S-equol, a major isoflavone from soybean, inhibits nitric oxide production in lipopolysaccharide-stimulated rat astrocytes partially via the GPR30-mediated pathway

Mitsuaki Moriyama, Ayano Hashimoto, Hideyo Satoh, Kenji Kawabe, Mizue Ogawa, Katsura Takano, Yoichi Nakamura

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number8496973
JournalInternational Journal of Inflammation
Volume2018
DOIs
Publication statusPublished - Jan 1 2018
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy

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