S-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.
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DOI：
10.1155/2018/8496973
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发表时间：
2018
影响因子：
2
通讯作者：
Nakamura Y
中科院分区：
文献类型：
--
作者：
Moriyama M;Hashimoto A;Satoh H;Kawabe K;Ogawa M;Takano K;Nakamura Y
累积的证据表明，雌激素受体（ER）激动剂减轻神经炎症。雌马酚是大豆中的一种主要代谢产物，具有雌激素样生物活性，但其对炎症反应的影响尚未完全确定。在这里，我们研究了S-雌马酚对一氧化氮（NO）产生的影响，这是脂多糖刺激星形胶质细胞的众所周知的炎症变化。S-雌马酚减弱LPS诱导的NO产生，同时诱导型NO合酶（iNOS）的表达减少。S-雌马酚不影响LPS诱导的细胞内ROS产生的增加。细胞内ER阻断剂ICI 182.780对S-雌马酚诱导的NO产生减少没有影响。加入G-15，G蛋白偶联受体30的拮抗剂，这是非基因组的ER和位于细胞表面，部分恢复S-雌马酚诱导的NO产生的衰减。这些发现表明，S-雌马酚的NO产生的衰减可以减轻LPS诱导的星形胶质细胞的神经炎症。S-雌马酚可以至少部分地通过非基因组效应发挥胶质细胞保护作用。
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.