The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats

Alzheimer disease (AD) seriously harms human health and its onset is insidious. Therefore, it is of great significance to find out the pathogenesis of AD disease for improving the prevention and treatment effect of the disease. The study drew attention to the influence of E2F-1/NF-κB/GSK-3β signalin...

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Autores principales: Mayila Tuerxun, Ajar Muhda, Lixin Yin
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Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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spelling oai:doaj.org-article:6e998041569946c7ad133b22a05cc7f22021-12-01T14:41:00ZThe molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats2165-59792165-598710.1080/21655979.2021.1989261https://doaj.org/article/6e998041569946c7ad133b22a05cc7f22021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1989261https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Alzheimer disease (AD) seriously harms human health and its onset is insidious. Therefore, it is of great significance to find out the pathogenesis of AD disease for improving the prevention and treatment effect of the disease. The study drew attention to the influence of E2F-1/NF-κB/GSK-3β signaling pathway on cognitive dysfunction of Alzheimer rats. 60 specific pathogen-free (SPF) SD rats were selected as research subjects. The, the AD model was created by injecting Aβ1-42 into hippocampus CA1 region of AD rats using a microscopic syringe. Besides, Morris water maze test and Western blot were performed to detect the cognitive function, the levels of destination protein and active oxidation products in the brain of rats. Compared to the Sham group, the escape latency and the distance of the model group significantly increased (P < 0.05), and the number of times to pass the target quadrant was significantly reduced (P < 0.05); the expression levels of E2F-1 and NF-κB protein in the hippocampus and the phosphorylation levels of Tau231, Tau262, Tau396, Tau404 and T216-GSK-3β protein of the model group were significantly increased (P < 0.05); the ROS/RNS value in the hippocampus of the model group significantly increased (P < 0.05). AD model rats exhibit obvious cognitive dysfunction, which is associated with the activation of E2F-1/NF-κB/GSK-3β signaling pathway and the heightened Tau protein phosphorylation level.Mayila TuerxunAjar MuhdaLixin YinTaylor & Francis Grouparticlealzheimer’s diseasecognitive learning abilitytau protein phosphorylatione2f-1/nf-κb/gsk-3β signaling pathwayBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 10000-10008 (2021)
institution DOAJ
collection DOAJ
language EN
topic alzheimer’s disease
cognitive learning ability
tau protein phosphorylation
e2f-1/nf-κb/gsk-3β signaling pathway
Biotechnology
TP248.13-248.65
spellingShingle alzheimer’s disease
cognitive learning ability
tau protein phosphorylation
e2f-1/nf-κb/gsk-3β signaling pathway
Biotechnology
TP248.13-248.65
Mayila Tuerxun
Ajar Muhda
Lixin Yin
The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
description Alzheimer disease (AD) seriously harms human health and its onset is insidious. Therefore, it is of great significance to find out the pathogenesis of AD disease for improving the prevention and treatment effect of the disease. The study drew attention to the influence of E2F-1/NF-κB/GSK-3β signaling pathway on cognitive dysfunction of Alzheimer rats. 60 specific pathogen-free (SPF) SD rats were selected as research subjects. The, the AD model was created by injecting Aβ1-42 into hippocampus CA1 region of AD rats using a microscopic syringe. Besides, Morris water maze test and Western blot were performed to detect the cognitive function, the levels of destination protein and active oxidation products in the brain of rats. Compared to the Sham group, the escape latency and the distance of the model group significantly increased (P < 0.05), and the number of times to pass the target quadrant was significantly reduced (P < 0.05); the expression levels of E2F-1 and NF-κB protein in the hippocampus and the phosphorylation levels of Tau231, Tau262, Tau396, Tau404 and T216-GSK-3β protein of the model group were significantly increased (P < 0.05); the ROS/RNS value in the hippocampus of the model group significantly increased (P < 0.05). AD model rats exhibit obvious cognitive dysfunction, which is associated with the activation of E2F-1/NF-κB/GSK-3β signaling pathway and the heightened Tau protein phosphorylation level.
format article
author Mayila Tuerxun
Ajar Muhda
Lixin Yin
author_facet Mayila Tuerxun
Ajar Muhda
Lixin Yin
author_sort Mayila Tuerxun
title The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
title_short The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
title_full The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
title_fullStr The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
title_full_unstemmed The molecular mechanisms of signal pathway activating effect of E2F-1/NF-κB/GSK-3β on cognitive dysfunction of Alzheimer rats
title_sort molecular mechanisms of signal pathway activating effect of e2f-1/nf-κb/gsk-3β on cognitive dysfunction of alzheimer rats
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/6e998041569946c7ad133b22a05cc7f2
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