Regulatory mechanism of pyrrolidine dithiocarbamate is mediated by nuclear factor-κB and inhibits neutrophil accumulation in ARDS mice.

摘要: The aim of the present study was to investigate regulatory mechanism nuclear factor (NF)-κB on polymorphonuclear neutrophil (PMN) accumulation and inflammatory response in lung tissues with acute respiratory distress syndrome (ARDS), as well therapeutic effect pyrrolidine dithiocarbamate (PDTC). Mouse models ARDS were established by intraperitoneal injection lipopolysaccharide (LPS). BALB/c mice divided into control, LPS PDTC + groups. expression PMN adhesion molecules, CD11b/CD18 intercellular molecule-1 (ICAM-1), detected immunohistochemistry, while protein levels NF-κB p65 tissue analyzed western blot analysis. In addition, flow cytometry used apoptosis rate PMNs bronchoalveolar fluid, interleukin (IL)-1β, IL-8 tumor necrosis (TNF)-α myeloperoxidase (MPO) activity also determined. Following an LPS, alveolar septum rupture, pulmonary interstitial hyperemia infiltration observed. cytoplasm decreased, nucleus increased. IL-8, IL-1β TNF-α increased high status maintained for 24 h. As time increased, ICAM-1 MPO activity, delayed. Compared group, following intervention, cytokines activity. Therefore, reduced production via pathway, which activation promoted apoptosis.