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Updated: Aug 23, 2026

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
11:22

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions

Published on: August 23, 2013

Cilostazol inhibits high glucose-mediated endothelial-neutrophil adhesion by decreasing adhesion molecule expression

Hitoshi Omi1, Naotsuka Okayama, Manabu Shimizu

  • 1Department of Internal Medicine and Bioregulation, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan.

Microvascular Research
|August 18, 2004
PubMed

Insights

Cilostazol inhibits high glucose-induced endothelial-neutrophil adhesion by reducing adhesion molecules. This effect may be mediated by increased nitric oxide (NO) production, offering potential benefits for diabetic vascular complications.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Diabetic Complications Research

Background:

  • Endothelial-neutrophil adhesion contributes to vascular injury in diabetes.
  • Platelet aggregation inhibitors are used for intermittent claudication but their direct endothelial effects in hyperglycemia are unclear.

Purpose of the Study:

  • To investigate the direct effects of platelet aggregation inhibitors on high glucose-induced endothelial-neutrophil adhesion and adhesion molecule expression.

Main Methods:

  • Human endothelial cells were exposed to high glucose.
  • Neutrophil adhesion was quantified via myeloperoxidase activity.
  • Expression of intercellular adhesion molecule-1 (ICAM-1) and P-selectin was measured.

Main Results:

  • Cilostazol significantly reduced neutrophil adhesion and ICAM-1/P-selectin expression.
  • Nitric oxide (NO) synthase inhibitors diminished cilostazol's inhibitory effect.
  • Protein kinase C (PKC) activator did not affect cilostazol's action.

Conclusions:

  • Cilostazol directly inhibits high glucose-induced endothelial adhesion molecules and neutrophil adhesion.
  • Increased nitric oxide (NO) production is implicated in cilostazol's mechanism.
  • Cilostazol shows potential for managing diabetic vascular complications.
Abstract

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