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Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice
BACKGROUND: Crocetin, an agent derived from saffron, has multiple pharmacological properties, such as neuroprotective, anti-oxidant, and anti-inflammatory actions. These properties might benefit the treatment of Alzheimer’s disease (AD). In the present study, we tested whether crocetin attenuates in...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208089/ https://www.ncbi.nlm.nih.gov/pubmed/30450117 http://dx.doi.org/10.1186/s12979-018-0132-9 |
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author | Zhang, Jin Wang, Yuchao Dong, Xueshuang Liu, Jianghua |
author_facet | Zhang, Jin Wang, Yuchao Dong, Xueshuang Liu, Jianghua |
author_sort | Zhang, Jin |
collection | PubMed |
description | BACKGROUND: Crocetin, an agent derived from saffron, has multiple pharmacological properties, such as neuroprotective, anti-oxidant, and anti-inflammatory actions. These properties might benefit the treatment of Alzheimer’s disease (AD). In the present study, we tested whether crocetin attenuates inflammation and amyloid-β (Aβ) accumulation in APPsw transgenic mice, AD mouse models. Cell viability and the levels of Aβ40 and Aβ42 in HeLa cells stably transfected with Swedish mutant APP751 were evaluated. Mice with Swedish mutant APP751 transgene were used as transgenic mouse models of AD, and were orally administrated with crocetin. Aβ protein and inflammatory cytokines were measured with ELISA. NF-κB and P53 were measured with western blot assay. Learning and memory were analyzed with Morris water maze and novel object recognition tests. RESULTS: Crocetin significantly reduced Aβ40 and Aβ42 secretion in Hela cells without effecting cell viability. In AD transgenic mice, crocetin significantly reduced the pro-inflammatory cytokines and enhanced anti-inflammatory cytokine in plasma, suppressed NF-κB activation and P53 expression in the hippocampus, decreased Aβ in various brain areas, and improved learning and memory deficits. CONCLUSION: Crocetin improves Aβ accumulation-induced learning and memory deficit in AD transgenic mice, probably due to its anti-inflammatory and anti-apoptotic functions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12979-018-0132-9) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6208089 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-62080892018-11-16 Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice Zhang, Jin Wang, Yuchao Dong, Xueshuang Liu, Jianghua Immun Ageing Research BACKGROUND: Crocetin, an agent derived from saffron, has multiple pharmacological properties, such as neuroprotective, anti-oxidant, and anti-inflammatory actions. These properties might benefit the treatment of Alzheimer’s disease (AD). In the present study, we tested whether crocetin attenuates inflammation and amyloid-β (Aβ) accumulation in APPsw transgenic mice, AD mouse models. Cell viability and the levels of Aβ40 and Aβ42 in HeLa cells stably transfected with Swedish mutant APP751 were evaluated. Mice with Swedish mutant APP751 transgene were used as transgenic mouse models of AD, and were orally administrated with crocetin. Aβ protein and inflammatory cytokines were measured with ELISA. NF-κB and P53 were measured with western blot assay. Learning and memory were analyzed with Morris water maze and novel object recognition tests. RESULTS: Crocetin significantly reduced Aβ40 and Aβ42 secretion in Hela cells without effecting cell viability. In AD transgenic mice, crocetin significantly reduced the pro-inflammatory cytokines and enhanced anti-inflammatory cytokine in plasma, suppressed NF-κB activation and P53 expression in the hippocampus, decreased Aβ in various brain areas, and improved learning and memory deficits. CONCLUSION: Crocetin improves Aβ accumulation-induced learning and memory deficit in AD transgenic mice, probably due to its anti-inflammatory and anti-apoptotic functions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12979-018-0132-9) contains supplementary material, which is available to authorized users. BioMed Central 2018-10-30 /pmc/articles/PMC6208089/ /pubmed/30450117 http://dx.doi.org/10.1186/s12979-018-0132-9 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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 Zhang, Jin Wang, Yuchao Dong, Xueshuang Liu, Jianghua Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title | Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title_full | Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title_fullStr | Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title_full_unstemmed | Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title_short | Crocetin attenuates inflammation and amyloid-β accumulation in APPsw transgenic mice |
title_sort | crocetin attenuates inflammation and amyloid-β accumulation in appsw transgenic mice |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208089/ https://www.ncbi.nlm.nih.gov/pubmed/30450117 http://dx.doi.org/10.1186/s12979-018-0132-9 |
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