4.4 Article

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

Journal

VETERINARY MEDICINE AND SCIENCE
Volume 8, Issue 2, Pages 700-709

Publisher

WILEY
DOI: 10.1002/vms3.693

Keywords

arctigenin; mice; NF-kappa B; PCV2; proinflammatory cytokine

Funding

  1. Hubei Provincial Natural Science Foundation of China [2018CFB678]
  2. OpenProject ofKey Laboratory ofAnimal Embryo Engineering and Molecular Breeding of Hubei Province [KLAEMB-2016-05]
  3. Science and Technology Innovation Platform Projects from Science and TechnologyDepartment of Hubei Province [2018BEC494]
  4. Innovation System ConstructionProject ofWuhan Academy ofAgricultural Sciences [CXJSFW202002-1]
  5. CentralGovernment Guides Local Science and Technology DevelopmentProject [2020ZYYD029]

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This study demonstrated that arctigenin (ACT) effectively inhibits proinflammatory cytokine production induced by PCV2 infection in vitro and in vivo by suppressing NF-κB signaling pathway activation. The results suggest that ACT could potentially be developed as a traditional Chinese herbal medicine remedy for the treatment of porcine circovirus-associated diseases.
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-kappa B signalling pathway activation following PCV2 infection in PK-15 cells. Furthermore, western blotting demonstrated that ACT suppressed the NF-kappa B signal pathway in PCV2 infection-stimulated PK-15 cells by inhibiting the translocation of p65 from the cytoplasm to the nucleus and I kappa B alpha 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-kappa B signal pathway in PCV2-infected mice by inhibiting the translocation of p65 from the cytoplasm to the nucleus and I kappa B alpha 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-kappa B 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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