Ginkgolide B Reduces Inflammatory Protein Expression in Oxidized Low-density Lipoprotein-stimulated Human Vascular Endothelial Cells

• DOI: 10.1097/fjc.0b013e31821a50a8
• Publication Date: 2011-03-25T04:59:42Z
• Authors: Shan Zhang; Beidong Chen; Wei Wu; Li Bao; Ruomei Qi
• Keywords: 0303 health sciences; Osmolar Concentration; Down-Regulation; NADPH Oxidases; Phospholipid Ethers; Platelet Membrane Glycoproteins; Intercellular Adhesion Molecule-1; 3. Good health; Lipoproteins, LDL; Lactones; Oxidative Stress; Protein Transport; 03 medical and health sciences; Ginkgolides; NADPH Oxidase 4; Humans; Endothelium, Vascular; RNA, Messenger; Inflammation Mediators; Reactive Oxygen Species; Oxidation-Reduction; Cells, Cultured; Chemokine CCL2

Ginkgolide B is a herbal constituent extracted from leaves of the ginkgo biloba tree. Previous studies have shown that ginkgolide B is a specific platelet activating factor (PAF) receptor antagonist, and it suppresses PAF-mediated platelet activation via competitive binding. In this study, the effect of ginkgolide B on nicotinamide adenine dinucleotide phosphate oxidase and other inflammatory proteins in ox-LDL (low-density lipoprotein)-stimulated human vascular endothelial cells was investigated. Another PAF receptor antagonist CV3988 was employed to compare with ginkgolide B in this study. Our results show that the enhancement of Nox4 expression and reactive oxygen species generation was attenuated by ginkgolide B in cells treated with ox-LDL but not with CV3988. Increases in monocyte chemoattractant protein-1 and intercellular adhesion molecule 1 expression induced by ox-LDL, however, were inhibited by both ginkgolide B and CV3988. The translocation of NF-kappaB p65 (NF-κB) into the nucleus was inhibited by both ginkgolide B and CV3988. In conclusion, both ginkgolide B and CV3988 can inhibit the expression of inflammatory proteins by blocking NF-κB translocation. It seems that ginkgolide B possesses some pharmacological action on intracellular oxidative stress in association with the downregulation of Nox4 expression.