Department of Obstetrics, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Microbiol Spectr. 2024 Feb 6;12(2):e0327923. doi: 10.1128/spectrum.03279-23. Epub 2024 Jan 3.
Endometritis, a local inflammatory disease, has been known as the most common cause of infertility in mares. In this study, we investigated the protective effects of luteolin on endometritis induced by () and further clarified the possible molecular mechanisms. An -induced endometritis model was established by the infusion of into the uterus. Luteolin was intraperitoneally administered to mice 1 h before treatment. The results showed that the mice of the group showed severe histological changes of uterine tissues, increased myeloperoxidase (MPO) activity, and elevated TNF-α, IL-1β, and IL-6 levels. These changes induced by were dose-dependently inhibited by luteolin. Furthermore, luteolin inhibited MDA and Fe production and increased the production of GSH decreased by . Luteolin prevented -induced endometrial barrier disruption through up-regulating ZO-1 and occludin expression. Luteolin dramatically inhibited -induced NF-κB activation. The expression of Nrf2 and HO-1 was increased by luteolin. In addition, the inhibitory effects of luteolin on -induced endometritis were reversed in Nrf2 knockdown mice. In conclusion, these data indicated that luteolin protected mice against -induced endometritis through inhibiting inflammation and ferroptosis via regulating the Nrf2 signaling pathway.IMPORTANCEEndometritis is an inflammatory disease of the endometrium, which is a common gynecological disease. Up to now, there is no evidence for the protective effects of luteolin on endometritis. The purpose of this study was to investigate whether luteolin has protective effects against -induced endometritis and attempts to clarify the mechanism.
子宫内膜炎是一种局部炎症性疾病，是导致母马不孕的最常见原因。在这项研究中，我们研究了木樨草素对（）诱导的子宫内膜炎的保护作用，并进一步阐明了可能的分子机制。通过将（）注入子宫来建立（）诱导的子宫内膜炎模型。在（）处理前 1 小时，通过腹腔内给予小鼠木樨草素。结果表明，（）组小鼠的子宫组织出现严重的组织学变化，髓过氧化物酶（MPO）活性增加，TNF-α、IL-1β和 IL-6 水平升高。木樨草素可剂量依赖性抑制（）引起的这些变化。此外，木樨草素抑制 MDA 和 Fe 的产生，增加（）减少的 GSH 的产生。木樨草素通过上调 ZO-1 和闭合蛋白的表达来防止（）诱导的子宫内膜屏障破坏。木樨草素显著抑制 NF-κB 的激活。木樨草素增加 Nrf2 和 HO-1 的表达。此外，在 Nrf2 敲低小鼠中，木樨草素对（）诱导的子宫内膜炎的抑制作用被逆转。总之，这些数据表明，木樨草素通过调节 Nrf2 信号通路抑制炎症和铁死亡来保护小鼠免受（）诱导的子宫内膜炎。
重要性子宫内膜炎是一种子宫内膜的炎症性疾病，是一种常见的妇科疾病。到目前为止，还没有证据表明木樨草素对子宫内膜炎有保护作用。本研究的目的是研究木樨草素是否对（）诱导的子宫内膜炎有保护作用，并试图阐明其机制。
