5. Oxidative stress:
There are many studies showing increased oxidative stress in COPD patients. The oxides mainly include superoxide anion (O2-), hydroxyl radical (OH), hypochlorous acid (HClO), H2O2 and nitric oxide (NO). Oxides can directly act on and destroy many biochemical macromolecules such as proteins, lipids and nucleic acids, resulting in cell dysfunction or cell death, and can also damage the extracellular matrix; cause protease-antiprotease imbalance; promote inflammatory responses, such as activation of transcription factors NF-κB is involved in the transcription of various inflammatory factors, such as IL-8, TNF-α, NO-induced synthase and epoxide-induced enzyme.
6. Inflammation mechanism:
Chronic inflammation of airways, lung parenchyma, and pulmonary vessels is a characteristic change of COPD. Inflammatory cells such as neutrophils, macrophages, and T lymphocytes are all involved in the pathogenesis of COPD. Activation and aggregation of neutrophils is an important link in the inflammatory process in COPD, causing a chronic mucus hypersecretion state through the release of neutrophil elastase, neutrophil cathepsin G, neutrophil protease 3 and matrix metalloproteinases and destroy the lung parenchyma.
Such as autonomic dysfunction, malnutrition, and temperature changes may all be involved in the occurrence and development of COPD.