Grape seed proanthocyanidin extract modulates cigarette smoke extract-induced epithelial cell apoptosis by inhibiting oxidative stress in chronic obstructive pulmonary disease

[Display omitted] •GSPE reduced CSE-induced increase in ROS and apoptosis levels in mouse lungs and AECs.•GSPE lowered Bax/Bcl-2 ratio, protecting against CSE-induced epithelial cell apoptosis.•GSPE ameliorated lung inflammation by reducing the number of inflammatory cells.•GSPE improved COPD phenotypes: airspace enlargement and alveolar wall damage. Chronic obstructive pulmonary disease (COPD) is a progressive, irreversible, inflammatory lung disease characterized by airway inflammation and emphysema. Cigarette smoke-induced oxidative stress and apoptosis of alveolar epithelial cells (AECs) are key factors in COPD pathogenesis. We investigated the effects of grape seed proanthocyanidin extract (GSPE) on cigarette smoke extract (CSE)-induced AEC apoptosis, emphysema, and inflammation. We exposed mice to CSE and evaluated histological changes, reactive oxygen species production, proinflammatory cytokine expression, and apoptosis levels in the lungs and AECs. GSPE exerted protective effects against CSE-induced COPD. The levels of reactive oxygen species were by GSPE in vitro and in vivo. GSPE significantly decreased the levels of reactive oxygen species in vitro and in vivo and reduced the number of macrophages, neutrophils and levels of cytokines in the bronchoalveolar lavage fluid and AECs, ameliorating lung inflammation. GSPE ameliorated the CSE-induced COPD development by inhibiting oxidative stress-induced epithelial cell apoptosis.