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      Cryptotanshinone suppressed inflammatory cytokines secretion in RAW264.7 macrophages through inhibition of the NF-κB and MAPK signaling pathways.

      Inflammation
      Animals, Anti-Inflammatory Agents, pharmacology, Blotting, Western, Cell Line, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Inflammation, immunology, metabolism, Interleukin-6, antagonists & inhibitors, Lipopolysaccharides, MAP Kinase Signaling System, drug effects, Macrophages, Mice, Mitogen-Activated Protein Kinases, NF-kappa B, Phenanthrenes, Phosphorylation, Signal Transduction, Tumor Necrosis Factor-alpha

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          Abstract

          Cryptotanshinone (CTS), a major constituent extracted from the medicinal herb Salvia miltiorrhiza Bunge, has well-documented antioxidative and anti-inflammatory effects. In the present study, the pharmacological effects and underlying molecular mechanisms of CTS on lipopolysaccharide (LPS)-induced inflammatory responses were investigated. By enzyme-linked immunosorbent assay, we observed that CTS reduced significantly the production of proinflammatory mediators (tumor necrosis factor-α and interleukin-6) induced by LPS in murine macrophage-like RAW264.7 cells. Mechanistically, CTS inhibited markedly the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, p38MAPK, and JNK, which are crucially involved in regulation of proinflammatory mediator secretion. Moreover, immunofluorescence and western blot analysis indicated that CTS abolished completely LPS-triggered nuclear factor-κB (NF-κB) activation. Taken together, these data implied that NF-κB and MAPKs might be the potential molecular targets for clarifying the protective effects of CTS on LPS-induced inflammatory cytokine production in macrophages.

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