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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Anti-Inflammatory Agents, Antioxidants, Cell Survival, Cells, Cultured, Cyclooxygenase 2, Dose-Response Relationship, Drug, Heme Oxygenase-1, Intramolecular Oxidoreductases, Lipopolysaccharides, Macrophage Activation, Macrophages, Peritoneal, Male, Melatonin, Membrane Proteins, Mice, NF-E2-Related Factor 2, NF-kappa B, Nitric Oxide, Nitric Oxide Synthase Type II, Nitrites, Phosphorylation, Prostaglandin-E Synthases, Signal Transduction, Time Factors, Transcription, Genetic, p38 Mitogen-Activated Protein Kinases.
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Does melatonin modulate microsomal PGE synthase 1 and NF-E2-related factor-2-regulated antioxidant enzyme expression in LPS-induced murine peritoneal macrophages? Context: Increasing evidence demonstrates that melatonin regulates inflammatory and immune processes acting as both an activator and inhibitor of these responses. Nevertheless, the molecular mechanisms of its anti-inflammatory action remain unclear. Here we have characterized the cellular mechanisms underlying the redox modulation of LPS-stimulated inflammatory responses in murine peritoneal macrophages by melatonin to provide insight into its anti-inflammatory effects. Murine peritoneal macrophages were isolated and treated with melatonin in the presence or absence of LPS (5 μg·mL(-1) ) for 18 h. Cell viability was determined using sulforhodamine B assay and NO production was measured using the Griess reaction. Pro-inflammatory enzymes and transcription factors were detected by Western blotting. Without affecting cell viability, melatonin (12.5, 25, 50 and 100 μM) reduced the level of nitrites, inducible NOS (iNOS), COX-2 and microsomal PGE synthase-1 (mPGES1) protein, and p38 MAPK phosphorylation, and prevented NF-κB translocation. Furthermore, melatonin treatment significantly increased NF-E2-related factor 2 (Nrf2) and haem oxygenase 1 (HO1) protein levels in murine macrophages exposed to LPS.
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Melatonin reduced pro-inflammatory mediators and enhanced the expression of HO1 via NF-κB, p38 MAPK and Nrf2 cascade signalling pathways in murine macrophages. Thus, melatonin might be a promising target for diseases associated with overactivation of macrophages. Final Decision: yes