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Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model

Arctigenin (ACT) is a novel anti‐inflammatory lignan extracted from Arctium lappa L, a herb commonly used in traditional Chinese herbal medicine. In this study, we investigated the molecular mechanism whereby ACT inhibits PCV2 infection‐induced proinflammatory cytokine production in vitro and in viv...

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Autores principales: Wu, Lijun, Chen, Jie, Zhou, Danna, Chen, Runshan, Chen, Xiabing, Shao, Zhiyong, Yang, Wenhai, He, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959337/
https://www.ncbi.nlm.nih.gov/pubmed/34914190
http://dx.doi.org/10.1002/vms3.693
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author Wu, Lijun
Chen, Jie
Zhou, Danna
Chen, Runshan
Chen, Xiabing
Shao, Zhiyong
Yang, Wenhai
He, Bin
author_facet Wu, Lijun
Chen, Jie
Zhou, Danna
Chen, Runshan
Chen, Xiabing
Shao, Zhiyong
Yang, Wenhai
He, Bin
author_sort Wu, Lijun
collection PubMed
description Arctigenin (ACT) is a novel anti‐inflammatory lignan extracted from Arctium lappa L, a herb commonly used in traditional Chinese herbal medicine. In this study, we investigated the molecular mechanism whereby ACT inhibits PCV2 infection‐induced proinflammatory cytokine production in vitro and in vivo. We observed that in PCV2 infection+ACT treated PK‐15 cells, proinflammatory cytokine production was significantly reduced, compared to the PCV2‐infected cells. The transfection and luciferase reporter assay confirmed that ACT suppressed NF‐κB signalling pathway activation following PCV2 infection in PK‐15 cells. Furthermore, western blotting demonstrated that ACT suppressed the NF‐κB signal pathway in PCV2 infection‐stimulated PK‐15 cells by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation. BALB/c mice were used as a model to evaluate the anti‐inflammatory effect of ACT in vivo. We found that the BALB/c mice inoculated with PCV2 infection + ACT treated showed a significant reduction of proinflammatory cytokine production in serum, lung and spleen tissue, compared to the PCV2‐infected mice. Western blotting confirmed that ACT suppressed the NF‐κB signal pathway in PCV2‐infected mice by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation in lung tissue. Our studies first demonstrate that ACT inhibits PCV2 infection‐induced proinflammatory cytokine production by suppressing the phosphorylation and nuclear translocation of NF‐κB in vitro and in vivo. These results will help further develop ACT as a Traditional Chinese herbal medicine remedy in the treatment of porcine circovirus‐associated diseases.
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spelling pubmed-89593372022-03-29 Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model Wu, Lijun Chen, Jie Zhou, Danna Chen, Runshan Chen, Xiabing Shao, Zhiyong Yang, Wenhai He, Bin Vet Med Sci REPTILES Arctigenin (ACT) is a novel anti‐inflammatory lignan extracted from Arctium lappa L, a herb commonly used in traditional Chinese herbal medicine. In this study, we investigated the molecular mechanism whereby ACT inhibits PCV2 infection‐induced proinflammatory cytokine production in vitro and in vivo. We observed that in PCV2 infection+ACT treated PK‐15 cells, proinflammatory cytokine production was significantly reduced, compared to the PCV2‐infected cells. The transfection and luciferase reporter assay confirmed that ACT suppressed NF‐κB signalling pathway activation following PCV2 infection in PK‐15 cells. Furthermore, western blotting demonstrated that ACT suppressed the NF‐κB signal pathway in PCV2 infection‐stimulated PK‐15 cells by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation. BALB/c mice were used as a model to evaluate the anti‐inflammatory effect of ACT in vivo. We found that the BALB/c mice inoculated with PCV2 infection + ACT treated showed a significant reduction of proinflammatory cytokine production in serum, lung and spleen tissue, compared to the PCV2‐infected mice. Western blotting confirmed that ACT suppressed the NF‐κB signal pathway in PCV2‐infected mice by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation in lung tissue. Our studies first demonstrate that ACT inhibits PCV2 infection‐induced proinflammatory cytokine production by suppressing the phosphorylation and nuclear translocation of NF‐κB in vitro and in vivo. These results will help further develop ACT as a Traditional Chinese herbal medicine remedy in the treatment of porcine circovirus‐associated diseases. John Wiley and Sons Inc. 2021-12-16 /pmc/articles/PMC8959337/ /pubmed/34914190 http://dx.doi.org/10.1002/vms3.693 Text en © 2021 The Authors. Veterinary Medicine and Science published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 REPTILES
Wu, Lijun
Chen, Jie
Zhou, Danna
Chen, Runshan
Chen, Xiabing
Shao, Zhiyong
Yang, Wenhai
He, Bin
Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title_full Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title_fullStr Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title_full_unstemmed Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title_short Anti‐inflammatory activity of arctigenin against PCV2 infection in a mouse model
title_sort anti‐inflammatory activity of arctigenin against pcv2 infection in a mouse model
topic REPTILES
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959337/
https://www.ncbi.nlm.nih.gov/pubmed/34914190
http://dx.doi.org/10.1002/vms3.693
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