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

Clicks: 314
ID: 37489
2019
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Popular

Ranked #24 of 62 articles by views in Antioxidants (Basel, Switzerland)

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
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.
Reference Key
kim2019driedantioxidants Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
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;
Journal Antioxidants (Basel, Switzerland)
Year 2019
DOI
E349
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.