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

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          Abstract

          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 µg/mL) in the presence of 10 µg/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-κB and MAPK signaling pathways was detected with western blotting.

          Results

          The results indicated that AP reduced the production of inflammatory mediators (TNF-α, IL-1β, 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-κB and MAPK signaling pathways evidenced by inhibition of the phosphorylation of IκBα, 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-κB and MAPK signaling pathways.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12917-021-02952-4.

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          Most cited references40

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          Inflammatory responses and inflammation-associated diseases in organs

          Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease. Both infectious and non-infectious agents and cell damage activate inflammatory cells and trigger inflammatory signaling pathways, most commonly the NF-κB, MAPK, and JAK-STAT pathways. Here, we review inflammatory responses within organs, focusing on the etiology of inflammation, inflammatory response mechanisms, resolution of inflammation, and organ-specific inflammatory responses.
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            A guide to chemokines and their receptors

            The chemokines (or chemotactic cytokines) are a large family of small, secreted proteins that signal through cell surface G protein‐coupled heptahelical chemokine receptors. They are best known for their ability to stimulate the migration of cells, most notably white blood cells (leukocytes). Consequently, chemokines play a central role in the development and homeostasis of the immune system, and are involved in all protective or destructive immune and inflammatory responses. Classically viewed as inducers of directed chemotactic migration, it is now clear that chemokines can stimulate a variety of other types of directed and undirected migratory behavior, such as haptotaxis, chemokinesis, and haptokinesis, in addition to inducing cell arrest or adhesion. However, chemokine receptors on leukocytes can do more than just direct migration, and these molecules can also be expressed on, and regulate the biology of, many nonleukocytic cell types. Chemokines are profoundly affected by post‐translational modification, by interaction with the extracellular matrix (ECM), and by binding to heptahelical ‘atypical’ chemokine receptors that regulate chemokine localization and abundance. This guide gives a broad overview of the chemokine and chemokine receptor families; summarizes the complex physical interactions that occur in the chemokine network; and, using specific examples, discusses general principles of chemokine function, focusing particularly on their ability to direct leukocyte migration.
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              Pathological roles of MAPK signaling pathways in human diseases.

              The mammalian family of mitogen-activated protein kinases (MAPKs) includes extracellular signal-regulated kinase (ERK), p38, and c-Jun NH(2)-terminal kinase (JNK), with each MAPK signaling pathway consisting of at least three components, a MAPK kinase kinase (MAP3K), a MAPK kinase (MAP2K), and a MAPK. The MAPK pathways are activated by diverse extracellular and intracellular stimuli including peptide growth factors, cytokines, hormones, and various cellular stressors such as oxidative stress and endoplasmic reticulum stress. These signaling pathways regulate a variety of cellular activities including proliferation, differentiation, survival, and death. Deviation from the strict control of MAPK signaling pathways has been implicated in the development of many human diseases including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and various types of cancers. Persistent activation of the JNK or p38 signaling pathways has been suggested to mediate neuronal apoptosis in AD, PD, and ALS, whereas the ERK signaling pathway plays a key role in several steps of tumorigenesis including cancer cell proliferation, migration, and invasion. In this review, we summarize recent findings on the roles of MAPK signaling pathways in human disorders, focusing on cancer and neurodegenerative diseases including AD, PD, and ALS. Copyright 2010 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                dkma@hebau.edu.cn
                Journal
                BMC Vet Res
                BMC Vet Res
                BMC Veterinary Research
                BioMed Central (London )
                1746-6148
                19 July 2021
                19 July 2021
                2021
                : 17
                : 248
                Affiliations
                [1 ]GRID grid.274504.0, ISNI 0000 0001 2291 4530, College of Veterinary Medicine, , Hebei Agricultural University, ; 2596 Lekai South Street, Hebei 071001 Baoding, China
                [2 ]GRID grid.43308.3c, ISNI 0000 0000 9413 3760, International Joint Research Laboratory for Fish Immunopharmacology, Freshwater Fisheries Research Center, , Chinese Academy of Fishery Sciences, ; 214081 Wuxi, Jiangsu China
                [3 ]GRID grid.412545.3, ISNI 0000 0004 1798 1300, College of Veterinary Medicine, , Shanxi Agricultural University, ; Shanxi 030801 Taigu, China
                Author information
                http://orcid.org/0000-0003-0101-5784
                Article
                2952
                10.1186/s12917-021-02952-4
                8287747
                34281532
                fac25388-7c1e-451a-9563-3c411f07a827
                © The Author(s) 2021

                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/. The Creative Commons Public Domain Dedication waiver ( http://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.

                History
                : 15 December 2020
                : 28 June 2021
                Funding
                Funded by: Hebei key research and development program
                Award ID: 19226611D
                Award Recipient :
                Funded by: Inovation ability training program of Hebei Province for Graduate candidate
                Award ID: CXZZBS2020101
                Award Recipient :
                Funded by: Project of Bureau of Hebei Animal Husbandry and Veterinary Medicine
                Award ID: 2013107
                Funded by: Hebei Dairy Cattle Innovation Team of Modern Agro-industry Technology Research System
                Award ID: HBCT2018120406
                Funded by: Hebei Beef Innovation Team of Modern Agro-industry Technology Research System
                Award ID: HBCT20181130405
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2021

                Veterinary medicine
                dairy cow,claw dermal cell,lps,angelica polysaccharide,nf-κb,mapk
                Veterinary medicine
                dairy cow, claw dermal cell, lps, angelica polysaccharide, nf-κb, mapk

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