aβ 1-42 peptide-induced Alzheimer's model + HSV-gB (AβH). Levels of complement proteins and cytokines were determined comparatively. In addition, specific markers of AD (hyperphosphorylated Tau proteins, Aβ 1-40 peptide and amyloid precursor protein) were measured in all groups. HSV-gB administration was found to increase Aβ and hyperphosphorylated Tau levels, similar to AD models. In addition, our data confirmed that the immune system and chronic inflammation might have a crucial role in AD development and that HSV-1 infection might also be an underlying factor of AD.
(© 2023 John Wiley & Sons Ltd.)
Databáze: MEDLINE
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