title: Ginkgolide B reduces inflammatory protein expression in oxidized low-density lipoprotein-stimulated human vascular endothelial cells.
abstract: 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.
authors: Department of Immunology, Beijing Institute of Geriatrics, Beijing Hospital and Key Laboratory of Geriatrics Ministry of Health, Beijing, China.
authors: Shan
authors: S
authors: Zhang
authors: Beidong
authors: B
authors: Chen
authors: Wei
authors: W
authors: Wu
authors: Li
authors: L
authors: Bao
authors: Ruomei
authors: R
authors: Qi
mesh_terms: D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D015536:Down-Regulation / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D046934:Ginkgolides / Q000494:pharmacology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007783:Lactones / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000633:toxicity*; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000235:genetics / Q000378:metabolism; D009994:Osmolar Concentration; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D010742:Phospholipid Ethers / Q000494:pharmacology; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors*; D021381:Protein Transport / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D046934:Ginkgolides; D018836:Inflammation Mediators; D007783:Lactones; D008077:Lipoproteins, LDL; D010742:Phospholipid Ethers; D010980:Platelet Membrane Glycoproteins; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D043562:Receptors, G-Protein-Coupled; D051996:Transcription Factor RelA; C099252:oxidized low density lipoprotein; C039351:platelet activating factor receptor; D018799:Intercellular Adhesion Molecule-1; C037913:CV 3988; C045856:ginkgolide B; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498910:NOX4 protein, human