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Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A
The plant Coleus forskohlii is distributed primarily in India, Thailand, China, Egypt and Brazil and has a history of use in the treatment of multiple diseases. Isoforskolin (ISOF) is the principle active component of C. forskohlii native to China and has previously been studied for its biological e...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740510/ https://www.ncbi.nlm.nih.gov/pubmed/29285146 http://dx.doi.org/10.3892/etm.2017.5300 |
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author | Zhao, Hua Liu, Aihua Shen, Longqiang Xu, Cuiping Zhu, Ziwei Yang, Jiaru Han, Xinling Bao, Fukai Yang, Weimin |
author_facet | Zhao, Hua Liu, Aihua Shen, Longqiang Xu, Cuiping Zhu, Ziwei Yang, Jiaru Han, Xinling Bao, Fukai Yang, Weimin |
author_sort | Zhao, Hua |
collection | PubMed |
description | The plant Coleus forskohlii is distributed primarily in India, Thailand, China, Egypt and Brazil and has a history of use in the treatment of multiple diseases. Isoforskolin (ISOF) is the principle active component of C. forskohlii native to China and has previously been studied for its biological effects. The aim of the present study was to evaluate the effect of ISOF on the proinflammatory responses induced by recombinant Borrelia burgdorferi basic membrane protein A (rBmpA). In in vitro experiments, the proinflammatory effects of rBmpA and the anti-inflammatory function of ISOF were evaluated in murine macrophages, human macrophages and dendritic cells by detecting the transcription and expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6. In in vivo experiments, mean arthritis index and X-ray and histopathological examinations were used to verify the role of ISOF in experimental Lyme arthritis in mice. The results indicated that rBmpA, which induced the transcription and expression of TNF-α and IL-6, activated proinflammatory responses in murine macrophages, human macrophages and dendritic cells. In turn, ISOF downregulated the transcription and expression of TNF-α and IL-6 induced by rBmpA. Additionally, the in vivo experiments demonstrated that ISOF could also inhibit the symptoms of experimental Lyme arthritis. These results suggest that ISOF may have a potential application as an anti-inflammatory agent for the treatment of Lyme arthritis. |
format | Online Article Text |
id | pubmed-5740510 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57405102017-12-28 Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A Zhao, Hua Liu, Aihua Shen, Longqiang Xu, Cuiping Zhu, Ziwei Yang, Jiaru Han, Xinling Bao, Fukai Yang, Weimin Exp Ther Med Articles The plant Coleus forskohlii is distributed primarily in India, Thailand, China, Egypt and Brazil and has a history of use in the treatment of multiple diseases. Isoforskolin (ISOF) is the principle active component of C. forskohlii native to China and has previously been studied for its biological effects. The aim of the present study was to evaluate the effect of ISOF on the proinflammatory responses induced by recombinant Borrelia burgdorferi basic membrane protein A (rBmpA). In in vitro experiments, the proinflammatory effects of rBmpA and the anti-inflammatory function of ISOF were evaluated in murine macrophages, human macrophages and dendritic cells by detecting the transcription and expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6. In in vivo experiments, mean arthritis index and X-ray and histopathological examinations were used to verify the role of ISOF in experimental Lyme arthritis in mice. The results indicated that rBmpA, which induced the transcription and expression of TNF-α and IL-6, activated proinflammatory responses in murine macrophages, human macrophages and dendritic cells. In turn, ISOF downregulated the transcription and expression of TNF-α and IL-6 induced by rBmpA. Additionally, the in vivo experiments demonstrated that ISOF could also inhibit the symptoms of experimental Lyme arthritis. These results suggest that ISOF may have a potential application as an anti-inflammatory agent for the treatment of Lyme arthritis. D.A. Spandidos 2017-12 2017-10-13 /pmc/articles/PMC5740510/ /pubmed/29285146 http://dx.doi.org/10.3892/etm.2017.5300 Text en Copyright: © Zhao et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zhao, Hua Liu, Aihua Shen, Longqiang Xu, Cuiping Zhu, Ziwei Yang, Jiaru Han, Xinling Bao, Fukai Yang, Weimin Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title | Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title_full | Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title_fullStr | Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title_full_unstemmed | Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title_short | Isoforskolin downregulates proinflammatory responses induced by Borrelia burgdorferi basic membrane protein A |
title_sort | isoforskolin downregulates proinflammatory responses induced by borrelia burgdorferi basic membrane protein a |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740510/ https://www.ncbi.nlm.nih.gov/pubmed/29285146 http://dx.doi.org/10.3892/etm.2017.5300 |
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