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Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis
BACKGROUND: Haemophilus parasuis (HPS) is the causative agent of Glässer’s disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to p...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434632/ https://www.ncbi.nlm.nih.gov/pubmed/30909903 http://dx.doi.org/10.1186/s12917-019-1840-x |
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author | Ye, Chun Li, Ruizhi Xu, Lei Qiu, Yinsheng Fu, Shulin Liu, Yu Wu, Zhongyuan Hou, Yongqing Hu, Chien-An Andy |
author_facet | Ye, Chun Li, Ruizhi Xu, Lei Qiu, Yinsheng Fu, Shulin Liu, Yu Wu, Zhongyuan Hou, Yongqing Hu, Chien-An Andy |
author_sort | Ye, Chun |
collection | PubMed |
description | BACKGROUND: Haemophilus parasuis (HPS) is the causative agent of Glässer’s disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to possess a series of activities, such as anti-bacterial, anti-viral, anti-tumor, anti-oxidant and anti-inflammatory activities. However, whether BA has anti-apoptotic effects following HPS infection is unclear. Here, we investigated the anti-apoptotic effects and mechanisms of BA in HPS-induced apoptosis via the protein kinase C (PKC)–mitogen-activated protein kinase (MAPK) pathway in piglet’s mononuclear phagocytes (PMNP). RESULTS: Our data demonstrated that HPS could induce reactive oxygen species (ROS) production, arrest the cell cycle and promote apoptosis via the PKC–MAPK signaling pathway in PMNP. Moreover, when BA was administered, we observed a reduction in ROS production, suppression of cleavage of caspase-3 in inducing apoptosis, and inhibition of activation of the PKC–MAPK signaling pathway for down-regulating p-JNK, p-p38, p-ERK, p-PKC-α and PKC-δ in PMNP triggered by HPS. CONCLUSIONS: Our data strongly suggest that BA can reverse the apoptosis initiated by HPS through regulating the PKC–MAPK signaling pathway, which represents a promising therapeutic agent in the treatment of HPS infection. |
format | Online Article Text |
id | pubmed-6434632 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-64346322019-04-08 Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis Ye, Chun Li, Ruizhi Xu, Lei Qiu, Yinsheng Fu, Shulin Liu, Yu Wu, Zhongyuan Hou, Yongqing Hu, Chien-An Andy BMC Vet Res Research Article BACKGROUND: Haemophilus parasuis (HPS) is the causative agent of Glässer’s disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to possess a series of activities, such as anti-bacterial, anti-viral, anti-tumor, anti-oxidant and anti-inflammatory activities. However, whether BA has anti-apoptotic effects following HPS infection is unclear. Here, we investigated the anti-apoptotic effects and mechanisms of BA in HPS-induced apoptosis via the protein kinase C (PKC)–mitogen-activated protein kinase (MAPK) pathway in piglet’s mononuclear phagocytes (PMNP). RESULTS: Our data demonstrated that HPS could induce reactive oxygen species (ROS) production, arrest the cell cycle and promote apoptosis via the PKC–MAPK signaling pathway in PMNP. Moreover, when BA was administered, we observed a reduction in ROS production, suppression of cleavage of caspase-3 in inducing apoptosis, and inhibition of activation of the PKC–MAPK signaling pathway for down-regulating p-JNK, p-p38, p-ERK, p-PKC-α and PKC-δ in PMNP triggered by HPS. CONCLUSIONS: Our data strongly suggest that BA can reverse the apoptosis initiated by HPS through regulating the PKC–MAPK signaling pathway, which represents a promising therapeutic agent in the treatment of HPS infection. BioMed Central 2019-03-25 /pmc/articles/PMC6434632/ /pubmed/30909903 http://dx.doi.org/10.1186/s12917-019-1840-x Text en © The Author(s). 2019 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 Article Ye, Chun Li, Ruizhi Xu, Lei Qiu, Yinsheng Fu, Shulin Liu, Yu Wu, Zhongyuan Hou, Yongqing Hu, Chien-An Andy Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title | Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title_full | Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title_fullStr | Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title_full_unstemmed | Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title_short | Effects of Baicalin on piglet monocytes involving PKC–MAPK signaling pathways induced by Haemophilus parasuis |
title_sort | effects of baicalin on piglet monocytes involving pkc–mapk signaling pathways induced by haemophilus parasuis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434632/ https://www.ncbi.nlm.nih.gov/pubmed/30909903 http://dx.doi.org/10.1186/s12917-019-1840-x |
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