S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway
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...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | International Journal of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/8496973 |
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| _version_ | 1832558755651256320 |
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| author | Mitsuaki Moriyama Ayano Hashimoto Hideyo Satoh Kenji Kawabe Mizue Ogawa Katsura Takano Yoichi Nakamura |
| author_facet | Mitsuaki Moriyama Ayano Hashimoto Hideyo Satoh Kenji Kawabe Mizue Ogawa Katsura Takano Yoichi Nakamura |
| author_sort | Mitsuaki Moriyama |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-cfb9bba319e240ca91674beb89b8ec76 |
| institution | Kabale University |
| issn | 2090-8040 2042-0099 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Inflammation |
| spelling | doaj-art-cfb9bba319e240ca91674beb89b8ec762025-02-03T01:31:37ZengWileyInternational Journal of Inflammation2090-80402042-00992018-01-01201810.1155/2018/84969738496973S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated PathwayMitsuaki Moriyama0Ayano Hashimoto1Hideyo Satoh2Kenji Kawabe3Mizue Ogawa4Katsura Takano5Yoichi Nakamura6Laboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, Izumisano, Osaka, JapanCumulative 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.http://dx.doi.org/10.1155/2018/8496973 |
| spellingShingle | Mitsuaki Moriyama Ayano Hashimoto Hideyo Satoh Kenji Kawabe Mizue Ogawa Katsura Takano Yoichi Nakamura S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway International Journal of Inflammation |
| title | S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway |
| title_full | S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway |
| title_fullStr | S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway |
| title_full_unstemmed | S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway |
| title_short | S-Equol, a Major Isoflavone from Soybean, Inhibits Nitric Oxide Production in Lipopolysaccharide-Stimulated Rat Astrocytes Partially via the GPR30-Mediated Pathway |
| title_sort | s equol a major isoflavone from soybean inhibits nitric oxide production in lipopolysaccharide stimulated rat astrocytes partially via the gpr30 mediated pathway |
| url | http://dx.doi.org/10.1155/2018/8496973 |
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