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...
Guardado en:
Autores principales: | , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Taylor & Francis Group
2021
|
Materias: | |
Acceso en línea: | https://doaj.org/article/6e998041569946c7ad133b22a05cc7f2 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:6e998041569946c7ad133b22a05cc7f2 |
---|---|
record_format |
dspace |
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 |
work_keys_str_mv |
AT mayilatuerxun themolecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats AT ajarmuhda themolecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats AT lixinyin themolecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats AT mayilatuerxun molecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats AT ajarmuhda molecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats AT lixinyin molecularmechanismsofsignalpathwayactivatingeffectofe2f1nfkbgsk3boncognitivedysfunctionofalzheimerrats |
_version_ |
1718404998411321344 |