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Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway
Parkinson's disease (PD) is a complex multi-system and age-related neurodegenerative disorder. The intervention targeting neuroinflammation in PD patients is one effective strategy to slow down or inhibit disease progression. Microglia-mediated inflammatory response plays an important role in P...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217967/ https://www.ncbi.nlm.nih.gov/pubmed/28060896 http://dx.doi.org/10.1371/journal.pone.0169560 |
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author | Jing, Haoran Wang, Shaoxia Wang, Min Fu, Wenliang Zhang, Chao Xu, Donggang |
author_facet | Jing, Haoran Wang, Shaoxia Wang, Min Fu, Wenliang Zhang, Chao Xu, Donggang |
author_sort | Jing, Haoran |
collection | PubMed |
description | Parkinson's disease (PD) is a complex multi-system and age-related neurodegenerative disorder. The intervention targeting neuroinflammation in PD patients is one effective strategy to slow down or inhibit disease progression. Microglia-mediated inflammatory response plays an important role in Parkinson's, Alzheimer's and other cerebral diseases. Isobavachalcone is a main component of Chinese herb medicine Psoralea corylifolia, which function includes immunoregulation, anti-oxidation and the regulation of β-amyloid (Aβ42) deposited in hippocampus in Alzheimer's patients. Whether it has the therapeutic effect on Parkinson's disease, however, is unclear. In this study, we found that isobavachalcone could effectively remit Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP), prolong the residence time of mice on Rota-rod and alleviate the neuronal necrosis. It also inhibited the over-activation of microglia, and decreased the expression of IL-6 and IL-1β in the brain of PD mice. In vitro, isobavachalcone could inhibit nuclear factor-kappaB (NF-κB) pathway through inhibiting the LPS-induced transfer of NF-κB subunit from cytoplasm to nucleus in BV-2 cells. Isobavachalcone decreased the LPS-induced oxidative stress and the expression of inflammatory cytokines, and provided a neuroprotective effect by antagonizing microglia-mediated inflammation. Our results indicated that isobavachalcone may be a candidated drug against Parkinson's disease with great clinical potential. |
format | Online Article Text |
id | pubmed-5217967 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-52179672017-01-19 Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway Jing, Haoran Wang, Shaoxia Wang, Min Fu, Wenliang Zhang, Chao Xu, Donggang PLoS One Research Article Parkinson's disease (PD) is a complex multi-system and age-related neurodegenerative disorder. The intervention targeting neuroinflammation in PD patients is one effective strategy to slow down or inhibit disease progression. Microglia-mediated inflammatory response plays an important role in Parkinson's, Alzheimer's and other cerebral diseases. Isobavachalcone is a main component of Chinese herb medicine Psoralea corylifolia, which function includes immunoregulation, anti-oxidation and the regulation of β-amyloid (Aβ42) deposited in hippocampus in Alzheimer's patients. Whether it has the therapeutic effect on Parkinson's disease, however, is unclear. In this study, we found that isobavachalcone could effectively remit Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP), prolong the residence time of mice on Rota-rod and alleviate the neuronal necrosis. It also inhibited the over-activation of microglia, and decreased the expression of IL-6 and IL-1β in the brain of PD mice. In vitro, isobavachalcone could inhibit nuclear factor-kappaB (NF-κB) pathway through inhibiting the LPS-induced transfer of NF-κB subunit from cytoplasm to nucleus in BV-2 cells. Isobavachalcone decreased the LPS-induced oxidative stress and the expression of inflammatory cytokines, and provided a neuroprotective effect by antagonizing microglia-mediated inflammation. Our results indicated that isobavachalcone may be a candidated drug against Parkinson's disease with great clinical potential. Public Library of Science 2017-01-06 /pmc/articles/PMC5217967/ /pubmed/28060896 http://dx.doi.org/10.1371/journal.pone.0169560 Text en © 2017 Jing et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Jing, Haoran Wang, Shaoxia Wang, Min Fu, Wenliang Zhang, Chao Xu, Donggang Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title | Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title_full | Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title_fullStr | Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title_full_unstemmed | Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title_short | Isobavachalcone Attenuates MPTP-Induced Parkinson's Disease in Mice by Inhibition of Microglial Activation through NF-κB Pathway |
title_sort | isobavachalcone attenuates mptp-induced parkinson's disease in mice by inhibition of microglial activation through nf-κb pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217967/ https://www.ncbi.nlm.nih.gov/pubmed/28060896 http://dx.doi.org/10.1371/journal.pone.0169560 |
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