Center for Reproductive Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Key Laboratory of Reproductive Endocrinology of Ministry of Education, Shandong University, Jinan, Shandong, China.
Am J Reprod Immunol. 2024 Mar;91(3):e13833. doi: 10.1111/aji.13833.
Endometritis is an inflammatory reaction of the lining of uterus, leading to the occurrence of infertility. Platelet rich plasma (PRP) has been proven to exhibit extremely effective for the treatment of endometrium-associated infertility, but the mechanism of its prevention for endometritis remains unclear.
The present study aimed to investigate the protective effect of PRP against endometritis induced by lipopolysaccharide (LPS) and elucidate the mechanism underlying these effects.
Mouse model of endometritis was established by intrauterine perfusion of LPS. PRP intrauterine infusion was administered at 24 h after LPS induction. After another 24 h, the uterine tissues were harvested to observe histopathological changes, production of proinflammatory cytokines, variation of the Toll-like receptor 4/nuclear factor κB (TLR4/NF-κB) signaling pathways, and validated the anti-inflammatory effect of PRP. The myeloperoxidase (MPO) activity and concentration of nitric oxide (NO) were determined using assay kit. Proinflammatory chemokines (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6)) were measured by ELISA and Real-Time PCR. The activity of TLR4/NF-κB pathway in uterine tissues was measured by Western blotting.
Hematoxylin-eosin staining (H&E) appeared that PRP remarkably relieved the impairment of uterine tissues. Detection of MPO activity and concentration of NO revealed that PRP treatment distinctly mitigated infiltration of inflammatory cells in mice with endometritis induced by LPS. PRP treatment significantly affected the expression of TNF-α, IL-1β, and IL-6. PRP was also found to suppress LPS-induced activation of TLR4/NF-κB pathway.
PRP effectively alleviates LPS-induced endometritis via restraining the signal pathway of TLR4/NF-κB. These findings provide a solid foundation for PRP as a potential therapeutic agent for endometritis.
子宫内膜炎是子宫内层的炎症反应，导致不孕的发生。富含血小板的血浆 (PRP) 已被证明对治疗与子宫内膜相关的不孕非常有效，但它预防子宫内膜炎的机制尚不清楚。
本研究旨在探讨 PRP 对脂多糖 (LPS) 诱导的子宫内膜炎的保护作用，并阐明其作用机制。
通过宫内灌注 LPS 建立子宫内膜炎小鼠模型。在 LPS 诱导后 24 小时进行 PRP 宫内灌注。再过 24 小时后，采集子宫组织观察组织病理学变化、促炎细胞因子的产生、Toll 样受体 4/核因子 κB (TLR4/NF-κB) 信号通路的变化，并验证 PRP 的抗炎作用。采用试剂盒测定髓过氧化物酶 (MPO) 活性和一氧化氮 (NO) 浓度。通过 ELISA 和 Real-Time PCR 测定促炎趋化因子（肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β) 和白细胞介素-6 (IL-6)）。采用 Western blot 测定子宫组织中 TLR4/NF-κB 通路的活性。
苏木精-伊红染色 (H&E) 显示 PRP 显著减轻了子宫内膜炎小鼠子宫组织的损伤。MPO 活性和 NO 浓度检测显示，PRP 治疗明显减轻了 LPS 诱导的子宫内膜炎小鼠炎症细胞的浸润。PRP 治疗显著影响 TNF-α、IL-1β 和 IL-6 的表达。还发现 PRP 抑制了 LPS 诱导的 TLR4/NF-κB 通路的激活。
PRP 通过抑制 TLR4/NF-κB 信号通路有效缓解 LPS 诱导的子宫内膜炎。这些发现为 PRP 作为子宫内膜炎潜在治疗剂提供了坚实的基础。
