Myricetin protects airway epithelial cells against cigarette smoke extract-induced inflammation and oxidative stress by suppressing autophagy.

Abstract

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease characterized by inflammation and oxidative stress, which is mainly caused by cigarette smoke (CS). The flavonoid myricetin was reported to exert protective effects in different diseases. This study aimed to explore the function of myricetin in COPD progression. Airway epithelial A549 cells were treated with CS extract (CSE) to establish an in vitro model, followed by the detection of inflammation, oxidative stress, and autophagy markers. Sprague-Dawley male rats were exposed to CS for 12 weeks to establish an in vivo model, followed by the evaluation of lung function parameters and lung histopathological changes. We found that myricetin relieved inflammation and oxidative stress in CSE-induced A549 cells, as demonstrated by the reduced MCP-1, IL-6, and IL-8 expression, ROS production, and MDA content and elevated SOD activity. Myricetin treatment reduced LC3B-II/LC3B-I ratio and Beclin-1 protein levels and elevated p62 protein level after CSE stimulation in A549 cells. In vivo results revealed that myricetin restored pulmonary function and ameliorated pulmonary inflammation and emphysema in CS-induced COPD rats. Collectively, the anti-inflammatory and antioxidant effects of myricetin in COPD may be attributed to its suppressive effects on autophagy.