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Title 

Effect of 5-O-methylhirsutanonol on nuclear factor-κB-dependent production of NO and expression of iNOS in lipopolysaccharide-Induced RAW264.7 cells

 

LPS처리에 의해 유도된 NF-kB에 의존하는 iNOS

Authors 

Jong Min HanWoo Song LeeJ R KimJ SonOh Hyung KwonHyun Jun LeeJung Joon LeeTae Sook Jeong

Publisher 

American Chemical Society

Issue Date 

2008

Citation 

Journal of Agricultural and Food Chemistry, vol. 56, no. 1, pp. 92-98

Keywords 

5-O-methylhirsutanonol (5-MH)diarylheptanoidsinducible nitric oxide synthease (iNOS)nitric oxide (NO)nuclear factor κB (NF-κB)reactive oxygen species (ROS)5 O methylhirsutanonol5-O-methylhirsutanonolantiinflammatory agentimmunoglobulin enhancer binding protein

Abstract 

Diarylheptanoids are known to have anti-inflammatory and anti-atherosclerotic activities in various cell types, including macrophages. 5-O-Methylhirsutanonol (5-MH) isolated from the leaves of Alnus japonica Steud exhibited the antioxidant activities on Cu2+- and AAPH-mediated low-density lipoprotein (LDL) oxidation in the thiobarbituric acid-reactive substances (TBARS) assay as well as the macrophage-mediated LDL oxidation. In the main study, we examined anti-inflammatory activities of 5-O- methylhirsutanonol (5-MH) on nuclear factor κB (NF-κB)-dependent nitric oxide (NO) production and expression of inducible nitric oxide synthease (iNOS) in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. 5-MH inhibited NO production with an IC50 value of 14.5 μM and expression of both iNOS protein and iNOS mRNA in a parallel dose-response manner. Then, expression of inflammation-associated genes, such as TNF-α, COX-2, and IL-1β, was suppressed by 5-MH, as determined by reverse transcriptase polymerase chain reaction analysis. Moreover, 5-MH attenuated NF-κB activation by inhibition of hyperphosphorylation of IκB-α and its subsequent proteolytic degradation and p65 nuclear translocation, as well as preventing DNA-binding ability. In addition, 5-MH suppressed the mRNA expression of the gene reactive oxygen species (ROS) concerned in the regulation of NF-κB signaling.

ISSN 

0021-8561

Link 

http://dx.doi.org/10.1021/jf0721085

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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