Estrogen has known anti-inflammatory effects, but the mechanism whereby 17β-estradiol (E2) protects oviduct sheep epithelial cells from inflammation remains unknown. In this study, we detected the E2 synthetase and E2 nuclear and membrane receptors in sheep oviducts, primarily in epithelial cells. Using lipopolysaccharide (LPS)-stimulated sheep oviduct epithelial cells as an in vitro inflammation model, we demonstrated that E2 attenuates the expression of inflammatory factors in a concentration-response manner. E2 also inhibited the LPS-stimulated phosphorylation of p38 MAPK and NF-κB p65 but did not reduce the phosphorylation of JNK and ERK 1/2. This attenuation was partially antagonized by an intracellular estrogen antagonist that was involved in genomic regulation and enhanced by a G protein-coupled estrogen receptor agonist that was involved in nongenomic cellular modulation. These results suggest that E2 has an inhibitory effect on LPS-induced oviduct epithelial cell inflammation in sheep, which is mediated by the downstream regulatory effects of estrogen receptors.

雌激素具有抗炎作用，但是17β-雌二醇（E2）保护输卵管绵羊上皮细胞免受炎症的机制仍然未知。在这项研究中，我们检测了绵羊输卵管（主要是上皮细胞）中的E2合成酶以及E2核和膜受体。使用脂多糖（LPS）刺激的绵羊输卵管上皮细胞作为体外炎症模型，我们证明E2以浓度-反应的方式减弱了炎症因子的表达。E2还抑制LPS刺激的p38 MAPK和NF-κBp65的磷酸化，但不降低JNK和ERK 1/2的磷酸化。这种衰减被参与基因组调节的细胞内雌激素拮抗剂部分拮抗，并被参与非基因组细胞调节的G蛋白偶联雌激素受体激动剂增强。这些结果表明，E2对LPS诱导的绵羊输卵管上皮细胞炎症具有抑制作用，这是由雌激素受体的下游调节作用介导的。