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.