Original ArticleGinkgolide B Reduces Inflammatory Protein Expression in Oxidized Low-density Lipoprotein-stimulated Human Vascular Endothelial CellsZhang, Shan MD*†; Chen, Beidong MD, PhD*; Wu, Wei BS*; Bao, Li BS*; Qi, Ruomei MD, PhD*Author Information From the *Department of Immunology, Beijing Institute of Geriatrics, Beijing Hospital and Key Laboratory of Geriatrics Ministry of Health, Beijing, China; and †Division of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China. Received for publication December 17, 2010; accepted March 14, 2011. Supported by a grant from the National Natural Science Foundation of China (grant no. 30572038 and grant no. 81070231). The authors declare no conflicts of interest. Shan Zhang, MD, and Beidong Chen, MD, PhD, contributed equally to this work. Reprints: Ruomei Qi, MD, PhD, No. 1 Dahua Road, Beijing Institute of Geriatrics, Beijing Hospital, Beijing 100730, China (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: June 2011 - Volume 57 - Issue 6 - p 721-727 doi: 10.1097/FJC.0b013e31821a50a8 Buy Metrics 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. © 2011 Lippincott Williams & Wilkins, Inc.