Perfluorocarbon reduces cell damage from blast injury by inhibiting signal paths of NF-κB, MAPK and Bcl-2/Bax signaling pathway in A549 cells

• DOI: 10.1371/journal.pone.0173884
• Publication Date: 2017-03-21T22:11:14Z
• Authors: Zhaorui Zhang; Zhixin Liang; Huaidong Li; Chunsun Li; Zhen Yang; Yanqin Li; Danyang She; Lu Cao; Wenjie Wang; Changlin Liu; Liangan Chen
• Keywords: 0301 basic medicine; MAP Kinase Signaling System; Science; Acute Lung Injury; Interleukin-1beta; Apoptosis; Models, Biological; 03 medical and health sciences; Blast Injuries; Humans; RNA, Messenger; Cell Shape; bcl-2-Associated X Protein; Fluorocarbons; Caspase 3; Interleukin-6; Tumor Necrosis Factor-alpha; Q; R; NF-kappa B; 3. Good health; Oxidative Stress; Proto-Oncogene Proteins c-bcl-2; A549 Cells; Medicine; Research Article; Signal Transduction

Blast lung injury is a common type of blast injury and has very high mortality. Therefore, research to identify medical therapies for blast injury is important. Perfluorocarbon (PFC) is used to improve gas exchange in diseased lungs and has anti-inflammatory functions in vitro and in vivo. The aim of this study was to determine whether PFC reduces damage to A549 cells caused by blast injury and to elucidate its possible mechanisms of action.A549 alveolar epithelial cells exposed to blast waves were treated with and without PFC. Morphological changes and apoptosis of A549 cells were recorded. PCR and enzyme-linked immunosorbent assay (ELISA) were used to measure the mRNA or protein levels of IL-1β, IL-6 and TNF-α. Malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity levels were detected. Western blot was used to quantify the expression of NF-κB, Bax, Bcl-2, cleaved caspase-3 and MAPK cell signaling proteins.A549 cells exposed to blast wave shrank, with less cell-cell contact. The morphological change of A549 cells exposed to blast waves were alleviated by PFC. PFC significantly inhibited the apoptosis of A549 cells exposed to blast waves. IL-1β, IL-6 and TNF-α cytokine and mRNA expression levels were significantly inhibited by PFC. PFC significantly increased MDA levels and decreased SOD activity levels. Further studies indicated that NF-κB, Bax, caspase-3, phospho-p38, phosphor-ERK and phosphor-JNK proteins were also suppressed by PFC. The quantity of Bcl-2 protein was increased by PFC.Our research showed that PFC reduced A549 cell damage caused by blast injury. The potential mechanism may be associated with the following signaling pathways: 1) the signaling pathways of NF-κB and MAPK, which inhibit inflammation and reactive oxygen species (ROS); and 2) the signaling pathways of Bcl-2/Bax and caspase-3, which inhibit apoptosis.