Linked Life Data

18170962

Source:http://linkedlifedata.com/resource/pubmed/id/18170962

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-1-3
pubmed:abstractText
The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes. Stimulation by the combination of 5 microg/ml of LPS and 100 ng/ml of TNF-alpha (LT) significantly enhanced NO production in 3T3-L1 adipocytes. Preincubation of the cells with NAC (5-20 mM) for 24 h suppressed the increased NO production in a dose-dependent manner. The production of NO was decreased by 49% at the concentration of 20 mM of NAC. The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis. Nuclear factor-kappa B (NF-kappa B) was significantly activated by LT-treatment, while the pretreatment with 20 mM of NAC prevented the activity by 42%. Pyrrolidine dithiocarbamate (PDTC), a NF-kappaB inhibitor, also inhibited the LT-mediated NO production dose-dependently. One hundred microM of PDTC inhibited the NO production by 46%. We also investigated the effect of NAC and PDTC on the production of interleukein-6 (IL-6), which is regulated transcriptionally by NF-kappa B in 3T3-L1 adipocytes. IL-6 production was markedly increased by LT stimulus, and the enhanced secretion of IL-6 was suppressed in a dose-dependent manner by pretreatment with NAC or PDTC. These results suggest that NAC regulates iNOS expression and NO production in adipocytes through the modulating activation of NF-kappa B.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0387-821X
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
417-29
pubmed:meshHeading
pubmed-meshheading:18170962-3T3-L1 Cells, pubmed-meshheading:18170962-Acetylcysteine, pubmed-meshheading:18170962-Animals, pubmed-meshheading:18170962-Antioxidants, pubmed-meshheading:18170962-Cells, Cultured, pubmed-meshheading:18170962-Depression, Chemical, pubmed-meshheading:18170962-Dose-Response Relationship, Drug, pubmed-meshheading:18170962-Enzyme Induction, pubmed-meshheading:18170962-Interleukin-6, pubmed-meshheading:18170962-Lipopolysaccharides, pubmed-meshheading:18170962-Mice, pubmed-meshheading:18170962-NF-kappa B, pubmed-meshheading:18170962-Nitric Oxide, pubmed-meshheading:18170962-Nitric Oxide Synthase, pubmed-meshheading:18170962-Oxidative Stress, pubmed-meshheading:18170962-Pyrrolidines, pubmed-meshheading:18170962-Stimulation, Chemical, pubmed-meshheading:18170962-Thiocarbamates, pubmed-meshheading:18170962-Tumor Necrosis Factor-alpha
pubmed:year
2007
pubmed:articleTitle
N-acetylcysteine inhibits induction of nitric oxide synthase in 3T3-L1 adipocytes.
pubmed:affiliation
Department of Pediatrics, School of Medicine, University of Occupational and Environmental Health, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't