4.6 Article

Angelica polysaccharide attenuates LPS-induced inflammation response of primary dairy cow claw dermal cells via NF-κB and MAPK signaling pathways

Journal

BMC VETERINARY RESEARCH
Volume 17, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12917-021-02952-4

Keywords

Dairy cow; Claw dermal cell; LPS; Angelica polysaccharide; NF-kappa B; MAPK

Funding

  1. Hebei key research and development program [19226611D]
  2. In novation ability training program of Hebei Province for Graduate candidate [CXZZBS2020101]
  3. Project of Bureau of Hebei Animal Husbandry and Veterinary Medicine [2013107]
  4. Hebei Dairy Cattle Innovation Team of Modern Agro-industry Technology Research System [HBCT2018120406]
  5. Hebei Beef Innovation Team of Modern Agroindustry Technology Research System [HBCT20181130405]

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The study demonstrated that Angelica polysaccharide (AP) can reduce inflammatory mediators production in dairy cow claw dermal cells, regulate the expression of TLR4, MyD88, and chemokines, and inhibit NF-kappa B and MAPK signaling pathways activation.
Background: Laminitis, an inflammation of the claw laminae, is one of the major causes of bovine lameness, which can lead to enormous economic losses and animal welfare problems in dairy farms. Angelica polysaccharide (AP) is proved to possess anti-inflammatory properties. But the role of AP on inflammatory response of the claw dermal cells has not been reported. The aim of this study was to investigate the anti-inflammatory effects of AP on lipopolysaccharide (LPS)-induced primary claw dermal cells of dairy cow and clarify the potential mechanisms. In the current research, the primary claw dermal cells were exposed to gradient concentrations of AP (10, 50, 100 mu g/mL) in the presence of 10 mu g/mL LPS. The levels of cytokines and nitric oxide (NO) were detected with ELISA and Griess colorimetric method. The mRNA expressions of TLR4, MyD88 and chemokines were measured with qPCR. The activation of NF-kappa B and MAPK signaling pathways was detected with western blotting. Results: The results indicated that AP reduced the production of inflammatory mediators (TNF-alpha, IL-1 beta, IL-6 and NO), downregulated the mRNA expression of TLR4, MyD88 and some pro-inflammatory chemokines (CCL2, CCL20, CXCL2, CXCL8, CXCL10), and suppressed the NF-kappa B and MAPK signaling pathways evidenced by inhibition of the phosphorylation of I kappa B alpha, p65 and ERK, JNK, p38. Conclusions: Our results demonstrated that AP may exert its anti-inflammatory effects on claw dermal cells of dairy cow by regulating the NF-kappa B and MAPK signaling pathways.

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