The present study revealed that YE blocked bronchiolar and alveolar inflammation and subsequent pulmonary emphysema in CS- and OVA-challenged COPD models, in which YE abrogated chronic inflammation, MMP-12 proteolytic activity, oxidative stress, and apoptosis of structural alveolar cells in the airways that might possibly be an important upstream event in the pathogenesis of COPD. The gene discussed is MMP12; the disease is pulmonary emphysema.