Aldosterone alleviates lipopolysaccharide-induced acute lung injury by regulating epithelial sodium channel through PI3K/Akt/SGK1 signaling pathway.
Xiu Fei, Yu Ziqian, Yang Bingwu, Li Min, Xian Xinmiao, Meng Zhen, Guo Lirong, Wang Song
Author Information
Xiu Fei: Department of Blood Transfusion, Liaocheng People's Hospital, #67 Dongchangxi Road, Liaocheng, 252000, China.
Yu Ziqian: Department of Clinical Laboratory, Liaocheng Veterans Hospital, #2 Gaodong Street, Liaocheng, 252000, China.
Yang Bingwu: Procesion Biomedical Lab, Liaocheng People's Hospital, Medical College of Liaocheng University, #67 Dongchangxi Road, Liaocheng, 252000, China.
Li Min: Procesion Biomedical Lab, Liaocheng People's Hospital, Medical College of Liaocheng University, #67 Dongchangxi Road, Liaocheng, 252000, China.
Xian Xinmiao: Procesion Biomedical Lab, Liaocheng People's Hospital, Medical College of Liaocheng University, #67 Dongchangxi Road, Liaocheng, 252000, China.
Meng Zhen: Procesion Biomedical Lab, Liaocheng People's Hospital, Medical College of Liaocheng University, #67 Dongchangxi Road, Liaocheng, 252000, China.
Guo Lirong: Nursing School of Jilin University, Changchun, Jilin, 130021, China. Electronic address: guolr@jlu.edu.cn.
Wang Song: Procesion Biomedical Lab, Liaocheng People's Hospital, Medical College of Liaocheng University, #67 Dongchangxi Road, Liaocheng, 252000, China. Electronic address: wslcrmyy@sina.com.
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 ALImice. 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.
