Source:http://linkedlifedata.com/resource/pubmed/id/19998383
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-6-14
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pubmed:abstractText |
Obese adipose tissues are characterized by the enhanced infiltration of macrophages. It is considered that the paracrine loop involving monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and the free fatty acid between adipocytes and macrophages establishes a vicious cycle that aggravates inflammatory changes and insulin resistance in obese adipose tissues. Diosgenin, a saponin aglycon found in a variety of plants, has anti-inflammatory properties. In the present study, we examined the effect of diosgenin on the inflammatory changes in the interaction between adipocytes and macrophages. A coculture of 3T3-L1 adipocytes and RAW 264 macrophages markedly enhanced the production of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and nitric oxide compared with the sum of their single cultures; however, treatment with diosgenin inhibited the production of these proinflammatory mediators. Diosgenin also suppressed the inflammation in RAW 264 macrophages that was induced by the conditioned medium derived from 3T3-L1 adipocytes. Furthermore, diosgenin inhibited the conditioned medium-induced degradation of inhibitor kappaB and the phosphorylation of c-jun N-terminal kinase in macrophages. These results indicate that diosgenin exhibits anti-inflammatory properties in the interaction of adipocytes and macrophages by inhibiting the inflammatory signals in macrophages. Diosgenin may be useful for ameliorating the inflammatory changes in obese adipose tissues.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Diosgenin,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappaB inhibitor alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Tlr4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1613-4133
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pubmed:author |
pubmed-author:HiraiShizukaS,
pubmed-author:HoshinoShoheiS,
pubmed-author:KawadaTeruoT,
pubmed-author:LeeJoo-YoungJY,
pubmed-author:MizoguchiNorikoN,
pubmed-author:NakanoYukiY,
pubmed-author:NarukamiToshihikoT,
pubmed-author:SICKHH,
pubmed-author:TakahashiNobuyukiN,
pubmed-author:TaketaniKeikoK,
pubmed-author:TsugeNobuakiN,
pubmed-author:UemuraTakuT
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pubmed:issnType |
Electronic
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
797-804
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pubmed:meshHeading |
pubmed-meshheading:19998383-3T3-L1 Cells,
pubmed-meshheading:19998383-Adipocytes,
pubmed-meshheading:19998383-Animals,
pubmed-meshheading:19998383-Anti-Inflammatory Agents,
pubmed-meshheading:19998383-Cell Communication,
pubmed-meshheading:19998383-Coculture Techniques,
pubmed-meshheading:19998383-Diosgenin,
pubmed-meshheading:19998383-Fatty Acids, Nonesterified,
pubmed-meshheading:19998383-I-kappa B Proteins,
pubmed-meshheading:19998383-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:19998383-Macrophages,
pubmed-meshheading:19998383-Mice,
pubmed-meshheading:19998383-Phosphorylation,
pubmed-meshheading:19998383-Toll-Like Receptor 4,
pubmed-meshheading:19998383-Tumor Necrosis Factor-alpha
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pubmed:year |
2010
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pubmed:articleTitle |
Diosgenin attenuates inflammatory changes in the interaction between adipocytes and macrophages.
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pubmed:affiliation |
Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Kyoto, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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