Saturday, 17 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Mitochondrial oxidative damage has been recognized as being involved in many diseases and in the aging process. Fibrotic changes appear as sequelae to insults by a diverse group of infectious, environmental, and therapeutic exposures. Therefore, this pathologic process can be involved in common pathway to final stage of various pulmonary disroders including senile pulmonary illness. To date, bloemycin-inhlaed animal model represents as a relatively well established experimental tool for pulmonary fibrotic chages. In this study, we aimed to investgate the role of mitochondrial ROS in the pathogenesis of bleomycin-induced lung inflammation and fibrosis and the related mechanisms. These results showed that the increased the gneeration of mitochondrial ROS in inflammatory cells and lung tissues, increased numbers of airway inflammatory cells, airway hyperresponsiveness, and increased levels of pro-inflammatory cytokines, TGF-β1, and increased nuclear translocation of NF-κB. In addition, the bloemycin-inhaled mice developed features of pulmonary fibrotic changes, including thickening of the peribronchial smooth muscle layer, subepithelial collagen deposition, and increased airway mucus production. Administration of NecroX compounds including NecroX-5 and -7 reduced the pathophysiological symptoms of pulmonary fibrosis, increased NF-κB activation, Th2 cytokines, and TGF-β1 in lungs as well as the increased generation of mitochondrial ROS in lung after bleomycin inhalation. These results indicate that reduction of mitochondrial ROS may attenuate pulmonary fibrotic changes through the regulation of NF-κB pathway, providing the therapeutic potential of NecroX compounds as an anti-fibrotic agent.