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A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway

INTRODUCTION: The pathology of Alzheimer’s disease (AD) includes β-amyloid (Aβ) (plaques) and neurofibrillary tangles (NFTs). This study aimed to explore the efficacy of Huatuo Zaizao pill (HTZP) in an AD mouse model induced by injecting Aβ(1-42), and the neuroprotective mechanism of HTZP in AD. MAT...

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Autores principales: Jiang, Su, Yu, Lin-Jie, Yang, Hui, Jin, Yuexinzi, Chen, Jian, Zhang, Jing-Hua, Liu, Ying, Xu, Yun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408018/
https://www.ncbi.nlm.nih.gov/pubmed/37560736
http://dx.doi.org/10.5114/aoms.2020.99427
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author Jiang, Su
Yu, Lin-Jie
Yang, Hui
Jin, Yuexinzi
Chen, Jian
Zhang, Jing-Hua
Liu, Ying
Xu, Yun
author_facet Jiang, Su
Yu, Lin-Jie
Yang, Hui
Jin, Yuexinzi
Chen, Jian
Zhang, Jing-Hua
Liu, Ying
Xu, Yun
author_sort Jiang, Su
collection PubMed
description INTRODUCTION: The pathology of Alzheimer’s disease (AD) includes β-amyloid (Aβ) (plaques) and neurofibrillary tangles (NFTs). This study aimed to explore the efficacy of Huatuo Zaizao pill (HTZP) in an AD mouse model induced by injecting Aβ(1-42), and the neuroprotective mechanism of HTZP in AD. MATERIAL AND METHODS: C57BL/6 (B6) mice were randomly divided into 4 groups (n = 10, per group): control group, AD model group, and 2 different doses of HTZP treated groups. The Morris water maze test was carried out on AD mice to assess the learning ability after treatment with HTZP for 15 day. The levels of inflammatory factors and the nuclear factor-κB (NF-κB) pathway were examined by western blot and real-time polymerase chain reaction (PCR). The content of microglia was investigated by immunofluorescence. RESULTS: This study revealed that a cognitive disorder could be mitigated when the AD mice were treated with HTZP, which might be associated with the decreased level of pro-inflammatory factors, and the inhibitory activities of microglia. Additionally, phosphorylation of IκB and NF-κB p65 could be reduced by prohibiting the neuroinflammation of NF-κB activation in the hippocampus of AD mice. CONCLUSIONS: These results showed that HTZP could mitigate a cognitive disorder, diminish the activation of microglia, and inhibit the content of inflammatory factors through the NF-κB pathway in Aβ(1-42)-induced AD mice. HTZP may be an appropriate agent for AD treatment in the future.
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spelling pubmed-104080182023-08-09 A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway Jiang, Su Yu, Lin-Jie Yang, Hui Jin, Yuexinzi Chen, Jian Zhang, Jing-Hua Liu, Ying Xu, Yun Arch Med Sci Experimental Research INTRODUCTION: The pathology of Alzheimer’s disease (AD) includes β-amyloid (Aβ) (plaques) and neurofibrillary tangles (NFTs). This study aimed to explore the efficacy of Huatuo Zaizao pill (HTZP) in an AD mouse model induced by injecting Aβ(1-42), and the neuroprotective mechanism of HTZP in AD. MATERIAL AND METHODS: C57BL/6 (B6) mice were randomly divided into 4 groups (n = 10, per group): control group, AD model group, and 2 different doses of HTZP treated groups. The Morris water maze test was carried out on AD mice to assess the learning ability after treatment with HTZP for 15 day. The levels of inflammatory factors and the nuclear factor-κB (NF-κB) pathway were examined by western blot and real-time polymerase chain reaction (PCR). The content of microglia was investigated by immunofluorescence. RESULTS: This study revealed that a cognitive disorder could be mitigated when the AD mice were treated with HTZP, which might be associated with the decreased level of pro-inflammatory factors, and the inhibitory activities of microglia. Additionally, phosphorylation of IκB and NF-κB p65 could be reduced by prohibiting the neuroinflammation of NF-κB activation in the hippocampus of AD mice. CONCLUSIONS: These results showed that HTZP could mitigate a cognitive disorder, diminish the activation of microglia, and inhibit the content of inflammatory factors through the NF-κB pathway in Aβ(1-42)-induced AD mice. HTZP may be an appropriate agent for AD treatment in the future. Termedia Publishing House 2020-10-21 /pmc/articles/PMC10408018/ /pubmed/37560736 http://dx.doi.org/10.5114/aoms.2020.99427 Text en Copyright: © 2020 Termedia & Banach https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Experimental Research
Jiang, Su
Yu, Lin-Jie
Yang, Hui
Jin, Yuexinzi
Chen, Jian
Zhang, Jing-Hua
Liu, Ying
Xu, Yun
A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title_full A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title_fullStr A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title_full_unstemmed A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title_short A study on inhibition of the Aβ(1-42)-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
title_sort study on inhibition of the aβ(1-42)-induced inflammatory response by the huatuo zaizao pill through the nf-κb signaling pathway
topic Experimental Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408018/
https://www.ncbi.nlm.nih.gov/pubmed/37560736
http://dx.doi.org/10.5114/aoms.2020.99427
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