Cargando…

Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells

BACKGROUND: The application of plant extracts has received great interest for the treatment of bovine mastitis. Isoliquiritigenin (ISL) is a rich dietary flavonoid that has significant antioxidative, anti-inflammatory and anticancer activities. This study was conducted to explore the protective effi...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Manman, Lu, Guicong, Ma, Xiao, Wang, Ruihong, Chen, Xihong, Yu, Yongxiong, Jiang, Caode
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392288/
https://www.ncbi.nlm.nih.gov/pubmed/35986317
http://dx.doi.org/10.1186/s12917-022-03414-1
_version_ 1784771029942403072
author Li, Manman
Lu, Guicong
Ma, Xiao
Wang, Ruihong
Chen, Xihong
Yu, Yongxiong
Jiang, Caode
author_facet Li, Manman
Lu, Guicong
Ma, Xiao
Wang, Ruihong
Chen, Xihong
Yu, Yongxiong
Jiang, Caode
author_sort Li, Manman
collection PubMed
description BACKGROUND: The application of plant extracts has received great interest for the treatment of bovine mastitis. Isoliquiritigenin (ISL) is a rich dietary flavonoid that has significant antioxidative, anti-inflammatory and anticancer activities. This study was conducted to explore the protective efficacy and related mechanism of ISL against lipopolysaccharide (LPS)-stimulated oxidation and inflammation in bovine mammary epithelial cells (MAC-T) by in vitro experiments. RESULTS: Real-time PCR and ELISA assays indicated that ISL treatment at 2.5, 5 and 10 μg/mL significantly reduced the mRNA and protein expression of the oxidative indicators cyclooxygenase-2 and inducible nitric oxide synthase (P < 0.01), and of the inflammatory cytokines interleukin-6 (P < 0.05), interleukin-1β (P < 0.01) and tumor necrosis factor-α (P < 0.01) in LPS-stimulated MAC-T cells. Moreover, Western blotting and immunofluorescence tests indicated that the phosphorylation levels of nuclear factor kappa (NF-κB) p65 and the inhibitor of NF-κB were significantly decreased by ISL treatment, thus blocking the nuclear transfer of NF-κB p65. In addition, ISL attenuated the phosphorylation levels of p38, extracellular signal-regulated kinase and c-jun NH2 terminal kinase. CONCLUSIONS: Our data demonstrated that ISL downregulated the LPS-induced inflammatory response in MAC-T cells. The anti-inflammatory and antioxidative activity of ISL involves the NF-κB and MAPK cascades. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12917-022-03414-1.
format Online
Article
Text
id pubmed-9392288
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-93922882022-08-21 Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells Li, Manman Lu, Guicong Ma, Xiao Wang, Ruihong Chen, Xihong Yu, Yongxiong Jiang, Caode BMC Vet Res Research BACKGROUND: The application of plant extracts has received great interest for the treatment of bovine mastitis. Isoliquiritigenin (ISL) is a rich dietary flavonoid that has significant antioxidative, anti-inflammatory and anticancer activities. This study was conducted to explore the protective efficacy and related mechanism of ISL against lipopolysaccharide (LPS)-stimulated oxidation and inflammation in bovine mammary epithelial cells (MAC-T) by in vitro experiments. RESULTS: Real-time PCR and ELISA assays indicated that ISL treatment at 2.5, 5 and 10 μg/mL significantly reduced the mRNA and protein expression of the oxidative indicators cyclooxygenase-2 and inducible nitric oxide synthase (P < 0.01), and of the inflammatory cytokines interleukin-6 (P < 0.05), interleukin-1β (P < 0.01) and tumor necrosis factor-α (P < 0.01) in LPS-stimulated MAC-T cells. Moreover, Western blotting and immunofluorescence tests indicated that the phosphorylation levels of nuclear factor kappa (NF-κB) p65 and the inhibitor of NF-κB were significantly decreased by ISL treatment, thus blocking the nuclear transfer of NF-κB p65. In addition, ISL attenuated the phosphorylation levels of p38, extracellular signal-regulated kinase and c-jun NH2 terminal kinase. CONCLUSIONS: Our data demonstrated that ISL downregulated the LPS-induced inflammatory response in MAC-T cells. The anti-inflammatory and antioxidative activity of ISL involves the NF-κB and MAPK cascades. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12917-022-03414-1. BioMed Central 2022-08-19 /pmc/articles/PMC9392288/ /pubmed/35986317 http://dx.doi.org/10.1186/s12917-022-03414-1 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Li, Manman
Lu, Guicong
Ma, Xiao
Wang, Ruihong
Chen, Xihong
Yu, Yongxiong
Jiang, Caode
Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title_full Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title_fullStr Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title_full_unstemmed Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title_short Anti-inflammation of isoliquiritigenin via the inhibition of NF-κB and MAPK in LPS-stimulated MAC-T cells
title_sort anti-inflammation of isoliquiritigenin via the inhibition of nf-κb and mapk in lps-stimulated mac-t cells
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392288/
https://www.ncbi.nlm.nih.gov/pubmed/35986317
http://dx.doi.org/10.1186/s12917-022-03414-1
work_keys_str_mv AT limanman antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT luguicong antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT maxiao antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT wangruihong antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT chenxihong antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT yuyongxiong antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells
AT jiangcaode antiinflammationofisoliquiritigeninviatheinhibitionofnfkbandmapkinlpsstimulatedmactcells