3,4-oxo-isopropylidene-shikimic acid inhibits adhesion of polymorphonuclear leukocyte to TNF-alpha-induced endothelial cells in vitro
Abstract
AIM:
To examine the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) on human polymorphonuclear leukocyte (PMN) adhesion to human umbilical vein endothelial cells (HUVEC) and explore its mechanism.
METHODS:
Adhesion of PMN to HUVEC was measured by rose bengal staining assay. Cell-ELISA and RT-PCR methods were used to examine the expression of adhesion molecules ICAM-1. Cell viability was detected with MTT assay.
RESULTS:
ISA (1-100 micromol/L) effectively reduced PMN adhesion to TNF-alpha-induced HUVEC with the inhibitory rate from 17.2 % to 53.5 %, and exerted no effect on PMN adhesion to normal HUVEC. Adhesion molecule ICAM-1 surface protein and mRNA expression induced by TNF-alpha (400 kU/L) were significantly inhibited by ISA. In addition, the cell viability of HUVEC was unchanged 48 h after treatment with ISA.
CONCLUSION:
ISA inhibited TNF-alpha-stimulated PMN-HUVEC adhesion and expression of ICAM-1.
Keywords:
To examine the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) on human polymorphonuclear leukocyte (PMN) adhesion to human umbilical vein endothelial cells (HUVEC) and explore its mechanism.
METHODS:
Adhesion of PMN to HUVEC was measured by rose bengal staining assay. Cell-ELISA and RT-PCR methods were used to examine the expression of adhesion molecules ICAM-1. Cell viability was detected with MTT assay.
RESULTS:
ISA (1-100 micromol/L) effectively reduced PMN adhesion to TNF-alpha-induced HUVEC with the inhibitory rate from 17.2 % to 53.5 %, and exerted no effect on PMN adhesion to normal HUVEC. Adhesion molecule ICAM-1 surface protein and mRNA expression induced by TNF-alpha (400 kU/L) were significantly inhibited by ISA. In addition, the cell viability of HUVEC was unchanged 48 h after treatment with ISA.
CONCLUSION:
ISA inhibited TNF-alpha-stimulated PMN-HUVEC adhesion and expression of ICAM-1.