Journal
INNATE IMMUNITY
Volume 16, Issue 5, Pages 333-339Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1753425909351880
Keywords
inflammation; lipopolysaccharide; nuclear factor-kappa B; pro-inflammatory mediators; sesamol
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Funding
- National Science Council, Taiwan [NSC-96-2221-E-006-029-MY3, NSC-96-2314-B-006-012-MY2, NSC-96-2628-B-006-038-MY3]
- Taiwan Department of Health [DOH92-TD-1009]
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We examined the effects of sesamol on the lipopolysaccharide (LPS)-induced inflammatory response. Sesamol inhibited serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and nitrite production in LPS-treated mice, and inhibited LPS-induced inducible nitric oxide synthase expression in mouse leukocytes. Sesamol also down-regulated TNF-alpha, IL-1 beta, and nitrite production as well as inducible nitric oxide synthase expression in LPS-treated RAW 264.7 cells. Further, sesamol inhibited LPS-induced nuclear factor (NF)-kappa B translocation and inhibitor (I) kappa B-alpha phosphorylation in RAW 264.7 cells. By inhibiting TNF-alpha, IL-1 beta, and nitrite levels, and interfering with the NFkB kappa B pathway, sesamol down-regulated the LPS-initiated inflammatory response.
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