Turmeronol A and turmeronol B from Curcuma longa prevent inflammatory mediator production by lipopolysaccharide-stimulated RAW264.7 macrophages, partially via reduced NF-κB signaling. Issue 9 (27th August 2019)

• Record Type: Journal Article
• Authors: Okuda-Hanafusa, Chinatsu; Uchio, Ryusei; Fuwa, Arisa; Kawasaki, Kengo; Muroyama, Koutarou; Yamamoto, Yoshihiro; Murosaki, Shinji
• Is Part Of: Food & function. Volume 10:Issue 9(2019)
• Page Start: 5779
• Page End: 5788
• Publication Date: 2019-08-27
• Subjects: Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Nutrition -- Periodicals; 664.07
• DOI: 10.1039/c9fo00336c
• Languages: English
• ISSNs: 2042-6496

Abstract

Abstract : Chronic inflammation depends on inflammatory mediators produced by activated macrophages and is the common pathological basis for various diseases. Abstract : Chronic inflammation depends on inflammatory mediators produced by activated macrophages and is the common pathological basis for various diseases. Turmeronol is a sesquiterpenoid found in the spice turmeric ( Curcuma longa ), which is known to have anti-inflammatory activity. To elucidate the anti-inflammatory mechanism of turmeronol, we investigated the influence of turmeronol A and turmeronol B in mouse macrophages (RAW264.7 cells) stimulated with lipopolysaccharide (LPS). Pretreatment of RAW264.7 cells with either turmeronol A or B significantly inhibited LPS-induced production of prostaglandin E2 and nitric oxide, as well as expression of mRNAs for the corresponding synthetic enzymes. In addition, the turmeronols significantly inhibited LPS-induced upregulation of interleukin-1β, interleukin-6, and tumor necrosis factor-α at the mRNA and protein levels. Both turmeronols also inhibited nuclear translocation of nuclear factor κB (NF-κB), with a similar time course to the NF-κB inhibitor pyrrolidine dithiocarbamate, but not curcumin (another NF-κB inhibitor). Thus, both turmeronols prevented activation of macrophages and inflammatory mediator production, possibly by suppressing activation of NF-κB, and therefore have potential for use in preventing chronic inflammatory diseases.