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The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide
Laminitis is one of the most important and intractable diseases in dairy cows, which can lead to enormous economic losses. Although many scholars have conducted a large number of studies on laminitis, the therapeutic test of medicinal plants in vitro is really rare. Licochalcone A is proved to posse...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803976/ https://www.ncbi.nlm.nih.gov/pubmed/35102233 http://dx.doi.org/10.1038/s41598-022-05653-6 |
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author | Tian, Mengyue Li, Nan Liu, Ruonan Li, Ke Du, Jinliang Zou, Dongmin Ma, Yuzhong |
author_facet | Tian, Mengyue Li, Nan Liu, Ruonan Li, Ke Du, Jinliang Zou, Dongmin Ma, Yuzhong |
author_sort | Tian, Mengyue |
collection | PubMed |
description | Laminitis is one of the most important and intractable diseases in dairy cows, which can lead to enormous economic losses. Although many scholars have conducted a large number of studies on laminitis, the therapeutic test of medicinal plants in vitro is really rare. Licochalcone A is proved to possess anti-inflammatory and anti-oxidant properties. But the effect of licochalcone A on LPS-induced inflammatory claw dermal cells has not been discovered yet. In this study, the primary dairy cow claw dermal cells were treated with gradient concentrations of licochalcone A (1, 5, 10 µg/mL) in the presence of 10 µg/mL lipopolysaccharides (LPS). The results indicated that licochalcone A reduced the concentrations of inflammation mediators (TNF-α, IL-1β and IL-6), increased the activity of SOD, reduced the levels of MDA and ROS, downregulated the mRNA expressions of TLR4 and MyD88, suppressed the protein levels of p-IκBα and p-p65, and upregulated the protein expression of PPARγ. In summary, licochalcone A protected dairy cow claw dermal cells against LPS-induced inflammatory response and oxidative stress through the regulation of TLR4/MyD88/NF-κB and PPARγ signaling pathways. |
format | Online Article Text |
id | pubmed-8803976 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-88039762022-02-01 The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide Tian, Mengyue Li, Nan Liu, Ruonan Li, Ke Du, Jinliang Zou, Dongmin Ma, Yuzhong Sci Rep Article Laminitis is one of the most important and intractable diseases in dairy cows, which can lead to enormous economic losses. Although many scholars have conducted a large number of studies on laminitis, the therapeutic test of medicinal plants in vitro is really rare. Licochalcone A is proved to possess anti-inflammatory and anti-oxidant properties. But the effect of licochalcone A on LPS-induced inflammatory claw dermal cells has not been discovered yet. In this study, the primary dairy cow claw dermal cells were treated with gradient concentrations of licochalcone A (1, 5, 10 µg/mL) in the presence of 10 µg/mL lipopolysaccharides (LPS). The results indicated that licochalcone A reduced the concentrations of inflammation mediators (TNF-α, IL-1β and IL-6), increased the activity of SOD, reduced the levels of MDA and ROS, downregulated the mRNA expressions of TLR4 and MyD88, suppressed the protein levels of p-IκBα and p-p65, and upregulated the protein expression of PPARγ. In summary, licochalcone A protected dairy cow claw dermal cells against LPS-induced inflammatory response and oxidative stress through the regulation of TLR4/MyD88/NF-κB and PPARγ signaling pathways. Nature Publishing Group UK 2022-01-31 /pmc/articles/PMC8803976/ /pubmed/35102233 http://dx.doi.org/10.1038/s41598-022-05653-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This 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/) . |
spellingShingle | Article Tian, Mengyue Li, Nan Liu, Ruonan Li, Ke Du, Jinliang Zou, Dongmin Ma, Yuzhong The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title | The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title_full | The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title_fullStr | The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title_full_unstemmed | The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title_short | The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
title_sort | protective effect of licochalcone a against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803976/ https://www.ncbi.nlm.nih.gov/pubmed/35102233 http://dx.doi.org/10.1038/s41598-022-05653-6 |
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