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

Abstract EN

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.