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- W2344404464 abstract "The therapeutic effectiveness of moracins as 2-arylbenzofuran derivatives against airway inflammation was examined. Moracin M, O, and R were isolated from the root barks of Morus alba, and they inhibited interleukin (IL)-6 production from IL-1β-treated lung epithelial cells (A549) at 101–00 μM. Among them, moracin M showed the strongest inhibitory effect (IC50=8.1 μM). Downregulation of IL-6 expression by moracin M was mediated by interrupting the c-Jun N-terminal kinase (JNK)/c-Jun pathway. Moracin derivatives inhibited inducible nitric oxide synthase (iNOS)-catalyzed NO production from lipopolysaccharide (LPS)-treated alveolar macrophages (MH-S) at 50–100 μM. In particular, moracin M inhibited NO production by downregulating iNOS. When orally administered, moracin M (20–60 mg/kg) showed comparable inhibitory action with dexamethasone (30 mg/kg) against LPS-induced lung inflammation, acute lung injury, in mice with that of dexamethasone (30 mg/kg). The action mechanism included interfering with the activation of nuclear transcription factor-κB in inflamed lungs. Therefore, it is concluded that moracin M inhibited airway inflammation in vitro and in vivo, and it has therapeutic potential for treating lung inflammatory disorders." @default.
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- W2344404464 date "2016-07-01" @default.
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- W2344404464 title "Moracin M inhibits airway inflammation by interrupting the JNK/c-Jun and NF-κB pathways in vitro and in vivo" @default.
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- W2344404464 doi "https://doi.org/10.1016/j.ejphar.2016.04.055" @default.
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