title: Apoptosis and surfactant protein-C expression inhibition induced by lipopolysaccharide in AEC II cell may associate with NF-κB pathway.
abstract: Lipopolysaccharide (LPS), a Gram-negative bacterial outer membrane component, is one of the major causes of septic shock. Herein we investigate LPS-induced apoptosis of rat alveolar epithelial type II cells (AEC II) and the effects of LPS on surfactant protein-C (SP-C) expression in AEC II, along with the possible molecular mechanisms. LPS exposure impaired cell viability and increased apoptosis of AEC II significantly in concentration-dependent manner embodied in increased caspase-3 expression and the activity of caspase-3. Simultaneously, our results also indicated that LPS inhibited surfactant protein-C (SP-C) expression in AEC II. Mechanistic studies revealed that LPS treatment significantly increased the expression of NF-κB p50, NF-κB p65 and IKKβ proteins as well as induced IκB-α phosphorylation. Moreover, pretreatment with IKK inhibitor IKK-16 or NF-κB inhibitor PDTC ameliorated LPS-caused alterations in cleaved caspase-3 expression, the activity of caspase-3 and SP-C expression. Taken together, these results demonstrate that LPS can induce apoptosis of AEC II and decrease SP-C expression partly through activating the NF-κB pathway.
authors.affiliation: Department of Emergency and Critical Care Medicine, Baoan Hospital, Nanfang Medical University, China.
authors.forename: Jinle
authors.initials: J
authors.lastname: Lin
authors.forename: Jun
authors.initials: J
authors.lastname: Tian
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.forename: Weigang
authors.initials: W
authors.lastname: Wu
authors.forename: Huaying
authors.initials: H
authors.lastname: Li
authors.forename: Xueyan
authors.initials: X
authors.lastname: Wang
authors.forename: Xiaobin
authors.initials: X
authors.lastname: Zeng
authors.forename: Wenwu
authors.initials: W
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D051550:I-kappa B Kinase / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D010455:Peptides / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000166:cytology; D017207:Rats, Sprague-Dawley; D051996:Transcription Factor RelA / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D010455:Peptides; D051996:Transcription Factor RelA; C077063:Sftpc protein, rat; D051550:I-kappa B Kinase; D053148:Caspase 3