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Melatonin protects against lipopolysaccharide-induced epididymitis in sheep epididymal epithelial cells in vitro.

Immunology letters
October 1, 2019
Wen-Bo Ge et al. (9 authors)
Journal ArticleResearch Support, Non-U.S. Gov'tAnimal StudyMolecular Study
Extracted Claims (8)
InterventionDirectionEndpointPopulationDosageImpactClaim #
LPS treatment
increase
interleukin (IL)-1β mRNA levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#1
LPS treatment
increase
IL-6 mRNA levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#2
LPS treatment
increase
tumor necrosis factor α mRNA levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#3
LPS treatment
increase
cyclooxygenase (COX)-2 mRNA levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#4
LPS treatment
increase
COX-2 protein levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#5
LPS treatment
increase
Toll-like receptor (TLR)-4 protein levels
LPS-stimulated sheep epididymal epithelial cells
-
increased
#6
LPS treatment
increase
nuclear factor (NF)-κB p65 phosphorylation
LPS-stimulated sheep epididymal epithelial cells
-
increased
#7
melatonin
decrease
effects of LPS treatment
LPS-stimulated sheep epididymal epithelial cells
-
reversed in a dose-dependent manner
#8
Abstract

Melatonin has protective effects against inflammation but its role in epididymitis is unknown. We addressed this in the present study using lipopolysaccharide (LPS)-stimulated sheep epididymal epithelial cells as an in vitro inflammation model. We found that interleukin (IL)-1β, IL-6, tumor necrosis factor α, and cyclooxygenase (COX)-2 mRNA levels; COX-2 and Toll-like receptor (TLR)-4 protein levels; and nuclear factor (NF)-κB p65 phosphorylation were increased by LPS treatment. These effects were reversed in a dose-dependent manner by melatonin (10

Medical Subject Headings (MeSH)
AnimalsCells, CulturedCytokinesEpididymisEpididymitisEpithelial CellsLipopolysaccharidesMaleReceptor, Melatonin, MT1Receptor, Melatonin, MT2SheepSignal TransductionToll-Like Receptor 4Transcription Factor RelA
Study Links
PubMed ID31491433
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