Researchers have reported that miR-124-3p is highly expressed in patients with chronic endometritis. However, the underlying mechanism of miR-124-3p in the development of endometritis remains unclear. This study constructed an in vitro endometrial cell injury model by treating HEECs with 2 μg/mL LPS for 48 h. Then, 1 mg/kg LPS was injected into both sides of the mouse uterus to construct an in vivo endometrial injury model. The expression of miR-124-3p in human endometrial epithelial cells (HEECs) was assessed using RT‒qPCR. Exosomes were separated from bone marrow-derived mesenchymal stem cells (BMSCs) and cocultured with HEECs. A dual-luciferase reporter assay was performed to confirm the relationship between miR-124-3p and DUSP6. The results indicated that LPS inhibited HEEC viability in a time- and dose-dependent manner. The miR-124-3p inhibitor reversed the LPS-induced apoptosis and inhibition of HEEC viability. In addition, miR-124-3p could be transferred from BMSCs to HEECs by exosomes. Exosomes were derived from BMSCs treated with an NC inhibitor (BMSCs/NC Exo) or miR-124-3p inhibitor (BMSCs/anti-miR-124-3p Exo). In addition, BMSCs/anti-miR-124-3p Exo abolished the LPS-induced inhibition of HEEC viability and proliferation by inducing HEEC apoptosis. Moreover, BMSCs/anti-miR-124-3p Exo alleviated the LPS-induced inflammation of HEECs by upregulating DUSP6 and downregulating p-p65 and p-ERK. Furthermore, in an LPS-induced in vivo endometrial injury model, BMSCs/anti-miR-124-3p Exo increased the expression level of DUSP6 and decreased the expression levels of p-p65 and p-ERK. BMSCs/anti-miR-124-3p Exo protected against LPS-induced endometrial damage in vitro and in vivo by upregulating DUSP6 and downregulating p-p65 and p-ERK1/2. This study showed that BMSCs/anti-miR-124-3p Exo might be a potential alternative for the treatment of endometritis.

研究人员报告称，miR-124-3p 在慢性子宫内膜炎患者中高表达。然而，miR-124-3p在子宫内膜炎发生过程中的潜在机制仍不清楚。本研究通过2 μg/mL LPS处理HEECs 48 h构建了体外子宫内膜细胞损伤模型。然后向小鼠子宫两侧注射1 mg/kg LPS，构建体内子宫内膜损伤模型。使用 RT-qPCR 评估人子宫内膜上皮细胞 (HEEC) 中 miR-124-3p 的表达。从骨髓间充质干细胞 (BMSC) 中分离出外泌体，并与 HEEC 共培养。进行双荧光素酶报告基因测定以确认 miR-124-3p 和 DUSP6 之间的关系。结果表明，LPS 以时间和剂量依赖性方式抑制 HEEC 活力。 miR-124-3p 抑制剂逆转 LPS 诱导的细胞凋亡和 HEEC 活力的抑制。此外，miR-124-3p可以通过外泌体从BMSC转移到HEEC。外泌体源自用 NC 抑制剂 (BMSCs/NC Exo) 或 miR-124-3p 抑制剂 (BMSCs/anti-miR-124-3p Exo) 处理的 BMSC。此外，BMSCs/抗miR-124-3p Exo通过诱导HEEC凋亡消除了LPS诱导的对HEEC活力和增殖的抑制。此外，BMSCs/抗miR-124-3p Exo通过上调DUSP6和下调p-p65和p-ERK减轻LPS诱导的HEEC炎症。此外，在 LPS 诱导的体内子宫内膜损伤模型中，BMSCs/抗 miR-124-3p Exo 增加了 DUSP6 的表达水平，并降低了 p-p65 和 p-ERK 的表达水平。 BMSCs/anti-miR-124-3p Exo通过上调 DUSP6 和下调 p-p65 和 p-ERK1/2，在体外和体内保护 LPS 诱导的子宫内膜损伤。这项研究表明 BMSCs/抗 miR-124-3p Exo 可能是治疗子宫内膜炎的潜在替代方案。