4. Influence of 3,3'-diindolylmethane on expression of inflammatory cytokines in periodontal ligament cells induced by lipopolysaccharide
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3,3′-Diindolylmethane Suppresses the Inflammatory Response to Lipopolysaccharide in Murine Macrophages
Article (PDF Available) in Journal of Nutrition138(1):17-23 · February 2008 with 50 Reads
DOI: 10.1093/jn/138.1.17 · Source: PubMed
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Han Jin Cho
Hallym University

Mi Ra Seon
+ 3

Yeo Myeong Lee

Jung Han Yoon Park
Hallym University
Show more authors
Abstract
3,3'-Diindolylmethane (DIM), a major acid-condensation product of indole-3-carbinol, has been shown to have multiple anticancer effects in experimental models. Because recurrent or chronic inflammation has been implicated in the development of a variety of human cancers, this study examined the antiinflammatory effects of DIM and the underlying mechanisms using lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. DIM significantly decreased the release of nitric oxide (NO), prostaglandin (PG)E2, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1beta by RAW264.7 cells treated with LPS. DIM inhibited LPS-induced increases in protein levels of inducible NO synthase (iNOS), which were accompanied by decreased iNOS mRNA levels and transcriptional activity. The mRNA levels of phospholipase A2 decreased, whereas neither cyclooxygenases-2 protein nor transcript was altered by DIM. In addition, DIM suppressed LPS-induced nuclear factor-kappaB (NF-kappaB) transcriptional activity, NF-kappaB DNA-binding activity, translocation of p65 (RelA) to the nucleus, and degradation of inhibitor of kappaB alpha. Furthermore, DIM decreased LPS-induced transcriptional activity of activator protein (AP)-1, AP-1 DNA-binding activity, and phosphorylation of stress-activated protein kinase/Jun-N-terminal kinase and c-Jun. We demonstrate that DIM inhibits LPS-induced release of proinflammatory mediators in murine macrophages. Downregulation of NF-kappaB and AP-1 signaling may be one of the mechanisms by which DIM inhibits inflammatory responses.
3,3′-Diindolylmethane Suppresses the Inflammatory Response to Lipopolysaccharide in Murine Macrophages
Article (PDF Available) in Journal of Nutrition138(1):17-23 · February 2008 with 50 Reads
DOI: 10.1093/jn/138.1.17 · Source: PubMed
Export this citation

Han Jin Cho
Hallym University

Mi Ra Seon
+ 3

Yeo Myeong Lee

Jung Han Yoon Park
Hallym University
Show more authors
Abstract
3,3'-Diindolylmethane (DIM), a major acid-condensation product of indole-3-carbinol, has been shown to have multiple anticancer effects in experimental models. Because recurrent or chronic inflammation has been implicated in the development of a variety of human cancers, this study examined the antiinflammatory effects of DIM and the underlying mechanisms using lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. DIM significantly decreased the release of nitric oxide (NO), prostaglandin (PG)E2, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1beta by RAW264.7 cells treated with LPS. DIM inhibited LPS-induced increases in protein levels of inducible NO synthase (iNOS), which were accompanied by decreased iNOS mRNA levels and transcriptional activity. The mRNA levels of phospholipase A2 decreased, whereas neither cyclooxygenases-2 protein nor transcript was altered by DIM. In addition, DIM suppressed LPS-induced nuclear factor-kappaB (NF-kappaB) transcriptional activity, NF-kappaB DNA-binding activity, translocation of p65 (RelA) to the nucleus, and degradation of inhibitor of kappaB alpha. Furthermore, DIM decreased LPS-induced transcriptional activity of activator protein (AP)-1, AP-1 DNA-binding activity, and phosphorylation of stress-activated protein kinase/Jun-N-terminal kinase and c-Jun. We demonstrate that DIM inhibits LPS-induced release of proinflammatory mediators in murine macrophages. Downregulation of NF-kappaB and AP-1 signaling may be one of the mechanisms by which DIM inhibits inflammatory responses.
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