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 remains unclear and the anti-inflammatory mechanism of Macrolide is complex and not exactly known.
Methods: We read and analysed 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 reduces 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 a 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