Two enone fatty acids isolated from Gracilaria verrucosa suppress the production of inflammatory mediators by down-regulating NF-κB and STAT1 activity in lipopolysaccharide-stimulated RAW 264.7 cells

被引:38
|
作者
Lee, Hye-Ja [1 ]
Dang, Hung-The [2 ]
Kang, Gyeoung-Jin [1 ]
Yang, Eun-Jin [1 ]
Park, Sun-Soon [1 ]
Yoon, Weon-Jong [1 ]
Jung, Jee H. [2 ]
Kang, Hee-Kyoung [1 ]
Yoo, Eun-Sook [1 ]
机构
[1] Cheju Natl Univ, Coll Med, Dept Pharmacol, Cheju 690756, South Korea
[2] Pusan Natl Univ, Coll Pharm, Pusan 609735, South Korea
关键词
Gracilaria verrucosa; Inflammation; Nitric oxide; Pro-inflammatory cytokines; NF-kappa B; STAT1; NITRIC-OXIDE SYNTHASE; ACTIVATED RECEPTOR-GAMMA; SIGNAL-TRANSDUCTION; CYCLOPENTENONE PROSTAGLANDINS; MACROPHAGE ACTIVATION; EXPRESSION; LPS; MECHANISMS; KINASE; PHOSPHORYLATION;
D O I
10.1007/s12272-009-1320-0
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Gracilaria verrucosa is a common marine red alga that has anti-oxidant and anti-cancer properties. Recently, we reported that anti-inflammatory constituents of G. verrucosa operate through an unknown mechanism. For this reason, we isolated two enone fatty acids from G. verrucosa and investigated their molecular mechanism in LPS-stimulated RAW264.7 cells. We found that the two compounds inhibited the production of inflammatory markers (nitric oxide, TNF-alpha, and IL-6) in a dose-dependent manner. We next studied the effects of G. verrucosa compounds on LPS-induced signaling pathways. The two compounds suppressed NF-kappa B reporter activity by interfering with nuclear translocation of NF-kappa B and suppressed JAK/STAT (p-STAT1) signaling. These results suggest that G. verrucosa inhibits the production of inflammatory mediators (NO, TNF-alpha, and IL-6) by suppressing the activation of NF-kappa B and the phosphorylation of STAT1.
引用
收藏
页码:453 / 462
页数:10
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