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.

Inhibitory Effect of Natural Anti-Inflammatory Compounds on Cytokines Released by Chronic Venous Disease Patient-Derived Endothelial Cells

“…In the next set of experiments, we have investigated whether the anti-inflammatory natural compounds α -Lipoic acid [23–28] and Ginkgo biloba derivatives [29, 30] affected the release of cytokines/chemokines by pathological VEC. Indeed, although it has already been reported that both compounds, and in particular α -Lipoic acid, exhibit anti-inflammatory activities both in vitro and in vivo in the context of endothelial biology of different pathologies [23–27], it remains to be established whether these compounds are active also on pathological VEC isolated from CVD patients.…”

Ginkgolide B Reduces LOX-1 Expression by Inhibiting Akt Phosphorylation and Increasing Sirt1 Expression in Oxidized LDL-Stimulated Human Umbilical Vein Endothelial Cells

“…Our previous studies showed that ginkgolide B inhibited inflammatory protein expression induced by ox-LDL in human umbilical vein endothelial cells (HUVECs), such as intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) expression, by inhibiting nuclear factor-kB (NF-kB) activation and reducing Nox4 expression in ox-LDL-treated endothelial cells [11], [12]. However, whether ginkgolide B influences LOX-1 expression in HUVECs has not yet been determined.…”

Ginkgolide B reduces neuronal cell apoptosis in the hemorrhagic rat brain: Possible involvement of Toll-like receptor 4/nuclear factor-kappa B pathway

“…Recently, it has been found that GB can reduce inflammatory protein expression in oxidized low-density lipoprotein-stimulated human vascular endothelial cells and lipopolysaccharidestimulated mouse peritoneal macrophages via blocking NF-B activation (Nie et al, 2004;Li et al, 2009;Zhang et al, 2011). In the central nervous system, after contusion spinal cord injury, treatment with GB led to significantly increased white matter tissue sparing as well as decreased mRNA levels for proinflammatory cytokines (Wang and Sun, 2000).…”