Oenothera paradoxa Defatted Seeds Extract and Its Bioactive Component Penta-O-galloyl-β-D-glucose Decreased Production of Reactive Oxygen Species and Inhibited Release of Leukotriene B4, Interleukin-8, Elastase, and Myeloperoxidase in Human Neutrophils

In this study, we analyzed ex vivo the effect of an aqueous extract of Oenothera paradoxa defatted seeds on the formation of neutrophil-derived oxidants. For defining active compounds, we also tested lypophilic extract constituents such as gallic acid, (+)-catechin, ellagic acid, and penta-O-galloyl-beta-D-glucose and a hydrophilic fraction containing polymeric procyanidins. The anti-inflammatory potential of the extract and compounds was tested by determining the release from activated neutrophils of elastase, myeloperoxidase, interleukin-8 (IL-8), and leukotriene B-4 (LTB4), which are considered relevant for the pathogenesis of cardiovascular diseases. The extract of O. paradoxa defatted seeds displays potent antioxidant effects against both 4 beta-phorbol-12 beta-myristate-alpha 13-acetate- and formyl-met-leu-phenylalanine-induced reactive oxygen species production in neutrophils with IC50 values around 0.2 mu g/mL. All types of polyphenolics present in the extract contributed to the extract antioxidant activity. According to their IC50 values, penta-O-galloyl-beta-D-glucose was the more potent constituent of the extract. In cell-free assays, we demonstrated that this effect is partially due to the scavenging of O-2(-) and H2O2 oxygen species. The extract and especially penta-O-galloyl-beta-D-glucose significantly inhibit elastase, myeloperoxidase IL-8, and LTB4 release with an IC50 for penta-O-galloyl-beta-D-glucose of 17 +/- 1, 15 +/- 1, 6.5 +/- 2.5, and around 20 mu M, respectively. The inhibition of penta-O-galloyl-beta-D-glucose on reactive oxygen species and especially on O-2(-) production, myeloperoxidase, and chemoattractant release may reduce the interaction of polymorphonuclear leukocyte with the vascular endothelium and by that potentially diminish the risk of progression of atherosclerosis development.