Lavandulyl flavonoids from Sophora flavescens suppress lipopolysaccharide-Induced activation of nuclear factor-kappaB and mitogen-activated protein kinases in RAW264.7 cells

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Title
Lavandulyl flavonoids from Sophora flavescens suppress lipopolysaccharide-Induced activation of nuclear factor-kappaB and mitogen-activated protein kinases in RAW264.7 cells
Author(s)
Jong Min Han; Y Y Jin; H Y Kim; K H Park; Woo Song LeeTae Sook Jeong
Bibliographic Citation
Biological & Pharmaceutical Bulletin, vol. 33, no. 6, pp. 1019-1023
Publication Year
2010
Abstract
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)-1 ß,and iNOS in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Moreover, compounds 1 and 2 attenuated NF-κB activation by inhibition of IkBa 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.
Keyword
Lavandulyl flavonoidMitogen-acti-vated protein kinaseNitric oxideNuclear factor-κBReactive oxygen speciesSophora flavescens
ISSN
0918-6158
Publisher
Pharmaceutical Soc Japan
DOI
http://dx.doi.org/10.1248/bpb.33.1019
Type
Article
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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