The hypothesis whether estrone (E₁) could exhibit a direct action at uterus and white adipose tissue (WAT), under obesity was tested. In uterine tissue of obese rats, E₁ increased nitric oxide (NO) synthesis, and reduced reactive oxygen species (ROS) production. The anti-oxidative action of E₁ was sustained under inflammatory stress or high glucose levels. ICI 182780 or G15 compounds were employed as ER or GPER antagonists respectively. The action of E₁ on ROS release involved ER participation; instead GPER mediated the acute stimulation on NO production. The antioxidative effect depends on NO-ROS balance. NO synthase (NOS) blockage suppressed the reduction in ROS synthesis elicited by E₁, effect mediated by cNOS and not by iNOS. On WAT explants, E₁ reduced ROS and thiobarbituric acid reactive substances production, and diminished leptin release. In summary, the data provide evidence that, in uterus and WAT, E₁ counteracts inflammatory and oxidative stress induced by obesity.

测试了在肥胖情况下雌酮（E _{1 ）}是否可以对子宫和白色脂肪组织（WAT）表现出直接作用的假设。在肥胖大鼠的子宫组织中，E ₁增加一氧化氮 (NO) 的合成，并减少活性氧 (ROS) 的产生。_{E 1}的抗氧化作用在炎症应激或高葡萄糖水平下持续存在。ICI 182780或G15化合物分别用作ER或GPER拮抗剂。_{E 1对ROS释放}的作用涉及ER参与；相反，GPER 介导对 NO 产生的急性刺激。抗氧化作用取决于NO-ROS平衡。_{NO 合酶 (NOS) 阻断抑制了 E 1}引起的 ROS 合成的减少，该效应是由 cNOS 介导的，而不是由 iNOS 介导的。在 WAT 外植体上，E ₁减少了 ROS 和硫代巴比妥酸反应物质的产生，并减少了瘦素的释放。总之，数据提供的证据表明，在子宫和 WAT 中，E ₁可以抵消肥胖引起的炎症和氧化应激。