Dried Yeast Extracts Curtails Pulmonary Oxidative Stress, Inflammation and Tissue Destruction in a Model of Experimental Emphysema

• Published in: Antioxidants 2019-09, Vol.8 (9), p.349
• Main Authors: Kim, Yun-Ho, Kang, Min-Kyung, Lee, Eun-Jung, Kim, Dong Yeon, Oh, Hyeongjoo, Kim, Soo-Il, Oh, Su Yeon, Kim, Kyung-Hee, Park, Sang-Jae, Choi, Yean-Jung, Kang, Young-Hee
• Format: Article
• Language: English
• Subjects: airway inflammation; Alveoli; Antioxidants; Apoptosis; Asthma; Bcl-2 protein; Bronchitis; Bronchus; Cell culture; Chronic obstructive pulmonary disease; Cigarette smoke; Cigarette smoking; Cigarettes; dried yeast extracts; Emphysema; Experiments; Flavorings; Food additives; Functional foods & nutraceuticals; Inflammation; Laboratory animals; Leukocytosis; Lipopolysaccharides; Lungs; Monocyte chemoattractant protein 1; Neutrophils; NF-κB protein; Oral administration; Ovalbumin; Oxidative stress; Penicillin; Polyclonal antibodies; pulmonary emphysema; Reactive oxygen species; Tumor necrosis factor-α; Umami; Yeast
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox8090349

Pulmonary emphysema is characterized by a loss of alveolar integrity due to prolonged cigarette smoking and inhaled irritants. Dried yeast extracts (YE) are employed as food additives, savory flavorings, or creation of umami taste sensations. Despite being rich in nutrition, their application as nutraceuticals and functional foods is not investigated much and little is known about the inhibition of pulmonary emphysema. This study examined whether YE ameliorated pulmonary emphysema in mice is evoked by cigarette smoke (CS) and ovalbumin (OVA). Mice were orally administrated with 25-100 mg/kg YE for 8 weeks. Alveolar epithelial A549 cells exposed to lipopolysaccharide or CS extracts (CSE) were supplemented with 10-100 µg/mL YE. Oral YE administration reduced bronchoalveolar lavage fluid leukocytosis in CS-/OVA-exposed mice. YE reduced induction of inflammatory mediators and MMP-12, and diminished reactive oxygen species production and emphysematous alterations in CS-challenged airways. The YE treatment blunted bax/bcl-2 ratio and activation of p53 and caspases in CS-exposed lungs. Apoptotic death was dampened in CSE-loaded YE-supplemented A549 cells. YE curtailed tissue levels of MMP-12 in inflammatory OVA-exposed lungs. YE abrogated the secretion of TNF-α and MCP-1 through blocking NF-κB signaling in endotoxin-loaded A549 cells. Thus, the antioxidant YE may therapeutically ameliorate oxidative stress and inflammatory tissue destruction in emphysematous diseases.