Hemeoxygenase 1 partly mediates the anti-inflammatory effect of dieckol in lipopolysaccharide stimulated murine macrophages

•Dieckol inhibited iNOS thereby reduced the release of nitric oxide from macrophages.•Dieckol inhibited NF-κB and PI-3K/Akt pathways in LPS stimulated macrophages.•Dieckol alone up-regulated hemeoxyginase-1 expression in murine macrophage cells.•Dieckol induced the phosphorylation of ERK and P38MAPK in unstimulated macrophages.

Eisenia bicyclis is edible brown algae recognized as a rich source of bioactive derivatives mainly phlorotannins reported for their anti-oxidant properties. Of all phlorotannins identified so far, dieckol has shown the most potent effect in anti-inflammatory, radical scavenging and neuroprotective functions. However, whether dieckol up-regulates hemeoxygenase 1 (HO-1) and this mediates its anti-inflammatory effect in murine macrophages remains poorly understood. Dieckol (12.5–50 μM) inhibited nitric oxide production and attenuated inducible nitric oxide synthase, phospho (p)-PI-3 K, p-Akt, p-IKK-α/β, p-IκB-α and nuclear p-NF-κBp65 protein expressions, and NF-κB transcriptional activity in LPS (0.1 μg/ml) stimulated murine macrophages. On the other hand, dieckol up-regulated HO-1which partly mediated its anti-inflammatory effect in murine macrophages. Thus, dieckol appeared to be a potential therapeutic agent against inflammation through HO-1 up-regulation.