Regulation of chronic obstructive pulmonary disease by parsnip polyphenols - PROJECT SUMMARY This proposal introduces a novel dietary approach targeting chronic obstructive pulmonary disease (COPD) caused by air pollution. Respiratory disorders, including asthma, COPD, and lung cancer, are significant global health concerns with high mortality rates. The primary risk factor for COPD is the inhalation of air pollutant cigarette smoke, leading to chronic pulmonary inflammation, mucus hypersecretion, airway remodeling, and emphysema, all contributing to lung dysfunction. Unfortunately, there are currently no effective medicinal therapies or dietary interventions for COPD. Cigarette smoke (CS) constitutes of over 7000 chemicals with known 93 harmful and potentially harmful chemicals such as acrolein. Repeated long-term environmental exposure to CS activates reactive oxygen species, inflammatory-oxidative stress and apoptosis that leads to alveolar space enlargement and development of COPD-emphysema, as well as compromising the ability to fight infection in the lungs, ultimately resulting in respiratory failure. Therefore, novel approaches that improve mitochondrial function in the lungs of COPD patients are urgently needed. Recent studies have indicated a potential protective effect of raw parsnip root (Pastinaca sativa), in combination with celery, against acrolein-induced pulmonary damage and inflammation. Moreover, our preliminary data demonstrate that an aging process involving high-temperature post-harvesting leads to the generation of polyphenol-enriched parsnip with enhanced antioxidative capacity compared to raw parsnip. We have observed that this aged parsnip effectively reduces lung inflammation and damage in mice acutely treated with acrolein intranasally. Based on these findings, we hypothesize that aged parsnip is a safe and bioactive dietary compound that can protect lungs from the pathogenesis of CS-induced COPD. To test this hypothesis, two aims have been developed using an animal model of chronic CS inhalation and primary human normal bronchial epithelial cells. Aim 1 will define the role of aged parsnip in chronic CS exposure-induced COPD. Aim 2 will determine the mechanism(s) underlying aged parsnip-ameliorated COPD. Successful completion of these aims will enable us to define the novel function of polyphenol-enriched aged parsnip and its bioactive components in air pollution-induced COPD.
