Intracellular Antioxidant Activity and Inhibition of Bee Pollens on the Production of Inflammatory Mediators (P06-081-19)

Abstract

ObjectivesThe purpose of this study is to present scientific evidences for health promotion of bee pollens through the investigation of the antioxidant and the anti-inflammatory effect. MethodsThe intracellular antioxidant activity of bee pollen ethanol extracts was investigated by DCFH-DA assay for the oxidative stress induced by lipopolysaccharide (LPS) in mitochondria of macrophages. Inhibition of nitric oxide (NO) and prostaglandin E2 (PGE2) production were confirmed by the addition of bee pollen extracts. Inhibition of transcription/expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and the inflammatory mediators-production were investigated by adding the bee pollen extracts. ResultsIntracellular oxidative stress by LPS was inhibited at approximately 53% by 0.25 and 3 mg/ml of the Darae-bee pollen extract. It was found that the Acorn- and Mixed bee pollen extract (3 mg/ml) reduced the intracellular oxidative stress at approximately 26.3 and 41.3%, respectively. For anti-inflammatory activity, all three bee pollen extracts (3 g/ml) inhibited effectively the production of NO to an equal to or rather lower than basal level in macrophages. Bee pollen extracts decreased the LPS-induced PGE2 production depending on the amount added, regardless of the kind of bee pollen added. Gene transcription and expression of iNOS and COX-2, an enzyme producing NO and PGE2, respectively, was suppressed by bee pollen extracts and confirmed by RT-PCR and western blot. Additionally, the production of IL-1b, IL-6 and TNF-α, which are inflammatory mediators in macrophages, were inhibited by Darae-, Acorn- and Mixed bee pollen extract. ConclusionsThe ethanol extracts of Darae-, Acorn- and Mixed bee pollen were verified to have the intracellular antioxidant activity and the inhibitory activity on the production of several anti-inflammatory mediators in macrophage cells. Funding SourcesN/A.