Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Tian, Mengyue, Li, Nan, Liu, Ruonan, Li, Ke, Du, Jinliang, Zou, Dongmin, Ma, Yuzhong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
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
Descripción
Sumario: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.