Purified polysaccharide from Ginkgo biloba leaves inhibits P-selectin-mediated leucocyte adhesion and inflammation

Aim: To investigate the anti-inflammatory mechanism of the polysaccharides of Ginkgo biloba leaves (PGBL) by inhibiting leucocyte adhesion. Methods: The rough PGBL were isolated and purified. The anti-inflammatory effects of purified PGBL (p-PGBL) were assayed by ear edema induced by xylol and the a...

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Published inActa pharmacologica Sinica Vol. 29; no. 4; pp. 499 - 506
Main Authors Fei, Rui, Fei, Yu, Zheng, Sheng, Gao, Yan-guang, Sun, Hong-xia, Zeng, Xian-lu
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.04.2008
Nature Publishing Group
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Summary:Aim: To investigate the anti-inflammatory mechanism of the polysaccharides of Ginkgo biloba leaves (PGBL) by inhibiting leucocyte adhesion. Methods: The rough PGBL were isolated and purified. The anti-inflammatory effects of purified PGBL (p-PGBL) were assayed by ear edema induced by xylol and the acute perito- nitis model in mice. The effect of p-PGBL on inhibiting the interaction between Pselectin and its ligands was investigated by flow cytometry and flow chamber. Results: p-PGBL could effectively inhibit the acute inflammation in mice and interfere with the adhesion of HL-60 cells, a human leukaemia cell line, or neutrophils to P-selectin in static conditions, as well as the adhesion of neutrophils to Chinese hamster ovary cells expressing human P-selectin and human umbilical vein endothelial cells in flow conditions in a dose-dependant manner. Conclusions: p-PGBL can inhibit the inflammatory process through interfering with the interaction between P-selectin and its ligands.
Bibliography:polysaccharides of Ginkgo biloba leaves
inflammation
polysaccharides of Ginkgo biloba leaves; celladhesion inhibition; inflammation; P-selectin
R285
P-selectin
celladhesion inhibition
31-1347/R
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1671-4083
1745-7254
DOI:10.1111/j.1745-7254.2008.00765.x