2--4--dihydroxy-6--methoxy-3--5--dimethylchalcone has been researched along with Inflammation* in 1 studies
1 other study(ies) available for 2--4--dihydroxy-6--methoxy-3--5--dimethylchalcone and Inflammation
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Dimethyl cardamonin inhibits lipopolysaccharide-induced inflammatory factors through blocking NF-kappaB p65 activation.
This study has found that dimethyl cardamonin (2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone; DMC), a naturally occurring chalcone, showed potent anti-inflammatory effects in vitro and in vivo. In a cellular model of inflammation, DMC inhibited production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) and attenuated expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1 beta, inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). DMC prevented nuclear translocation of the nuclear factor-kappaB (NF-kappaB) p65 subunit by reducing inhibitor of kappaB alpha (I-kappaB alpha) phosphorylation and degradation, which resulted in a suppression of NF-kappaB activities for its target genes. In a mouse model of endotoxin shock, the intraperitoneal injection (i.p.) of DMC (1-50mg/kg) suppressed TNF-alpha, IL-6 and IL-1 beta secretion in LPS-induced mouse blood serum. These results suggest that DMC exerts anti-inflammatory effects through blocking NF-kappaB activation, therefore, DMC may act as an effective therapeutic strategy against a variety of inflammatory diseases. Topics: Animals; Anti-Inflammatory Agents; Chalcones; Cyclooxygenase 2; Dinoprostone; Inflammation; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Macrophages; Male; Mice; Mice, Inbred ICR; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; Shock, Septic; Transcription Factor RelA; Tumor Necrosis Factor-alpha | 2010 |