Lipopolysaccharide (LPS) is isolated from the genital tract of animals suffering from uterine damage and ovarian dysfunction. This study provides direct molecular evidence about the mechanism through which endotoxins cause reproductive disorders. Granulosa cells and ovaries were collected from immature mice treated with eCG or with eCG and LPS injection intraperitoneally. Normal large antral follicles were observed in ovaries obtained from eCG and LPS coinjected mice, and the morphology of the ovaries was similar to that observed in the control group. These antral follicles were not deemed atretic because few TUNEL-positive cells were observed. However, the granulosa cells of large antral follicles did not acquire the ability to respond to hCG stimulation. The number of ovulated oocytes was significantly lower in LPS-injected mice after superovulation compared to mice that were not exposed to LPS. The low reactivity was caused by the limited expression of the Lhcgr gene, which encodes the LH receptor in granulosa cells as well as an LPS-induced increase in the level of Dnmt1 expression. The methylation rate of the Lhcgr promoter region was significantly higher in granulosa cells obtained from the LPS treatment group compared with the control group. Together, these findings demonstrated that the decrease in the expression of Lhcgr due to LPS was a result of the epigenetic regulatory action of LPS. Our studies suggest that ovarian follicular cysts that is characterized by bacterial infection in humans and animals, is closely connected to the level of methylation of the Lhcgr promoter region.

脂多糖 (LPS) 从患有子宫损伤和卵巢功能障碍的动物的生殖道中分离出来。这项研究提供了关于内毒素导致生殖障碍机制的直接分子证据。从用eCG或腹膜内注射eCG和LPS处理的未成熟小鼠收集颗粒细胞和卵巢。从eCG和LPS共注射小鼠获得的卵巢中观察到正常的大窦卵泡，并且卵巢的形态与在对照组中观察到的相似。这些窦卵泡不被认为是闭锁的，因为观察到的 TUNEL 阳性细胞很少。然而，大窦卵泡的颗粒细胞没有获得对 hCG 刺激的反应能力。与未接触 LPS 的小鼠相比，超排卵后注射 LPS 的小鼠的排卵卵母细胞数量显着降低。低反应性是由 Lhcgr 基因的有限表达引起的，该基因编码颗粒细胞中的 LH 受体以及 LPS 诱导的 Dnmt1 表达水平的增加。与对照组相比，LPS 治疗组获得的颗粒细胞中 Lhcgr 启动子区域的甲基化率显着更高。总之，这些发现表明 与对照组相比，LPS 治疗组获得的颗粒细胞中 Lhcgr 启动子区域的甲基化率显着更高。总之，这些发现表明 与对照组相比，LPS 治疗组获得的颗粒细胞中 Lhcgr 启动子区域的甲基化率显着更高。总之，这些发现表明由 LPS 引起的Lhcgr是 LPS 表观遗传调控作用的结果。我们的研究表明，以人类和动物细菌感染为特征的卵泡囊肿与Lhcgr启动子区域的甲基化水平密切相关。