Department of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Mol Cell Probes. 2020 Jun;51:101529. doi: 10.1016/j.mcp.2020.101529. Epub 2020 Feb 6.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease with long-term sequelae including neurodevelopmental delay. Although the precise mechanism of BPD is not well defined, oxidative stress is thought to be involved in the pathogenesis process of BPD. Nrf2 (Nuclear factor erythroid 2-related factor 2)-Keap1 (Kelch-like ECH associated protein 1)-ARE (Antioxidant Reaction Elements) signaling pathway is one of the main protective mechanisms of BPD, which can induce cytoprotective gene expression, such as heme oxygenase-1 (HO-1), nicotinamide quinone oxidoreductase 1 (NQO1) and so on. We exposed premature rats to hyperoxia and identified lung developmental retardation in preterm rats, with similar pathological changes as BPD. The expression of Nrf2 and HO-1 in premature rats was significantly higher after hyperoxia exposure. To explore the changes of Nrf2 and HO-1 in premature rats and enhance their beneficial functions may provide new treatment strategies for infants at risk of BPD.
支气管肺发育不良（BPD）是一种慢性肺部疾病，具有长期的后遗症，包括神经发育迟缓。尽管 BPD 的确切机制尚未明确，但氧化应激被认为参与了 BPD 的发病机制。Nrf2（核因子红细胞 2 相关因子 2）-Keap1（Kelch 样 ECH 相关蛋白 1）-ARE（抗氧化反应元件）信号通路是 BPD 的主要保护机制之一，可诱导细胞保护基因表达，如血红素加氧酶-1（HO-1）、烟酰胺醌氧化还原酶 1（NQO1）等。我们使早产儿暴露于高氧环境中，并发现早产儿的肺发育迟缓，其病理变化与 BPD 相似。高氧暴露后，早产儿 Nrf2 和 HO-1 的表达明显升高。探讨早产儿 Nrf2 和 HO-1 的变化并增强其有益功能，可能为有发生 BPD 风险的婴儿提供新的治疗策略。
