n(6)-(1-iminoethyl)lysine has been researched along with Inflammation* in 2 studies
2 other study(ies) available for n(6)-(1-iminoethyl)lysine and Inflammation
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Repurposing mosloflavone/5,6,7-trimethoxyflavone-resveratrol hybrids: Discovery of novel p38-α MAPK inhibitors as potent interceptors of macrophage-dependent production of proinflammatory mediators.
Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Dose-Response Relationship, Drug; Drug Discovery; Flavones; Flavonoids; Inflammation; Inflammation Mediators; Macrophages; Mice; Molecular Structure; p38 Mitogen-Activated Protein Kinases; Protein Kinase Inhibitors; RAW 264.7 Cells; Resveratrol; Structure-Activity Relationship | 2019 |
Chlojaponilactone B from Chloranthus japonicus: Suppression of Inflammatory Responses via Inhibition of the NF-κB Signaling Pathway.
Bioassay-guided fractionation of an ethanolic extract of Chloranthus japonicus led to the isolation of the known lindenane-type sesquiterpenoid chlojaponilactone B (1). This compound exhibited pronounced inhibition of nitric oxide (NO) production in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. Further anti-inflammatory assays showed that 1 suppressed the levels of some key inflammation mediators, such as iNOS, TNF-α, and IL-6, in a dose-dependent manner, and reduced the ear thickness and neutrophil infiltration in 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated mice. A mechanistic study revealed that compound 1 exerted its anti-inflammatory effects via the suppression of the NF-κB signaling pathway, which inhibited NF-κB-dependent transcriptional activity, IκBα phosphorylation, and p65 nuclear translocation. In contrast, chlojaponilactone B (1) was found to exert little influence on the MAPK signaling pathway. Topics: Animals; Anti-Inflammatory Agents; Cyclooxygenase 2; Cytokines; Inflammation; Inflammation Mediators; Interleukin-6; Lipopolysaccharides; Macrophages; Mice; Molecular Structure; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; Sesquiterpenes; Signal Transduction; Transcription Factor RelA; Tumor Necrosis Factor-alpha | 2016 |