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β-Carotene has shown antioxidant and anti- inflammatory activities; however, its molecular mechanism has not been clearly defined. We exa-mined in vitro and in vivo regulatory function of β-carotene on the production of nitric oxide (NO) and PGE2 as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2, TNF-α, and IL-1β. β- Carotene inhibited the expression and production of these inflammatory mediators in both LPS- stimulated RAW264.7 cells and primary macro-phages in a dose-dependent fashion as well as in LPS-administrated mice. Furthermore, this com-pound suppressed NF-κB activation and iNOS promoter activity in RAW264.7 cells stimulated with LPS. β-Carotene blocked nuclear translocation of NF-κB p65 subunit, which correlated with its inhibitory effect on IκBα phosphorylation and degradation. This compound directly blocked the intracellular accumulation of reactive oxygen species in RAW264.7 cells stimulated with LPS as both the NADPH oxidase inhibitor diphenylene t pyrrolidine dithiocar-bamate did. The inhibition of NADPH oxidase also inhibited NO production, iNOS expression, and iNOS promoter activity. These results suggest that β- carotene possesses anti-inflammatory activity by functioning as a potential inhibitor for redox-based NF-κB activation, probably due to its antioxidant activity.

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