Enterolactone is more effective than enterodiol in down‐regulating nitric oxide production in RAW 264.7 macrophages challenged with lipopolysaccharides (LPS).

Abstract

Our earlier study showed that flaxseed prevents vascular lesion development in ovariectomized hamsters. Flaxseed contains significant amounts of phenolic compounds, lignan, which are metabolized by colonic microflora to enterodiol (END) and enterolactone (ENL). The objective of this study was to evaluate and compare the anti‐inflammatory effects of END and ENL using the murine Raw 264.7 macrophage cell line. Cells were incubated in DMEM containing 10% FBS and 1% penicillin and then treated with increasing concentrations (0, 1, 10, 100, 500, 1000, 2500 and 5000μM) of END or ENL for 24 hrs. Subsequently, cells were challenged with LPS (500 ng/mL) for 24 hrs to induce an inflammatory response. Nitric oxide (NO) and cell viability were assessed using the Griess and Resazurin assays, respectively. Cell viability was not affected by any concentrations of END and ENL used in the study. As expected, the addition of LPS induced a significant increase in the production of NO and both END and ENL significantly decreased NO production. However, lower concentrations of ENL compared to END were required to significantly reduce NO production. These findings may in part explain the anti‐atherosclerotic effect of flaxseed and suggest that ENL may have more potent anti‐inflammatory properties.