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Florfenicol alleviated lipopolysaccharide (LPS)-induced inflammatory responses in Ctenopharyngodon idella through inhibiting toll / NF-κB signaling pathways.

Authors
  • Li, Pei1
  • Ye, Jianzhi2
  • Zeng, Shaodong2
  • Yang, Chunliang3
  • 1 Center for Food Quality Supervision and Testing (Zhanjiang)Ministry of Agriculture and Rural Affairs PR China, Agricultural Products Processing Research Institute, Chinese Academy of Tropical Agricultural Sciences, Zhanjiang, 52400, China; Institute for Fisheries Sciences, Guangxi University, Nanning, 53000, China. , (China)
  • 2 Center for Food Quality Supervision and Testing (Zhanjiang)Ministry of Agriculture and Rural Affairs PR China, Agricultural Products Processing Research Institute, Chinese Academy of Tropical Agricultural Sciences, Zhanjiang, 52400, China. , (China)
  • 3 Center for Food Quality Supervision and Testing (Zhanjiang)Ministry of Agriculture and Rural Affairs PR China, Agricultural Products Processing Research Institute, Chinese Academy of Tropical Agricultural Sciences, Zhanjiang, 52400, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Fish & Shellfish Immunology
Publisher
Elsevier
Publication Date
Nov 01, 2019
Volume
94
Pages
479–484
Identifiers
DOI: 10.1016/j.fsi.2019.08.073
PMID: 31472264
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The present study was conducted to evaluate the anti-inflammatory activity of florfenicol (FFC) against lipopolysaccharide (LPS)-induced inflammatory responses in Ctenopharyngodon idella in vivo and in vitro. Head-kidney (HK) macrophages were pre-treated with 10 μg/mL LPS and then exposed to different concentrations of FFC to determine its in vitro anti-inflammatory activity. Inhibitory effect of FFC on inflammatory mediators TNF-α, IL-6 and IL-1β, as well as LPS-induced nitric oxide (NO) and prostaglandin E 2 (PGE 2) production were assayed by ELISA. The expression level of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were investigated by RT-PCR. Expression level of TLR-related genes (TLR1, TLR2, TLR4, TLR7, TLR8) expression, tumor necrosis factor receptor-associated factor 6 (TRAF6), transforming growth factor-b-activated kinase 1 (TAK1), Myeloid differentiation factor 88 (MyD88), nucleus p65, NF-κBα (IκBα) were measured by RT-PCR after grass carp were treated with 50, 100 and 200 mg FFC/kg body weight for 3 days. Results from in vitro tests demonstrated that FFC dose-dependently inhibited LPS-induced inflammatory cytokines TNF-α, IL-6 and IL-1β, inflammatory factors NO and PGE 2 production in macrophages. In addition, iNOS and COX-2 expression levels decreased significantly as compared with LPS treated group. In vivo test demonstrated that treatment with FFC prevented the LPS-induced upregulation of TNF-α, IL-6, IL-1β, NO and PGE 2. The expression level of iNOS, and COX-2 in FFC-treated grass carp were also downregulated as compared with LPS treated fish. Besides, FFC blocked the expression of Toll-like receptor 2 (TLR2) and then suppressed the phosphorylation of nuclear transcription factor-kappa B (NF-κB) p65 and degradation inhibitor of IκBα. Furthermore, administration of FFC inhibited the up-regulation of IRAK4, TRAF6 and TAK1 induced by LPS. These results suggest that the anti-inflammatory properties of FFC might be the results from the inhibition of iNOS, COX-2, IL-6, IL-1β, and TNF-α expressions through the down-regulation of Toll/NF-κB signaling pathways. Copyright © 2019 Elsevier Ltd. All rights reserved.

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