Effect of Wenmaitong on adhesion of monocytes to vascular endothelial cell induced by hyperlipidemic serum.
- Author:
Yu HAO
1
;
Xiao-tong HANG
;
De-xian JIA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Adhesion; drug effects; Cell Line; Down-Regulation; drug effects; Drugs, Chinese Herbal; pharmacology; Endothelial Cells; cytology; drug effects; metabolism; Enzyme-Linked Immunosorbent Assay; Humans; Hyperlipidemias; blood; Intercellular Adhesion Molecule-1; biosynthesis; Male; Monocytes; cytology; drug effects; metabolism; Rabbits; Serum; Vascular Cell Adhesion Molecule-1; biosynthesis
- From: Chinese Journal of Integrated Traditional and Western Medicine 2007;27(4):335-338
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of Wenmaitong (WMT) and its disassembled formulas on the adhesion of monocytes to endothelial cells induced by hyperlipidemic serum to explore the mechanism of WMT on early arteriosclerosis obliterans (ASO).
METHODSSerums containing whole WMT and its disassembled formulas, including the formula consisted of warming Jing and boosting qi part (Wenjin Yiqi, WY) and that of promoting blood circulation part (Huoxue Tongmai, HT), as well as the serum contained high concentration of lipids were prepared conventionally, respectively. The adhesion of monocytes cell strain THP-1 to human umbilical vascular endothelial cells (HUVEC) was determined by rose bengal stain method, and ELISA was used to detect expressions of intercellular adhesion molecule (ICAM-1), vascular cellular adhesion molecule (VCAM-1) and P-selectin on HUVEC surface.
RESULTSWMT could inhibit THP-1 to HUVEC adhesion induced by hyperlipidemic serum, and down-regulate the expression of ICAM-1, VCAM-1, P-selectin on HUVEC surface, the two disassembled formulas could down-regulate different adhesion molecules.
CONCLUSIONOne mechanism of WMT on ASO may be its inhibition on arteriosclerosis by way of down-regulating the expression of vascular endothelial cells adhesion molecules to decrease the adhesion of monocyte to VEC, therefore to inhibit the monocytes migrating into vascular intima to develop foam cells.