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Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it...

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Detalles Bibliográficos
Autores principales: Jun, Fang, Yue, Zheng Qin, Bin, Wang Hong, Wen, Ju Dian, Hua, Yi Yang
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365368/
https://www.ncbi.nlm.nih.gov/pubmed/18475487
http://dx.doi.org/10.1155/S0962935192000565
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author Jun, Fang
Yue, Zheng Qin
Bin, Wang Hong
Wen, Ju Dian
Hua, Yi Yang
author_facet Jun, Fang
Yue, Zheng Qin
Bin, Wang Hong
Wen, Ju Dian
Hua, Yi Yang
author_sort Jun, Fang
collection PubMed
description Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.
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spelling pubmed-23653682008-05-12 Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages Jun, Fang Yue, Zheng Qin Bin, Wang Hong Wen, Ju Dian Hua, Yi Yang Mediators Inflamm Research Article Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect. Hindawi Publishing Corporation 1992 /pmc/articles/PMC2365368/ /pubmed/18475487 http://dx.doi.org/10.1155/S0962935192000565 Text en Copyright © 1992 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Jun, Fang
Yue, Zheng Qin
Bin, Wang Hong
Wen, Ju Dian
Hua, Yi Yang
Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title_full Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title_fullStr Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title_full_unstemmed Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title_short Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages
title_sort effects of esculentoside a on turnour necrosis factor production by mice peritoneal macrophages
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365368/
https://www.ncbi.nlm.nih.gov/pubmed/18475487
http://dx.doi.org/10.1155/S0962935192000565
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