Lavandulyl Flavonoids from Sophora flavescens Suppress Lipopolysaccharide-Induced Activation of Nuclear Factor-κB and Mitogen-Activated Protein Kinases in RAW264.7 Cells

Oxidized low-density lipoprotein (oxLDL) and reactive oxygen species (ROS) play key roles in the early stage of atherosclerosis. Nitric oxide (NO) and ROS are responsible for regulation of the transcriptional pathways of nuclear Factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK), key regu...

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Published inBiological & pharmaceutical bulletin Vol. 33; no. 6; pp. 1019 - 1023
Main Authors Han, Jong-Min, Jin, Yue-Yan, Kim, Hoi Young, Park, Ki Hun, Lee, Woo Song, Jeong, Tae-Sook
Format Journal Article
LanguageEnglish
Published The Pharmaceutical Society of Japan 2010
Subjects
Arteriosclerosis
c-Jun amino-terminal kinase
Extracellular signal-regulated kinase
Flavonoids
Gene regulation
Immune response
Inflammation
Interleukins
lavandulyl flavonoid
Lipoproteins
Macrophages
MAP kinase
mitogen-activated protein kinase
NF- Kappa B protein
Nitric oxide
Nitric-oxide synthase
nuclear factor-κB
Nuclear transport
Phosphorylation
Proteolysis
Reactive oxygen species
Sophora
Sophora flavescens
Tumor necrosis factor
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Summary:Oxidized low-density lipoprotein (oxLDL) and reactive oxygen species (ROS) play key roles in the early stage of atherosclerosis. Nitric oxide (NO) and ROS are responsible for regulation of the transcriptional pathways of nuclear Factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK), key regulators of cellular inflammatory and immune responses. Previously, we examined LDL-antioxidant activities of the nine flavonoids isolated from Sophora flavescens. Among these, two lavandulyl flavonoids, kurarinone (1) and kuraridin (2) inhibited inducible nitric oxide synthase (iNOS)-dependent NO production and ROS generation, and suppressed remarkably the expression of inflammatory cytokines, CCL2, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and iNOS in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Moreover, compounds 1 and 2 attenuated NF-κB activation by inhibition of IκBα proteolysis and p65 nuclear translocation, as well as phosphorylation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK), and p38 MAP kinases.
Bibliography:ObjectType-Article-2
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ISSN:0918-6158
1347-5215
1347-5215
DOI:10.1248/bpb.33.1019