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Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner
BACKGROUND: Activation of microglia plays a crucial role in immune and inflammatory processes after ischemic stroke. Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2). Inhibiting M1 while stimulating M2 has been suggested...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4378556/ https://www.ncbi.nlm.nih.gov/pubmed/25889216 http://dx.doi.org/10.1186/s12974-015-0270-3 |
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author | Pan, Jie Jin, Jia-li Ge, Hui-ming Yin, Kai-lin Chen, Xiang Han, Li-juan Chen, Yan Qian, Lai Li, Xiao-xi Xu, Yun |
author_facet | Pan, Jie Jin, Jia-li Ge, Hui-ming Yin, Kai-lin Chen, Xiang Han, Li-juan Chen, Yan Qian, Lai Li, Xiao-xi Xu, Yun |
author_sort | Pan, Jie |
collection | PubMed |
description | BACKGROUND: Activation of microglia plays a crucial role in immune and inflammatory processes after ischemic stroke. Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2). Inhibiting M1 while stimulating M2 has been suggested as a potential therapeutic approach in the treatment of stroke. FINDINGS: In this study, we indicated that a novel natural anti-oxidant extracted from the Chinese plant Hopea hainanensis, malibatol A (MA), decreased the infarct size and alleviated the brain injury after mice middle cerebral artery occlusion (MCAO). MA inhibited expression inflammatory cytokines in not only MCAO mice but also lipopolysaccharide (LPS)-stimulated microglia. Moreover, treatment of MA decreased M1 markers (CD16, CD32, and CD86) and increased M2 markers (CD206, YM-1) while promoting the activation of nuclear receptor PPARγ. CONCLUSIONS: MA has anti-inflammatory effects in MCAO mice in a PPARγ-dependent manner, making it a potential candidate for stroke treatment. |
format | Online Article Text |
id | pubmed-4378556 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-43785562015-03-31 Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner Pan, Jie Jin, Jia-li Ge, Hui-ming Yin, Kai-lin Chen, Xiang Han, Li-juan Chen, Yan Qian, Lai Li, Xiao-xi Xu, Yun J Neuroinflammation Research BACKGROUND: Activation of microglia plays a crucial role in immune and inflammatory processes after ischemic stroke. Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2). Inhibiting M1 while stimulating M2 has been suggested as a potential therapeutic approach in the treatment of stroke. FINDINGS: In this study, we indicated that a novel natural anti-oxidant extracted from the Chinese plant Hopea hainanensis, malibatol A (MA), decreased the infarct size and alleviated the brain injury after mice middle cerebral artery occlusion (MCAO). MA inhibited expression inflammatory cytokines in not only MCAO mice but also lipopolysaccharide (LPS)-stimulated microglia. Moreover, treatment of MA decreased M1 markers (CD16, CD32, and CD86) and increased M2 markers (CD206, YM-1) while promoting the activation of nuclear receptor PPARγ. CONCLUSIONS: MA has anti-inflammatory effects in MCAO mice in a PPARγ-dependent manner, making it a potential candidate for stroke treatment. BioMed Central 2015-03-14 /pmc/articles/PMC4378556/ /pubmed/25889216 http://dx.doi.org/10.1186/s12974-015-0270-3 Text en © Pan et al.; licensee BioMed Central. 2015 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 work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Pan, Jie Jin, Jia-li Ge, Hui-ming Yin, Kai-lin Chen, Xiang Han, Li-juan Chen, Yan Qian, Lai Li, Xiao-xi Xu, Yun Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title | Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title_full | Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title_fullStr | Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title_full_unstemmed | Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title_short | Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner |
title_sort | malibatol a regulates microglia m1/m2 polarization in experimental stroke in a pparγ-dependent manner |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4378556/ https://www.ncbi.nlm.nih.gov/pubmed/25889216 http://dx.doi.org/10.1186/s12974-015-0270-3 |
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