The study aimed to investigate whether recombinant human elafin can prevent hyperoxia-induced pulmonary inflammation in newborn mice, and to explore the mechanism underlying the inhibitory effects of elafin on nuclear factor-kappa B (NF-κB) signaling pathway. Neonatal C57BL/6J mice were exposed to 85% O₂ for 1, 3, 7, 14, or 21 days. Then, elafin was administered daily for 20 days through intraperitoneal injection. After treatment, morphometric analysis, quantitative real-time polymerase chain reaction, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and Western blotting were carried out to determine the key markers involved in inflammatory process and the potential signaling pathways in hyperoxia-exposed newborn mice treated with elafin. In neonatal bronchopulmonary dysplasia (BPD) mice, hyperoxia induced apoptosis by increasing Bcl-2-associated X protein expression, and triggered inflammation by upregulating the expression levels of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α. Moreover, hyperoxia activated NF-κB signaling pathway by promoting the nuclear translocation of p65 in lung tissue. However, all these changes could be inhibited or reversed by elafin at least partially. Elafin reduced apoptosis, suppressed inflammation cytokines, and improved NF-κB p65 nuclear accumulation in hyperoxia-exposed neonatal mice, indicating that this recombinant protein can serve as a novel target for the treatment of BPD.

中文翻译：

---

重组人Elafin通过抑制新生小鼠中的核因子-κB信号传导减轻慢性高氧血症引起的肺损伤。

该研究旨在调查重组人弹性蛋白是否可以预防高氧诱导的新生小鼠肺部炎症，并探讨弹性蛋白对核因子-κB（NF-κB）信号通路抑制作用的潜在机制。新生儿C57BL / 6J小鼠暴露于85％O ₂1、3、7、14或21天。然后，通过腹膜内注射每天给药elafin，持续20天。治疗后，进行形态计量学分析，定量实时聚合酶链反应，末端脱氧核苷酸转移酶dUTP缺口末端标记染色和蛋白质印迹，以确定参与高氧暴露的新生小鼠炎症过程中涉及的关键标志物和潜在的信号通路。与elafin。在新生儿支气管肺发育不良（BPD）小鼠中，高氧通过增加Bcl-2相关X蛋白表达诱导凋亡，并通过上调白介素（IL）-1β，IL-6，IL-8和肿瘤坏死的表达水平来引发炎症。因子-α。此外，高氧通过促进肺组织中p65的核易位激活了NF-κB信号通路。然而，elafin至少可以部分抑制或逆转所有这些变化。Elafin减少了高氧暴露新生小鼠的细胞凋亡，抑制了炎症细胞因子并改善了NF-κBp65核积累，表明该重组蛋白可以作为BPD治疗的新靶标。