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Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway

Neuroinflammation plays a very important role in the pathogenesis of Parkinson’s disease (PD). After activation, microglia produce pro-inflammatory mediators that damage surrounding neurons. Consequently, the inhibition of microglial activation might represent a new therapeutic approach of PD. Vanil...

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Autores principales: Yan, Xuan, Liu, Dian-Feng, Zhang, Xiang-Yang, Liu, Dong, Xu, Shi-Yao, Chen, Guang-Xin, Huang, Bing-Xu, Ren, Wen-Zhi, Wang, Wei, Fu, Shou-Peng, Liu, Ju-Xiong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343924/
https://www.ncbi.nlm.nih.gov/pubmed/28208679
http://dx.doi.org/10.3390/ijms18020389
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author Yan, Xuan
Liu, Dian-Feng
Zhang, Xiang-Yang
Liu, Dong
Xu, Shi-Yao
Chen, Guang-Xin
Huang, Bing-Xu
Ren, Wen-Zhi
Wang, Wei
Fu, Shou-Peng
Liu, Ju-Xiong
author_facet Yan, Xuan
Liu, Dian-Feng
Zhang, Xiang-Yang
Liu, Dong
Xu, Shi-Yao
Chen, Guang-Xin
Huang, Bing-Xu
Ren, Wen-Zhi
Wang, Wei
Fu, Shou-Peng
Liu, Ju-Xiong
author_sort Yan, Xuan
collection PubMed
description Neuroinflammation plays a very important role in the pathogenesis of Parkinson’s disease (PD). After activation, microglia produce pro-inflammatory mediators that damage surrounding neurons. Consequently, the inhibition of microglial activation might represent a new therapeutic approach of PD. Vanillin has been shown to protect dopaminergic neurons, but the mechanism is still unclear. Herein, we further study the underlying mechanisms in lipopolysaccharide (LPS)-induced PD models. In vivo, we firstly established rat models of PD by unilateral injection of LPS into substantia nigra (SN), and then examined the role of vanillin in motor dysfunction, microglial activation and degeneration of dopaminergic neurons. In vitro, murine microglial BV-2 cells were treated with vanillin prior to the incubation of LPS, and then the inflammatory responses and the related signaling pathways were analyzed. The in vivo results showed that vanillin markedly improved the motor dysfunction, suppressed degeneration of dopaminergic neurons and inhibited microglial over-activation induced by LPS intranigral injection. The in vitro studies demonstrated that vanillin reduces LPS-induced expression of inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2), IL-1β, and IL-6 through regulating ERK1/2, p38 and NF-κB signaling. Collectively, these data indicated that vanillin has a role in protecting dopaminergic neurons via inhibiting inflammatory activation.
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spelling pubmed-53439242017-03-16 Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway Yan, Xuan Liu, Dian-Feng Zhang, Xiang-Yang Liu, Dong Xu, Shi-Yao Chen, Guang-Xin Huang, Bing-Xu Ren, Wen-Zhi Wang, Wei Fu, Shou-Peng Liu, Ju-Xiong Int J Mol Sci Article Neuroinflammation plays a very important role in the pathogenesis of Parkinson’s disease (PD). After activation, microglia produce pro-inflammatory mediators that damage surrounding neurons. Consequently, the inhibition of microglial activation might represent a new therapeutic approach of PD. Vanillin has been shown to protect dopaminergic neurons, but the mechanism is still unclear. Herein, we further study the underlying mechanisms in lipopolysaccharide (LPS)-induced PD models. In vivo, we firstly established rat models of PD by unilateral injection of LPS into substantia nigra (SN), and then examined the role of vanillin in motor dysfunction, microglial activation and degeneration of dopaminergic neurons. In vitro, murine microglial BV-2 cells were treated with vanillin prior to the incubation of LPS, and then the inflammatory responses and the related signaling pathways were analyzed. The in vivo results showed that vanillin markedly improved the motor dysfunction, suppressed degeneration of dopaminergic neurons and inhibited microglial over-activation induced by LPS intranigral injection. The in vitro studies demonstrated that vanillin reduces LPS-induced expression of inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2), IL-1β, and IL-6 through regulating ERK1/2, p38 and NF-κB signaling. Collectively, these data indicated that vanillin has a role in protecting dopaminergic neurons via inhibiting inflammatory activation. MDPI 2017-02-12 /pmc/articles/PMC5343924/ /pubmed/28208679 http://dx.doi.org/10.3390/ijms18020389 Text en © 2017 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
Yan, Xuan
Liu, Dian-Feng
Zhang, Xiang-Yang
Liu, Dong
Xu, Shi-Yao
Chen, Guang-Xin
Huang, Bing-Xu
Ren, Wen-Zhi
Wang, Wei
Fu, Shou-Peng
Liu, Ju-Xiong
Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title_full Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title_fullStr Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title_full_unstemmed Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title_short Vanillin Protects Dopaminergic Neurons against Inflammation-Mediated Cell Death by Inhibiting ERK1/2, P38 and the NF-κB Signaling Pathway
title_sort vanillin protects dopaminergic neurons against inflammation-mediated cell death by inhibiting erk1/2, p38 and the nf-κb signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343924/
https://www.ncbi.nlm.nih.gov/pubmed/28208679
http://dx.doi.org/10.3390/ijms18020389
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