Xuejiao Sun, Lin Chen and Zhiyi He* Pages 301 - 304 ( 4 )
Background: Chronic Obstructive Pulmonary Disease (COPD) is a systematic inflammatory disease, and smoking is an important risk factor for COPD. Macrolide can reduce COPD inflammation. However, the inflammatory mechanism of COPD is remain unclear and the anti-inflammatory mechanism of Macrolide is complex and not exactly known.Methods: We read and analysis thirty-eight articles, including original articles and reviews. Results: The expression of Nrf2 was lower in COPD patients and might have a protective role against apoptosis caused by CSE-induced oxidative stress. Nrf2 may play an important role in COPD inflammation. Nrf2 is a key factor in downstream of PI3K/Akt and is involved in the regulation of oxidative stress and inflammatory response. Therefore, PI3K/Akt pathway may play an important role in the activation of Nrf2 and COPD inflammation. Macrolide reduce lung and systemic inflammation of COPD by regulating PI3K/Akt pathway. Conclusion: This review indicates that PI3K/Ak-Nrf2 may play an important role in COPD inflammation and macrolides may reduce lung and systemic inflammation of COPD by regulating PI3K/Akt-Nrf2 pathway. However, many crucial and essential questions remain to be answered. Further understanding of the mechanisms of macrolide efficacy and PI3K/Akt-Nrf2-mediated inflammatory responses may provide new clue for exploring COPD treatment in the future.
PI3K/Akt pathway, Nrf2 protein, oxidative stress, inflammation, macrolides, chronic obstructive pulmonary disease.
Department of Respiratory and Critical Care Medicine, Liuzhou General Hospital, Liuzhou, Guangxi 545006, , Department of Respiratory and Critical Care Medicine, Liuzhou General Hospital, Liuzhou, Guangxi 545006, , Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021