title: Irisin-mediated protective effect on LPS-induced acute lung injury via suppressing inflammation and apoptosis of alveolar epithelial cells.
abstract: It is considered that the essence of acute lung injury (ALI) is an excessive and uncontrolled inflammatory response in lung, of which mainly is attributed to the release of inflammatory mediators. Recent studies demonstrated that irisin, which is a metabolism associated factor after physical exercise could suppression of inflammation by regulating cellular signaling pathways, however, the underlying molecular mechanism remains to be determined. The present study aimed to reveal the potential mechanism responsible for the anti-inflammatory effects of irisin on LPS-induced acute lung injury in mice and in A549 cells. The results of histopathological changes showed that irisin ameliorated the lung injury that was induced by LPS in time- and dose-dependent manner. QRT-PCR assays demonstrated that irisin suppressed the production of IL-1β, IL-6, MCP-1 and TNF-α, and western blot assays demonstrated that irisin suppressed apoptosis of ALI. The expression of caspase-3 and Bax were decreased and Bcl-2 was increased by irisin administration. Further study was conducted on nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) using pathways using western blots. The results showed that irisin inhibited reduced LPS-induced activation of MAPK and NF-κB signaling. All results indicated that irisin has protective effect on LPS-induced ALI in mice and in A549 cells. Thus, irisn related with physical exercise may be a potential therapy for the treatment of pulmonary inflammation.
authors.affiliation: Center for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan 250012, PR China; Jinan Central Hospital Affiliated to Shandong University, Jinan 250012, PR China.
authors.forename: Lei
authors.initials: L
authors.lastname: Shao
authors.affiliation: Jinan Central Hospital Affiliated to Shandong University, Jinan 250012, PR China.
authors.forename: Di
authors.initials: D
authors.lastname: Meng
authors.affiliation: Jinan Central Hospital Affiliated to Shandong University, Jinan 250012, PR China.
authors.forename: Fei
authors.initials: F
authors.lastname: Yang
authors.affiliation: Center for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan 250012, PR China.
authors.forename: Haibo
authors.initials: H
authors.lastname: Song
authors.affiliation: Center for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan 250012, PR China. Electronic address: tangdq@sdu.edu.cn.
authors.forename: Dongqi
authors.initials: D
authors.lastname: Tang
mesh_terms: D000072283:A549 Cells; D055371:Acute Lung Injury / Q000139:chemically induced / Q000276:immunology* / Q000517:prevention & control*; D056809:Alveolar Epithelial Cells / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D005353:Fibronectins / Q000008:administration & dosage*; D006801:Humans; D008070:Lipopolysaccharides; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011014:Pneumonia / Q000139:chemically induced / Q000276:immunology* / Q000517:prevention & control*; D016896:Treatment Outcome
chemical_list: C571428:FNDC5 protein, mouse; D005353:Fibronectins; D008070:Lipopolysaccharides
keywords: Acute lung injury (ALI); Apoptosis; Inflammation; Irisin; p38AMRK/NF-κB signaling pathway