Effect of esculentoside A on cellular adhesion.
- Author:
Zhen-yu XIAO
1
;
Jun-ping ZHANG
;
Feng LU
;
Da-zhi ZHANG
;
Qin-yue ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Adult; CD18 Antigens; biosynthesis; genetics; Cell Adhesion; drug effects; Cell Line; Drugs, Chinese Herbal; isolation & purification; pharmacology; Endothelial Cells; metabolism; physiology; Humans; Intercellular Adhesion Molecule-1; biosynthesis; genetics; Neutrophils; metabolism; physiology; Oleanolic Acid; analogs & derivatives; isolation & purification; pharmacology; Phytolacca; chemistry; Plants, Medicinal; chemistry; RNA, Messenger; genetics; Reverse Transcriptase Polymerase Chain Reaction; Saponins; isolation & purification; pharmacology; Umbilical Veins; cytology
- From: Acta Pharmaceutica Sinica 2003;38(10):728-730
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the anti-inflammatory mechanism of esculentoside A (EsA) and to observe the effects of EsA on cellular adhesion between human umbilical vein endothelial cell (VEC304) and human neutrophil and to further observe the mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and cluster of differentiation 18(CD18).
METHODSThe hemocyte counting method was used for assaying the adhesion rate between VEC304 and neutrophil. The RT-PCR method was used for measuring the mRNA expression of ICAM-1 and CD18.
RESULTSThe adhesion rate between VEC304 and neutrophil was increased with treatment of lipopolysaccharide(LPS). EsA (3 - 12 x 10(-6) mumol.L-1) was shown to inhibit the high cellular adhesion induced by LPS. A further investigation of adhesion molecules mRNA expression was undertaken using semi-quantitative reverse transcribed polymerase chain reaction (RT-PCR). The results of RT-PCR from VEC304 and human neutrophil treating with LPS showed that ICAM-1 and CD18 mRNA expressions were higher than those of normal cells, while this increased expression of ICAM-1 and CD18 mRNA was remarkably attenuated by the addition of EsA.
CONCLUSIONEsA was found to inhibit the increased adhesion rate induced by LPS. Moreover, LPS induced high expression of ICAM-1 and CD18 was inhibited with treatment of EsA. It might be involved in the mechanisms of anti-inflammation of EsA.