Abstract
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.
Highlights
A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide Mengyue Tian[1,5], Nan Li2,5, Ruonan Liu[1], Ke Li1, Jinliang Du1,3, Dongmin Zou4 & Yuzhong Ma1*
The results indicated that licochalcone A reduced the concentrations of inflammation mediators (TNF-α, IL-1β and IL-6), increased the activity of superoxide dismutase (SOD), reduced the levels of MDA and reactive oxygen species (ROS), downregulated the mRNA expressions of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), suppressed the protein levels of p-IκBα and p-p65, and upregulated the protein expression of PPARγ
LPS markedly upregulated the mRNA expressions of TLR4 and MyD88 (P < 0.01), these gene expressions were suppressed significantly by licochalcone A treatment for 12 h, 24 h and 48 h in a dose-dependent manner (P < 0.01) (Fig. 7). It demonstrated that licochalcone A was able to attenuate the inflammation response caused by LPS on claw dermal cells with the regulation of TLR4/MyD88/nuclear factor-κB (NF-κB) pathway and PPARγ expression, which provided a new idea for the possibility of licochalcone A being used for the treatment of bovine laminitis
Summary
A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide Mengyue Tian[1,5], Nan Li2,5, Ruonan Liu[1], Ke Li1, Jinliang Du1,3, Dongmin Zou4 & Yuzhong Ma1*. 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). 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. Animal models are widely used for the study of bovine laminitis[3], but the cell models are rarely reported It showed that inflammatory injury was one of the most important pathological events occurring in the early stages of laminitis[3,4,5]. Stimulating the dairy cow claw dermal cells with LPS to establish inflammatory model may be a novel way for the research of laminitis. Licochalcone A, one of the major flavonoid compounds isolated from the liquorice[12], is proved to exert multiple beneficial properties, such as anti-inflammation[13], Scientific Reports | (2022) 12:1593
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