Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation

In order to explore the effect of root-securing and brain-fortifying Liquid- (RSBFL-) mediated caveolin-1 (CAV-1) on phosphorylation of Tau protein and to uncover underlying mechanisms of RSBFL for the prevention and treatment of Alzheimer’s disease (AD), hippocampal neurons isolated from neonatal S...

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Main Authors: Depei Yuan, Chuhua Zeng, Qianfeng Chen, Fengjie Wang, Lin Yuan, Yaoqian Zhu, Ziyang Shu, Ning Chen
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Neurology Research International
Online Access:http://dx.doi.org/10.1155/2017/6248351
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author Depei Yuan
Chuhua Zeng
Qianfeng Chen
Fengjie Wang
Lin Yuan
Yaoqian Zhu
Ziyang Shu
Ning Chen
author_facet Depei Yuan
Chuhua Zeng
Qianfeng Chen
Fengjie Wang
Lin Yuan
Yaoqian Zhu
Ziyang Shu
Ning Chen
author_sort Depei Yuan
collection DOAJ
description In order to explore the effect of root-securing and brain-fortifying Liquid- (RSBFL-) mediated caveolin-1 (CAV-1) on phosphorylation of Tau protein and to uncover underlying mechanisms of RSBFL for the prevention and treatment of Alzheimer’s disease (AD), hippocampal neurons isolated from neonatal SD rats and cultured in DMEM-F12 medium were induced by exogenous Aβ1–42 to establish a cell model with AD. Meanwhile, pEGFP-C1-CAV1 and CAV1-shRNA plasmids were transfected into hippocampal neurons for CAV-1 overexpression and silence, respectively. The serum containing RSBFL was prepared for the intervention of AD model cells. The expression of CAV-1, GSK-3β, and p-Tau in normal hippocampal neurons and AD model cells in the presence of serum containing RSBFL was evaluated. The model hippocampal neurons with AD induced by Aβ1–42 revealed an obvious CAV-1 inhibition, enhanced GSK-3β activity, and abnormal Tau phosphorylation. In contrast, the treatment with serum containing RSBFL could upregulate CAV-1 in AD hippocampal neurons (P<0.05) with improved p-GSK-3βSer9 and reduced p-GSK-3βTyr216 (P<0.01), as well as suppressed abnormal phosphorylation of Tau protein. Therefore, RSBFL has an excellent protective effect on hippocampal neurons through increasing CAV-1 expression, inhibiting GSK-3β activity, and reducing excessive abnormal phosphorylation of Tau protein.
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spelling doaj-art-1fdddba0a45d4e4a8c8a16076dca7d702025-08-20T02:03:47ZengWileyNeurology Research International2090-18522090-18602017-01-01201710.1155/2017/62483516248351Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau PhosphorylationDepei Yuan0Chuhua Zeng1Qianfeng Chen2Fengjie Wang3Lin Yuan4Yaoqian Zhu5Ziyang Shu6Ning Chen7College of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaCollege of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaCollege of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaCollege of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaCollege of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaCollege of Medicine, Hubei University for Nationalities, Enshi 445000, ChinaTianjiu Research and Development Center for Exercise Nutrition and Foods, College of Health Science, Wuhan Sports University, Wuhan 430079, ChinaTianjiu Research and Development Center for Exercise Nutrition and Foods, College of Health Science, Wuhan Sports University, Wuhan 430079, ChinaIn order to explore the effect of root-securing and brain-fortifying Liquid- (RSBFL-) mediated caveolin-1 (CAV-1) on phosphorylation of Tau protein and to uncover underlying mechanisms of RSBFL for the prevention and treatment of Alzheimer’s disease (AD), hippocampal neurons isolated from neonatal SD rats and cultured in DMEM-F12 medium were induced by exogenous Aβ1–42 to establish a cell model with AD. Meanwhile, pEGFP-C1-CAV1 and CAV1-shRNA plasmids were transfected into hippocampal neurons for CAV-1 overexpression and silence, respectively. The serum containing RSBFL was prepared for the intervention of AD model cells. The expression of CAV-1, GSK-3β, and p-Tau in normal hippocampal neurons and AD model cells in the presence of serum containing RSBFL was evaluated. The model hippocampal neurons with AD induced by Aβ1–42 revealed an obvious CAV-1 inhibition, enhanced GSK-3β activity, and abnormal Tau phosphorylation. In contrast, the treatment with serum containing RSBFL could upregulate CAV-1 in AD hippocampal neurons (P<0.05) with improved p-GSK-3βSer9 and reduced p-GSK-3βTyr216 (P<0.01), as well as suppressed abnormal phosphorylation of Tau protein. Therefore, RSBFL has an excellent protective effect on hippocampal neurons through increasing CAV-1 expression, inhibiting GSK-3β activity, and reducing excessive abnormal phosphorylation of Tau protein.http://dx.doi.org/10.1155/2017/6248351
spellingShingle Depei Yuan
Chuhua Zeng
Qianfeng Chen
Fengjie Wang
Lin Yuan
Yaoqian Zhu
Ziyang Shu
Ning Chen
Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
Neurology Research International
title Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
title_full Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
title_fullStr Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
title_full_unstemmed Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
title_short Root-Securing and Brain-Fortifying Liquid Upregulates Caveolin-1 in Cell Model with Alzheimer’s Disease through Inhibiting Tau Phosphorylation
title_sort root securing and brain fortifying liquid upregulates caveolin 1 in cell model with alzheimer s disease through inhibiting tau phosphorylation
url http://dx.doi.org/10.1155/2017/6248351
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