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Anti-inflammatory effects of cordycepin in lipopolysaccharide-stimulated RAW 264.7 macrophages through Toll-like receptor 4-mediated suppression of mitogen-activated protein kinases and NF-kappa B signaling pathways
- Anti-inflammatory effects of cordycepin in lipopolysaccharide-stimulated RAW 264.7 macrophages through Toll-like receptor 4-mediated suppression of mitogen-activated protein kinases and NF-kappa B signaling pathways
- Choi, YH[Choi, Yung Hyun]; Kim, GY[Kim, Gi-Young]; Lee, HH[Lee, Hye Hyeon]
- DGIST Authors
- Lee, HH[Lee, Hye Hyeon]
- Issue Date
- Drug Design Development and Therapy, 8, 1941-1953
- Article Type
- Animal; Animal Cell; Animals; Antagonists and Inhibitors; Anti-Inflammation; Anti-Inflammatory Activity; Anti-Inflammatory Agents, Non-Steroidal; Cell Culture; Cell Nucleus Transplantation; Cells, Cultured; Chemistry; Controlled Study; Cordycepin; Cyclooxygenase 2; Cytokine Release; Deoxyadenosine Derivative; Deoxyadenosines; Dose-Response; Dose-Response Relationship, Drug; Drug Effect; Drug Effects; Drug Mechanism; Enzyme Inactivation; Enzyme Inhibition; Enzyme Phosphorylation; Enzyme Repression; Fatty Acid Synthesis; Gene Expression Regulation; Immunoglobulin Enhancer Binding Protein; Inducible Nitric Oxide Synthase; Interleukin-1 Beta; Lipopolysaccharide; Lipopolysaccharides; Macrophage; Macrophages; Metabolism; Mice; Mitogen-Activated Protein Kinase; Mitogen-Activated Protein Kinases; Mouse; NF-Kappa B; Nitric Oxide; Non-Human; Non-Steroid Antiinflammatory Agent; Oxidation-Reduction Potential; Prostaglandin E2; Protein Binding; Protein Carbohydrate Interaction; Protein Degradation; Protein Phosphorylation; Protein Synthesis Inhibition; Raw 264.7 Macrophage; Signal Transduction; Structure-Activity Relationship; Structure Activity Relation; Synaptotagmin I; Toll-Like Receptor4; Tumor Necrosis Factor-Alpha
- Cordycepin is the main functional component of the Cordyceps species, which has been widely used in traditional Oriental medicine. This compound possesses many pharmacological properties, such as an ability to enhance immune function, as well as antioxidant, antiaging, and anticancer effects. In the present study, we investigated the anti-inflammatory effects of cordycepin using a murine macrophage RAW 264.7 cell model. Our data demonstrated that cordycepin suppressed production of proinflammatory mediators such as nitric oxide (NO) and prostaglandin E2 by inhibiting inducible NO synthase and cyclooxygenase-2 gene expression. Cordycepin also inhibited the release of proinflammatory cytokines, including tumor necrosis factor-alpha and interleukin-1-beta, through downregulation of respective mRNA expression. In addition, pretreatment with cordycepin significantly inhibited lipopolysaccharide (LPS)-induced phosphorylation of mitogen-activating protein kinases and attenuated nuclear translocation of NF-κB by LPS, which was associated with abrogation of inhibitor kappa B-alpha degradation. Furthermore, cordycepin potently inhibited the binding of LPS to macrophages and LPS-induced Toll-like receptor 4 and myeloid differentiation factor 88 expression. Taken together, the results suggest that the inhibitory effects of cordycepin on LPS-stimulated inflammatory responses in RAW 264.7 macrophages are associated with suppression of mitogen-activating protein kinases and activation of NF-κB by inhibition of the Toll-like receptor 4 signaling pathway. © 2014 Choi et al.
- Dove Medical Press Ltd.
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