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Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways
Neuroinflammation, characterized marked by microglial activation, plays a very important role in the pathogenesis of Parkinson’s disease (PD). Upon activation, pro-inflammatory mediators are produced by microglia, triggering excessive inflammatory responses and ultimately damaging dopaminergic neuro...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877682/ https://www.ncbi.nlm.nih.gov/pubmed/29534526 http://dx.doi.org/10.3390/ijms19030821 |
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author | Chen, Guangxin Liu, Juxiong Jiang, Liqiang Ran, Xin He, Dewei Li, Yuhang Huang, Bingxu Wang, Wei Liu, Dianfeng Fu, Shoupeng |
author_facet | Chen, Guangxin Liu, Juxiong Jiang, Liqiang Ran, Xin He, Dewei Li, Yuhang Huang, Bingxu Wang, Wei Liu, Dianfeng Fu, Shoupeng |
author_sort | Chen, Guangxin |
collection | PubMed |
description | Neuroinflammation, characterized marked by microglial activation, plays a very important role in the pathogenesis of Parkinson’s disease (PD). Upon activation, pro-inflammatory mediators are produced by microglia, triggering excessive inflammatory responses and ultimately damaging dopaminergic neurons. Therefore, the identification of agents that inhibit neuroinflammation may be an effective approach for developing novel treatments for PD. In this study, we sought to investigate whether peiminine protects dopaminergic neurons by inhibiting neuroinflammation. We evaluated the effects of peiminine on behavioural dysfunction, microglial activation and the loss of dopaminergic neurons in a rat model of lipopolysaccharide (LPS)-induced PD. BV-2 cells were pretreated with peiminine for 1 h and then stimulated with LPS for different times. Then, inflammatory responses and the related signalling pathways were analysed. Peiminine markedly attenuated behavioural dysfunction and inhibited the loss of dopaminergic neurons and microglial activation in the LPS-induced PD rat model. In BV-2 cells, peiminine significantly decreased LPS-induced expression of the pro-inflammatory mediators TNF-α, IL-6 and IL-1β, COX-2 and iNOS by inhibiting the phosphorylation of ERK1/2, AKT and NF-κB p65. Based on these results demonstrated that peiminine has a role in protecting dopaminergic neurons in the LPS-induced PD rat model by inhibiting neuroinflammation. |
format | Online Article Text |
id | pubmed-5877682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-58776822018-04-09 Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways Chen, Guangxin Liu, Juxiong Jiang, Liqiang Ran, Xin He, Dewei Li, Yuhang Huang, Bingxu Wang, Wei Liu, Dianfeng Fu, Shoupeng Int J Mol Sci Article Neuroinflammation, characterized marked by microglial activation, plays a very important role in the pathogenesis of Parkinson’s disease (PD). Upon activation, pro-inflammatory mediators are produced by microglia, triggering excessive inflammatory responses and ultimately damaging dopaminergic neurons. Therefore, the identification of agents that inhibit neuroinflammation may be an effective approach for developing novel treatments for PD. In this study, we sought to investigate whether peiminine protects dopaminergic neurons by inhibiting neuroinflammation. We evaluated the effects of peiminine on behavioural dysfunction, microglial activation and the loss of dopaminergic neurons in a rat model of lipopolysaccharide (LPS)-induced PD. BV-2 cells were pretreated with peiminine for 1 h and then stimulated with LPS for different times. Then, inflammatory responses and the related signalling pathways were analysed. Peiminine markedly attenuated behavioural dysfunction and inhibited the loss of dopaminergic neurons and microglial activation in the LPS-induced PD rat model. In BV-2 cells, peiminine significantly decreased LPS-induced expression of the pro-inflammatory mediators TNF-α, IL-6 and IL-1β, COX-2 and iNOS by inhibiting the phosphorylation of ERK1/2, AKT and NF-κB p65. Based on these results demonstrated that peiminine has a role in protecting dopaminergic neurons in the LPS-induced PD rat model by inhibiting neuroinflammation. MDPI 2018-03-12 /pmc/articles/PMC5877682/ /pubmed/29534526 http://dx.doi.org/10.3390/ijms19030821 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Chen, Guangxin Liu, Juxiong Jiang, Liqiang Ran, Xin He, Dewei Li, Yuhang Huang, Bingxu Wang, Wei Liu, Dianfeng Fu, Shoupeng Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title | Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title_full | Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title_fullStr | Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title_full_unstemmed | Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title_short | Peiminine Protects Dopaminergic Neurons from Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways |
title_sort | peiminine protects dopaminergic neurons from inflammation-induced cell death by inhibiting the erk1/2 and nf-κb signalling pathways |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877682/ https://www.ncbi.nlm.nih.gov/pubmed/29534526 http://dx.doi.org/10.3390/ijms19030821 |
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