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

Jae Hoon Choi, Tae Sook Jeong, Dae Yong Kim, Young Myeong Kim, Hee Jun Na, Ki Hwan Nam, Sae Bom Lee, Hyoung Chin Kim, Sei Ryang Oh, Yang Kyu Choi, Song Hae Bok, Goo Taeg Oh

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

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.

Original languageEnglish
Pages (from-to)287-295
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume42
Issue number2
DOIs
StatePublished - 1 Aug 2003

Keywords

  • Anti-inflammation
  • Antiatherogenesis
  • Hematein
  • NF-κB
  • Reactive oxygen species

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