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Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action
High mobility group box 1 (HMGB1) is an evolutionarily conserved protein and is constitutively expressed in virtually all types of cells. In response to microbial infections, HMGB1 is secreted from activated immune cells to orchestrate rigorous inflammatory responses. Here we review the distinct mec...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363608/ https://www.ncbi.nlm.nih.gov/pubmed/25821489 http://dx.doi.org/10.1155/2015/456305 |
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author | Wu, Andrew H. He, Li Long, Wei Zhou, Qiuping Zhu, Shu Wang, Ping Fan, Saijun Wang, Haichao |
author_facet | Wu, Andrew H. He, Li Long, Wei Zhou, Qiuping Zhu, Shu Wang, Ping Fan, Saijun Wang, Haichao |
author_sort | Wu, Andrew H. |
collection | PubMed |
description | High mobility group box 1 (HMGB1) is an evolutionarily conserved protein and is constitutively expressed in virtually all types of cells. In response to microbial infections, HMGB1 is secreted from activated immune cells to orchestrate rigorous inflammatory responses. Here we review the distinct mechanisms by which several herbal components inhibit HMGB1 action or secretion, such as by modulating inflammasome activation, autophagic degradation, or endocytic uptake. In light of the reciprocal interactions between these cellular processes, it is possible to develop more effective combinational herbal therapies for the clinical management of inflammatory diseases. |
format | Online Article Text |
id | pubmed-4363608 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-43636082015-03-29 Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action Wu, Andrew H. He, Li Long, Wei Zhou, Qiuping Zhu, Shu Wang, Ping Fan, Saijun Wang, Haichao Evid Based Complement Alternat Med Review Article High mobility group box 1 (HMGB1) is an evolutionarily conserved protein and is constitutively expressed in virtually all types of cells. In response to microbial infections, HMGB1 is secreted from activated immune cells to orchestrate rigorous inflammatory responses. Here we review the distinct mechanisms by which several herbal components inhibit HMGB1 action or secretion, such as by modulating inflammasome activation, autophagic degradation, or endocytic uptake. In light of the reciprocal interactions between these cellular processes, it is possible to develop more effective combinational herbal therapies for the clinical management of inflammatory diseases. Hindawi Publishing Corporation 2015 2015-03-02 /pmc/articles/PMC4363608/ /pubmed/25821489 http://dx.doi.org/10.1155/2015/456305 Text en Copyright © 2015 Andrew H. Wu et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Wu, Andrew H. He, Li Long, Wei Zhou, Qiuping Zhu, Shu Wang, Ping Fan, Saijun Wang, Haichao Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title | Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title_full | Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title_fullStr | Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title_full_unstemmed | Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title_short | Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action |
title_sort | novel mechanisms of herbal therapies for inhibiting hmgb1 secretion or action |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363608/ https://www.ncbi.nlm.nih.gov/pubmed/25821489 http://dx.doi.org/10.1155/2015/456305 |
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