Yuyao Health Training School, Ningbo, Zhejiang, China.
Department of Pediatrics, Jiande First People's Hospital, Hangzhou, Zhejiang, China.
Comb Chem High Throughput Screen. 2024;27(18):2681-2690. doi: 10.2174/0113862073246710231002042239.
Bronchopulmonary dysplasia (BPD) is a chronic lung condition that occurs in premature infants who undergo prolonged mechanical ventilation and oxygen therapy. Existing treatment methods have shown limited efficacy, highlighting the urgent need for new therapeutic strategies. Artesunate (AS) is a compound known for its potential anti-inflammatory properties, and studies have shown its protective effects against acute lung injury. However, its impact on BPD and the underlying mechanisms remain unclear.
To investigate the effect and underlying mechanism of AS on chronic hyperoxiainduced BPD in neonatal mice.
Full-term C57BL/6J mice were randomly assigned to the Air+lactate Ringer's solution (L/R) group, O + L/R group, and O + AS group. Analysis was performed using assay methods such as ELISA, RT-qPCR, hematoxylin-eosin staining, and Western blotting.
Compared with the O+L/R group, the expression of inflammatory factors in the serum, tissue, and BALF of the O+AS group was significantly reduced, the lung function of the mice was improved, and the inflammatory infiltrates were significantly alleviated. AS inhibited the mRNA expression of inflammatory factors in mice. We found that the expression of nuclear p65 and cytoplasmic p-IκBα in the NF-κB pathway was inhibited after adding AS.
AS ameliorated chronic hyperoxia-induced BPD in neonatal mice probably by inhibiting the expression of NF-κB pathway and inflammatory factors.
支气管肺发育不良（BPD）是一种在经历长时间机械通气和氧疗的早产儿中发生的慢性肺部疾病。现有的治疗方法显示疗效有限，这突显了对新治疗策略的迫切需求。青蒿琥酯（AS）是一种具有潜在抗炎特性的化合物，研究表明其对急性肺损伤具有保护作用。然而，其对 BPD 的影响及其潜在机制尚不清楚。
探讨青蒿琥酯（AS）对新生鼠慢性高氧诱导 BPD 的作用及机制。
将足月 C57BL/6J 小鼠随机分为空气+乳酸林格氏液（L/R）组、O+L/R 组和 O+AS 组。采用 ELISA、RT-qPCR、苏木精-伊红染色和 Western blot 等检测方法进行分析。
与 O+L/R 组相比，O+AS 组血清、组织和 BALF 中的炎症因子表达明显减少，小鼠肺功能改善，炎症浸润明显减轻。AS 抑制了小鼠炎症因子的 mRNA 表达。我们发现，加入 AS 后 NF-κB 通路中的核 p65 和胞质 p-IκBα 的表达受到抑制。
AS 通过抑制 NF-κB 通路和炎症因子的表达，改善了新生鼠慢性高氧诱导的 BPD。
