Fei Xiu, Ziqian Yu, Bingwu Yang, Min Li, Xinmiao Xian, Zhen Meng, Lirong Guo, Song Wang
Department of Blood Transfusion, Liaocheng People's Hospital, #67 Dongchangxi Road, Liaocheng, 252000, China.
Department of Clinical Laboratory, Liaocheng Veterans Hospital, #2 Gaodong Street, Liaocheng, 252000, China.
Mol Cell Probes. 2021 Jun;57:101709. doi: 10.1016/j.mcp.2021.101709. Epub 2021 Mar 10.
Reduced alveolar fluid clearance (AFC) is a major pathological feature of acute lung injury (ALI). Epithelial sodium channel (ENaC) plays a key role in regulating the transport of Na and clearing alveolar edema fluid effectively. ENaC has been reported to be regulated by aldosterone in the distal collecting tube of the kidney. We hypothesized whether aldosterone regulated ENaC in alveolar epithelium and correspondingly played a role in ALI. In this study we found that the expression of aldosterone synthesis encoding gene, CYP11B2, and ENaC were decreased in the lung tissue of LPS-induced ALI mice. Furthermore, aldosterone alleviated ALI by increasing the expression of ENaC-α and relieving pulmonary edema. Besides, we found that aldosterone upregulated ENaC-α through PI3K/Akt/SGK1 pathway. In conclusion, our study demonstrated that aldosterone attenuated pulmonary edema by upregulating ENaC-α through the PI3K/Akt/SGK1 pathway in LPS-induced ALI, indicating that aldosterone might be a promising adjuvant drug for ALI treatment.
肺泡液体清除率（AFC）降低是急性肺损伤（ALI）的主要病理特征。上皮钠通道（ENaC）在调节Na转运及有效清除肺泡水肿液中起关键作用。据报道，ENaC在肾远曲小管受醛固酮调节。我们推测醛固酮是否调节肺泡上皮中的ENaC并相应地在ALI中发挥作用。在本研究中，我们发现脂多糖诱导的ALI小鼠肺组织中醛固酮合成编码基因CYP11B2和ENaC的表达降低。此外，醛固酮通过增加ENaC-α的表达和减轻肺水肿来缓解ALI。此外，我们发现醛固酮通过PI3K/Akt/SGK1途径上调ENaC-α。总之，我们的研究表明，在脂多糖诱导的ALI中，醛固酮通过PI3K/Akt/SGK1途径上调ENaC-α来减轻肺水肿，表明醛固酮可能是一种有前景的ALI治疗辅助药物。
