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[Effect of esculentoside A on cellular adhesion].
Zhen-yu Xiao1, Jun-ping Zhang, Feng Lu
1College of Pharmacy, Second Military Medical University, Shanghai 200433, China. zhyxiao@yahoo.com
Yao Xue Xue Bao = Acta Pharmaceutica Sinica
|January 21, 2004
Summary
Esculentoside A (EsA) reduces inflammation by inhibiting cellular adhesion between endothelial cells and neutrophils. EsA also downregulates the mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and cluster of differentiation 18 (CD18).
Area of Science:
- Pharmacology
- Immunology
- Molecular Biology
Background:
- Inflammation involves increased cellular adhesion between endothelial cells and neutrophils.
- Intercellular adhesion molecule-1 (ICAM-1) and cluster of differentiation 18 (CD18) play crucial roles in this adhesion process.
- Esculentoside A (EsA) is a compound with potential anti-inflammatory properties.
Purpose of the Study:
- To investigate the anti-inflammatory mechanism of EsA.
- To assess EsA's effect on endothelial cell-neutrophil adhesion.
- To examine EsA's impact on ICAM-1 and CD18 mRNA expression.
Main Methods:
- Cellular adhesion assays using hemocyte counting.
- Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) for mRNA analysis.
- Utilized human umbilical vein endothelial cells (VEC304) and human neutrophils.
Main Results:
- Lipopolysaccharide (LPS) significantly increased VEC304-neutrophil adhesion.
- EsA (3-12 x 10(-6) mumol.L-1) inhibited LPS-induced cellular adhesion.
- LPS elevated ICAM-1 and CD18 mRNA expression, which EsA treatment markedly reduced.
Conclusions:
- EsA effectively inhibits LPS-induced cellular adhesion.
- EsA downregulates the expression of ICAM-1 and CD18 mRNA.
- These findings suggest EsA possesses anti-inflammatory activity potentially mediated by modulating adhesion molecule expression.