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Cumulative evidence indicates that estrogen receptor (ER) agonists attenuate neuroinflammation. Equol, a major isoflavone from soybean, exhibits estrogen-like biological activity, but their effect on inflammatory response has not been well established. Here, we investigated the effect of  S -equol on nitric oxide (NO) production, well-known inflammatory change in astrocytes stimulated by LPS.  S -Equol attenuated LPS-induced NO production with a concomitant decrease in expression of inducible NO synthase (iNOS).  S -Equol did not affect LPS-induced increase in intracellular ROS production. Intracellular ER blocker ICI 182.780 had no effect on  S -equol-induced decrease in NO production. Addition of G-15, antagonist of G protein-coupled receptor 30 which is nongenomic ER and located on cell surface, partially recovered  S -equol-induced attenuation of NO production. These findings suggest that attenuation of NO production by  S -equol may mitigate LPS-induced neuroinflammation in astrocytes.  S -Equol may exert a glioprotective effect, at least in part, via a nongenomic effect.

international journal of inflammation

<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>S</mml:mi></mml:mrow></mml:math>-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway

S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway