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

我认为新生儿慢性肺病可能是通过胎儿期氧化还原状态的改变而发展起来的，并在细胞模型中验证了这一假设。将肿瘤坏死因子α和转化生长因子β暴露于L2细胞可促进上皮间充质转化。加入转化生长因子β后，细胞内谷胱甘肽含量降低，而谷胱甘肽耗竭和肿瘤坏死因子α预负荷对细胞内谷胱甘肽转化率的影响更为显著。细胞内过氧化氢由肿瘤坏死因子α预负荷增加，而过氧化氢酶模拟物的加入则降低细胞内过氧化氢含量。我认为细胞的氧化还原状态会影响细胞对产前应激的反应。

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.