Arctigenin improves vascular tone and decreases inflammation in human saphenous vein

The goal of this study was to test the effects of bioactive phenylpropanoid dibenzylbutyrolactone lignan arctigenin (ATG) in vascular tone. Human bypass graft vessel, from a saphenous vein (SV), were set up in organ bath system and contracted with potassium chloride (KCl, 40 mM). Two concentration response curves of noradrenaline (NE) (10 nM-100 mu M) separated with an incubation period of 30 min without (Control) or with ATG (3-100 mu M) were established. Inhibitors of nitric oxide, prostaglandins, K+ related channels or calcium influx were used to delineate the molecular mechanisms beyond ATG effects. To investigate anti-inflammatory actions, SV were treated with 10 mu M or 100 mu M ATG and incubated for 18 h in the absence or presence of both interleukin-lbeta (IL-beta) and lipopolysaccharide (LPS) to mimic the physiological or inflamed tissue conditions. Proatherogenic and inflammatory mediators interleuldne-1 beta (IL-beta), Monocyte Chemoattractant Proteine-1 (MCP -1), Tumor Necrosis Factor-alpha (TNF-alpha), Interleuldne-6 (IL-6), Prostaglandin E-2 (PGE(2)) and interleuldne-8 (IL-8) in the supernatant were measured. ATG significantly decreased vascular contractile response to NE. Moreover, it reduced contractions induced by KCl and cumulative addition of CaCl2. The mediators were significantly increased in inflammatory conditions compared to normal conditions, an effect which was inhibited by ATG (10 and 100 mu M). ATG reduces contractions in SV and decreases the production of proinflammatory-proatherogenic mediators, setting the stage for further evaluating the effect of ATG in cardiovascular diseases.