Endometritis is an inflammatory of the inner lining of the uterus caused by bacterial infections that affect female reproductive health in humans and animals. Neutrophil extracellular traps (NETs) have the ability to resist infections that caused by pathogenic invasions. It has been proved that the formation of NETs is related to certain inflammatory diseases, such as mastitis and chronic obstructive pulmonary disease (COPD). However, there are sparse studies related to NETs and endometritis. In this study, we investigated the role of NETs in lipopolysaccharide (LPS)-induced acute endometritis in mice and evaluated the therapeutic efficiency of DNaseI. We established LPS-induced endometritis model in mice and found that the formation of NETs can be detected in the mice uterine tissues in vivo. In addition, DNaseI treatment can inhibit NETs construction in LPS-induced endometritis in mice. Moreover, myeloperoxidase (MPO) activity assay indicated that DNaseI treatment remarkably alleviated the inflammatory cell infiltrations. ELISA test indicated that the treatment of DNaseI significantly inhibited the expression of the proinflammatory cytokines TNF-α, and IL-1β. Also, DNaseI was found to increase proteins expression of the uterine tissue tight junctions and suppress LPS-induced NF-κB activation. All the results indicated that DNaseI effectively inhibits the formation of NETs by blocking the NF-κB signaling pathway and enhances the expression of tight junction proteins, consequently, alleviates inflammatory reactions in LPS-induced endometritis in mice.

子宫内膜炎是由细菌感染引起的子宫内膜炎症，影响人类和动物的女性生殖健康。中性粒细胞胞外诱捕器（NET）具有抵抗由病原体入侵引起的感染的能力。已经证明NET的形成与某些炎性疾病有关，例如乳腺炎和慢性阻塞性肺疾病（COPD）。但是，与NET和子宫内膜炎相关的研究稀疏。在这项研究中，我们调查了NETs在脂多糖（LPS）诱导的小鼠急性子宫内膜炎中的作用，并评估了DNaseI的治疗效果。我们建立了LPS诱导的小鼠子宫内膜炎模型，发现可以在小鼠子宫组织中检测到NETs的形成。此外，DNaseI处理可以抑制LPS诱导的小鼠子宫内膜炎中NETs的构建。而且，髓过氧化物酶（MPO）活性测定表明DNaseI处理显着减轻了炎性细胞浸润。ELISA试验表明，DNaseI的处理显着抑制了促炎细胞因子TNF-α和IL-1β的表达。此外，发现DNaseI可增加子宫组织紧密连接的蛋白质表达，并抑制LPS诱导的NF-κB活化。所有结果表明，DNaseI通过阻断NF-κB信号通路有效抑制NETs的形成，并增强紧密连接蛋白的表达，从而减轻LPS诱导的子宫内膜炎的炎症反应。髓过氧化物酶（MPO）活性测定表明DNaseI处理显着减轻了炎症细胞浸润。ELISA试验表明，DNaseI的处理显着抑制了促炎细胞因子TNF-α和IL-1β的表达。此外，发现DNaseI可增加子宫组织紧密连接的蛋白质表达，并抑制LPS诱导的NF-κB活化。所有结果表明，DNaseI通过阻断NF-κB信号通路有效抑制NETs的形成，并增强紧密连接蛋白的表达，从而减轻LPS诱导的子宫内膜炎的炎症反应。髓过氧化物酶（MPO）活性测定表明DNaseI处理显着减轻了炎症细胞浸润。ELISA试验表明，DNaseI的处理显着抑制了促炎细胞因子TNF-α和IL-1β的表达。此外，发现DNaseI可增加子宫组织紧密连接的蛋白质表达，并抑制LPS诱导的NF-κB活化。所有结果表明，DNaseI通过阻断NF-κB信号通路有效抑制NETs的形成，并增强紧密连接蛋白的表达，从而减轻LPS诱导的子宫内膜炎的炎症反应。ELISA试验表明，DNaseI的处理显着抑制了促炎细胞因子TNF-α和IL-1β的表达。此外，发现DNaseI可增加子宫组织紧密连接的蛋白质表达，并抑制LPS诱导的NF-κB活化。所有结果表明，DNaseI通过阻断NF-κB信号通路有效抑制NETs的形成，并增强紧密连接蛋白的表达，从而减轻LPS诱导的子宫内膜炎的炎症反应。ELISA试验表明，DNaseI的处理显着抑制了促炎细胞因子TNF-α和IL-1β的表达。此外，发现DNaseI可增加子宫组织紧密连接的蛋白质表达，并抑制LPS诱导的NF-κB活化。所有结果表明，DNaseI通过阻断NF-κB信号通路有效抑制NETs的形成，并增强紧密连接蛋白的表达，从而减轻LPS诱导的子宫内膜炎的炎症反应。