分析铁死亡(ferroptosis)在海水暴露后支气管上皮细胞损伤中的作用。

将培养至对数生长期的人支气管上皮细胞分为四组：Con(Control)组，SW(Seawater)组，Con＋F(Fer-1)组，SW＋F组。Con组使用DMEM完全培养基进行培养，Con＋F组使用含有10 μM Fer-1的DMEM完全培养基培养6 h，SW组使用含有25.0%中国一级标准海水的DMEM完全培养基培养6 h，SW＋F组使用含有10 μM Fer-1的25.0%一级标准海水DMEM完全培养基培养6 h。后检测每组细胞的增殖活力，测定GSH、MDA的含量，SOD的活力，并用蛋白免疫印迹检测GPX4、FTH1、COX2、ACSL4的相对蛋白表达量。

海水组的细胞活性显著下降(P<0.0001)，呈时间依赖性，平均每两小时下降13.0%，而Fer-1能够显著改善细胞活性的下降(P<0.0001)，相对活性升高8.897%。Fer-1可显著缓解海水诱导的细胞GSH降低、MDA积累和SOD活力降低(P<0.001)，Fer-1处理后相较于海水组分别升高3.985 μmol/gprot，降低1.414 nM/mgprot，升高1.288 U/mgprot。并可减轻海水诱导的细胞FTH1、GPX4表达量的降低，以及COX2、ACSL4表达量的升高(P<0.05)，分别相对升高25.02%、29.84%，降低68.98%、39.17%。

海水暴露使支气管上皮细胞发生铁死亡，Fer-1可减轻海水诱导的支气管上皮细胞损伤。

This study aims to investigate the role of ferroptosis in human bronchial epithelial cells injury following exposure to seawater.

bronchial epithelial cells were cultured to the logarithmic growth phase and divided into four groups: Control (Con), Seawater treated (SW), Fer-1 treated control (Con+ F), and Fer-1 treated seawater (SW+ F) groups. The Con group was cultured with DMEM complete medium, the Con+ F group was cultured with DMEM complete medium containing 10 μM Fer-1 for 6 hours, the SW group was cultured with DMEM complete medium containing 25% Chinese primary standard seawater for 6 hours, and the SW+ F group was cultured with DMEM complete medium containing 25% primary standard seawater and 10 μM Fer-1 for 6 hrs. Subsequently, the cell viability, GSH and MDA levels, SOD vigor, and protein expression levels of GPX4, FTH1, COX2, and ACSL4 were measured.

The viability of cells in the seawater group significantly decreased (P<0.0001), following a time-dependent pattern, with an average decrease of 13% every two hours. However, treatment with Fer-1 was able to significantly ameliorate this decline in cell viability (P<0.0001), resulting in a relative increase of 8.897%. Moreover, Fer-1 was capable of significantly mitigating the reduction in cellular GSH, MDA accumulation, and SOD activity induced by seawater (P<0.001). Compared to the seawater group, treatment with Fer-1 led to an increase of 3.985 μmol/gprot, a decrease of 1.414 nM/mgprot, and an increase of 1.288 U/mgprot. Furthermore, Fer-1 was able to mitigate the reduction in cellular FTH1 and GPX4 expression levels and the increase in COX2 and ACSL4 expression levels induced by seawater (P<0.05), resulting in relative increases of 25.02% and 29.84% and reductions of 68.98% and 39.17%, respectively.

Seawater exposure induces ferroptosis in bronchial epithelial cells, while Fer-1 attenuates the seawater-induced cell injury.