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Title 

Hematein inhibits atherosclerosis by inhibition of reactive oxygen generation and NF-κB-dependent inflammatory mediators in hyperlipidemic mice

Authors 

J H ChoiTae Sook JeongD Y KimY M KimH J NaKi Hoan NamSae Bom LeeHyoung-Chin KimSei Ryang OhYang Kyu ChoiSong Hae BokGoo Taeg Oh

Publisher 

Raven Press Publishers

Issue Date 

2003

Citation 

Journal of Cardiovascular Pharmacology, vol. 42, no. 2, pp. 287-295

Keywords 

anti-inflammationantiatherogenesishemateinNF-κBreactive oxygen speciesantiinflammatory agentimmunoglobulin enhancer binding proteininterleukin 1betareactive oxygen metaboliteatherosclerosis

Abstract 

Hematein, a natural compound, is a known antiinflammatory and antiatherogenic agent in the rabbit model. The authors investigated the effects of this compound on atherogenesis and possible mechanisms of the actions in the hyperlipidemic mice. Low-density lipoprotein receptor-deficient (Ldlr-/-) mice fed a high-cholesterol diet alone for 8 weeks developed the fatty streak lesion in the aortic sinus, whereas this lesion was significantly reduced by hematein treatment without a change in plasma lipid levels compared with control mice. Hematein treatment reduced plasma levels of lipid peroxide and superoxide generation in LPS-stimulated peritoneal macrophage. Hematein treatment inhibited NF-κB-DNA binding activity in peritoneal macrophages from Ldlr-/- mice and the activation of NF-κB in RAW264.7 macrophages. This compound suppressed plasma nitrite/nitrate levels in Ldlr-/- mice and NO production and iNOS expression in LPS+IFNγ-stimulated peritoneal macrophages. Hematein treatment also suppressed the activity of iNOS promoters in RAW264.7 macrophages, and reduced the plasma levels of TNF-α and IL-1β and the production of these cytokines in LPS+IFNγ-stimulated peritoneal macrophages. These results suggest that hematein inhibits atherosclerotic lesion formation, possibly by reducing proinflammatory mediators through a decrease in reactive oxygen species generation and NF-κB activation.

ISSN 

0160-2446

Link 

http://dx.doi.org/10.1097/00005344-200308000-00019

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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