Antenatal priming theory about induction of neonatal chronic lung disease: collapse of redox balance.

关于诱发新生儿慢性肺病的产前启动理论：氧化还原平衡崩溃。

• 批准号: 23791239
• 负责人: HASEGAWA Masashi
• 金额: $ 2.33万
• 依托单位: Osaka Medical College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791239/
• 关键词: 未熟児医学; 慢性肺疾患; 上皮間質転換; 酸化還元状態; 活性酸素

I think that neonatal chronic lung disease may have been developed by prenatal changes of the redox state, and tested the assumption in a cell model. Epithelial mesenchymal transition (EMT) is enhanced by exposure of TNFα and TGFβ to L2 cells. Intracellular GSH decreased after addition of TGFβ, and EMT is more enhanced by GSH depletion and TNFα preload. Intracellular hydrogen peroxide increased by TNFα preload and EMT is reduced by the addition of catalase mimic. I think that redox status of cells influence the cellular response to prenatal stress.

我认为，新生儿慢性肺病可能是由产前氧化还原状态的变化发展而来的，并在细胞模型中验证了这一假设。L2细胞暴露于TNFα和TGFβ可增强上皮间质转化（EMT）。加入TGFβ后，细胞内GSH减少，GSH耗竭和TNFα预负荷使EMT进一步增强。细胞内过氧化氢增加TNFα预负荷和EMT减少过氧化氢酶模拟。我认为细胞的氧化还原状态影响细胞对产前压力的反应。