作者: Irfan Rahman
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摘要: Inflammatory lung diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD) are characterised by systemic local chronic inflammation oxidative stress. The sources of the increased stress in patients with COPD derive from burden inhaled oxidants, amounts reactive oxygen species (ROS) generated several inflammatory, immune structural cells airways. Increased levels ROS produced airways reflected markers airspaces, sputum, breath, lungs blood COPD. ROS, either directly or via formation lipid peroxidation products acrolein, 4-hydroxy-2-nonenal F(2)-isoprostanes, may play a role enhancing through activation kinases (JNK, MAPK, p38, phosphoinositide 3 (PI-3)-kinase/PI-3K-activated serine-threonine kinase Akt) redox sensitive transcription factors NF-kappaB AP-1. Recent data have also indicated that pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for factor DNA binding leading to enhanced gene expression various cells. Furthermore, balance between antioxidant enzymes favor inflammatory lung. Thus, presence important consequences pathogenesis Identification genes predispose development identify novel therapeutic targets. Future work is directed understand molecular mechanisms antioxidants on ROS-mediated cell signaling pathways inhibition response would provide information targets Effective wide spectrum therapy has good bioavailability potency urgently needed control localised processes occur In addition, compounds be therapeutically useful monitoring biomarkers progression/severity