2'-Methoxy-4'6'-Bis(Methoxymethoxy)Chalcone Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages

Title
2'-Methoxy-4'6'-Bis(Methoxymethoxy)Chalcone Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages
Author(s)
Jin XY[Jin XY]이성희[이성희]박필훈허진[허진]김순애[김순애]김학성[김학성]손동환[손동환]
Keywords
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; ANTIOXIDANT RESPONSE ELEMENT; HEME OXYGENASE-1; CHALCONE DERIVATIVES; RAW-264.7 CELLS; COORDINATE REGULATION; CHRONIC INFLAMMATION; OXIDATIVE STRESS; EXPRESSION
Issue Date
201006
Publisher
WILEY-BLACKWELL
Citation
BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY, v.106, no.6, pp.454 - 460
Abstract
Chalcones have anti-inflammatory properties. Here, we synthesized 2'-methoxy-4'6'-bis(methoxymethoxy)chalcone (MBMC) and examined its anti-inflammatory effects. MBMC inhibited nitric oxide production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages. MBMC also blocked LPS-induced activation of nuclear factor kappa B (NF-kappa B), p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK). MBMC increased haem oxygenase 1 (HO-1) expression and nuclear accumulation of nuclear factor-erythroid 2-related factor 2 (Nrf2), an essential transcription factor for HO-1 induction. Treatment with tin protoporphyrin, a selective inhibitor of HO-1, reversed the inhibition of nitric oxide production by MBMC, suggesting that HO-1 induction mediates MBMC-mediated suppression of nitric oxide production. MBMC treatment rapidly and transiently decreased glutathione (GSH) levels, and treatment with GSH-Et (cell permeable form of GSH) or N-acetylcysteine (precursor of GSH) counteracted the HO-1 and Nrf2 expression elicited by MBMC, indicating that MBMC-induced HO-1 expression requires transient depletion of GSH. In summary, MBMC inhibits LPS-stimulated nitric oxide production via down-regulation of inflammatory pathways (NF-kappa B, p38 and JNK) and induction of the protective enzyme, HO-1.
URI
http://hdl.handle.net/YU.REPOSITORY/22386http://dx.doi.org/10.1111/j.1742-7843.2009.00524.x
ISSN
1742-7835
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약학대학 > 약학부 > Articles
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