Neurochemical Research of LOXBlock-1 and ZnSO4 against Neurodegenerative Damage Induced by Amyloid Beta(1-42)

Küçük Resim Yok

Tarih

2024

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

Springernature

Erişim Hakkı

info:eu-repo/semantics/closedAccess

Özet

Synaptosomes offer an intriguing ex vivo model system for investigating the molecular mechanisms of neurodegenerative processes. Lipoxygenases significantly affect the course of neurodegenerative diseases. Homeostasis of trace elements such as zinc is necessary for the continuity of brain functions. In this study, we purpose to determine whether LOXBlock-1, a 12/15 lipoxygenase inhibitor, and zinc sulfate (ZnSO4) provide any biochemical protection during neurodegenerative damage in synaptosomes induced by amyloid beta 1-42 (A beta 1-42). In this study, animals (30 Wistar Albino male rats 30) were divided into 5 groups (6 animals in each group): Control, 10 mu M A beta 1-42, 10 mu M A beta 1-42+25mM LOXBlock-1, 10 mu M A beta 1-42+10 mu M ZnSO4, and 10 mu M A beta 1-42+25mM LOXBlock-1+10 mu M ZnSO4. Synaptosomes were isolated from the rat cerebral cortex. Following, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, malondialdehyde (MDA) levels, adenosine deaminase (ADA) levels, reduced-glutathione (GSH) levels, neuronal nitric oxide synthase (nNOS) levels, acetylcholinesterase (AChE) activity, catalase (CAT) activity, and 8-OHdG levels in synaptosomes were detected according to the ELISA method. ADA and AChE expression and protein levels were analyzed. MDA, nNOS, AChE, and 8-OHdG levels in synaptosomes treated with A beta 1-42 resulted in an increase, while there was a decrease in ADA, GSH, and CAT levels (p<0.001 vs. control). Conversely, LOXBlock-1 and ZnSO4 treatments in synaptosomes treated with A beta 1-42 decreased MDA, nNOS, AChE, and 8-OHdG levels, while ADA, GSH, and CAT levels increased. Moreover, the most effective improvement was seen in the co-treatment group of LOXBlock-1 and ZnSO4. Our data showed that LOXBlock-1 and ZnSO4 co-treatment may protect against A beta 1-42 exposure in rat brain synaptosomes.

Açıklama

Anahtar Kelimeler

Alzheimer's diseases, LOXBlock-1, Nitrosative stress, Oxidative stress, Synaptosome, Zinc sulfate, Alzheimers-Disease, Oxidative Stress, Memory Deficits, A-Beta, Brain, Zinc, Tau, 12/15-Lipoxygenase, Dysfunction, Inhibition

Kaynak

Biological Trace Element Research

WoS Q Değeri

Q2

Scopus Q Değeri

Q1

Cilt

202

Sayı

7

Künye