title: Epigallocatechin-3-gallate suppresses alveolar epithelial cell apoptosis in seawater aspiration-induced acute lung injury via inhibiting STAT1-caspase-3/p21 associated pathway.
abstract: The apoptosis of alveolar epithelial cells is important in seawater aspiration‑induced acute lung injury (ALI). The present study aimed to investigate whether epigallocatechin-3-gallate (EGCG) is able to suppress apoptosis in alveolar epithelial cells in seawater aspiration‑induced ALI in vivo and in vitro, and the possible mechanisms underlying it. The results indicated that seawater aspiration‑induced ALI in rats is accompanied by increased apoptosis in lung tissue cells and the expression of apoptosis‑associated proteins, caspase‑3 and p21. EGCG pretreatment significantly ameliorated seawater aspiration‑induced ALI. Furthermore, EGCG decreased seawater aspiration‑induced apoptosis and the expression of caspase‑3 and p21 in lung tissue cells. Seawater‑challenged A549 cells experienced increased apoptosis and elevated levels of phosphorylated‑signal transducer and activator of transcription 1 (P‑STAT1). EGCG pretreatment of the cells resulted in significantly decreased seawater‑induced apoptosis and lower levels of STAT1 and P‑STAT1 in A549 cells. This suggests that EGCG suppresses alveolar epithelial cell apoptosis in seawater aspiration‑induced ALI via inhibiting the STAT1-caspase-3/p21 associated pathway.
authors.affiliation: Department of Pulmonary Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
authors.forename: Mingqing
authors.initials: M
authors.lastname: Dong
authors.affiliation: Department of Pulmonary Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
authors.forename: Liyan
authors.initials: L
authors.lastname: Bo
authors.affiliation: Department of Pulmonary Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
authors.forename: Congcong
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Pulmonary Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
authors.forename: Zhichao
authors.initials: Z
authors.lastname: Li
authors.affiliation: Department of Pulmonary Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
authors.forename: Faguang
authors.initials: F
authors.lastname: Jin
mesh_terms: D055371:Acute Lung Injury / Q000150:complications / Q000201:enzymology / Q000473:pathology*; D056809:Alveolar Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D045744:Cell Line, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism*; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D010766:Phosphorylation / Q000187:drug effects; D011654:Pulmonary Edema / Q000150:complications / Q000201:enzymology / Q000473:pathology; D017207:Rats, Sprague-Dawley; D053120:Respiratory Aspiration / Q000201:enzymology / Q000473:pathology*; D050794:STAT1 Transcription Factor / Q000378:metabolism*; D012623:Seawater; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D050794:STAT1 Transcription Factor; C494080:Stat1 protein, mouse; D002392:Catechin; C045651:epigallocatechin gallate; D053148:Caspase 3