Linked Life Data

16952378

Source:http://linkedlifedata.com/resource/pubmed/id/16952378

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25
pubmed:dateCreated
2006-11-14
pubmed:abstractText
TNF-alpha is a key molecule in obesity-related metabolic disturbances. This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines. The treatment of well-differentiated 3T3-L1 cells with 20 mM of NAC significantly increased the reduced glutathione concentration up to 150% of control. The treatment with 10 ng/ml of TNF-alpha decreased antioxidant enzyme levels such as CuZn-superoxide dismutase (SOD), MnSOD and catalase, and activated NF-kappaB in 3T3-L1 adipocytes. The activation of NF-kappaB was significantly prevented by the pretreatment with 20 mM of NAC. TNF-alpha (1-10 ng/ml) dose-dependently increased interleukin (IL)-6 and plasminogen activator inhibitor-1 (PAI-1) secretion from 3T3-L1 adipocytes, while decreased adiponectin secretion. NAC (5-20 mM) attenuated the TNF-alpha-induced changes in these adipocytokine secretions in a dose-dependent manner. The effect of TNF-alpha and NAC on the adipocytokine productions was exerted at the m-RNA level, judging from results of the real time RT-PCR analysis. The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes. NAC may have the potential to improve the obesity-related abnormal adipocytokine metabolism by attenuating the TNF-alpha-induced oxidant-antioxidant imbalance in adipocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2405-12
pubmed:meshHeading
pubmed-meshheading:16952378-3T3-L1 Cells, pubmed-meshheading:16952378-Acetylcysteine, pubmed-meshheading:16952378-Adipocytes, pubmed-meshheading:16952378-Adiponectin, pubmed-meshheading:16952378-Animals, pubmed-meshheading:16952378-Antioxidants, pubmed-meshheading:16952378-Catalase, pubmed-meshheading:16952378-Cell Differentiation, pubmed-meshheading:16952378-Cell Nucleus, pubmed-meshheading:16952378-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:16952378-Glutathione, pubmed-meshheading:16952378-Interleukin-6, pubmed-meshheading:16952378-Mice, pubmed-meshheading:16952378-NF-kappa B, pubmed-meshheading:16952378-Plasminogen Activator Inhibitor 1, pubmed-meshheading:16952378-RNA, Messenger, pubmed-meshheading:16952378-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16952378-Superoxide Dismutase, pubmed-meshheading:16952378-Tumor Necrosis Factor-alpha
pubmed:year
2006
pubmed:articleTitle
N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes.
pubmed:affiliation
Department of Pediatrics, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, 807-8555, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't