Emodin mitigates diesel exhaust particles-induced increase in airway resistance, inflammation and oxidative stress in mice.

Abstract

Clinical and experimental studies have reported that short-term exposure to particulate air pollution is associated with inflammation, oxidative stress and impairment of lung function. Emodin (1,3,8-trihydroxy-6-methylanthraquinone) has a strong antioxidant and anti-inflammatory actions. Therefore, in the present study, we evaluated the possible ameliorative effect of emodin on diesel exhaust particles (DEP)-induced impairment of lung function, inflammation and oxidative stress in mice. Mice were intratracheally instilled with DEP (20 μg/mouse) or saline (control). Emodin was administered intraperitoneally 1h before and 7h after pulmonary exposure to DEP. Twenty-four hours following DEP exposure, we evaluated airway resistance measured by forced oscillation technique, lung inflammation and oxidative stress. Emodin treatment abated the DEP-induced increase in airway resistance, and prevented the influx of neutrophils in bronchoalveolar lavage fluid. Similarly, lung histopathology confirmed the protective effect of emodin on DEP-induced lung inflammation. DEP induced a significant increase of proinflammatory cytokines in the lung including tumor necrosis factor α, interleukin 6 and interleukin 1β. The latter effect was significantly ameliorated by emodin. DEP caused a significant increase in lung lipid peroxidation, reactive oxygen species and a significant decrease of reduced glutathione concentration. These effects were significantly mitigated by emodin. We conclude that emodin significantly mitigated DEP-induced increase of airway resistance, lung inflammation and oxidative stress. Pending further pharmacological and toxicological studies, emodin may be considered a potentially useful pulmonary protective agent against particulate air pollution-induced lung toxicity.

• Authors: Abderrahim Nemmar, Suhail Al-Salam, Priya Yuvaraju, Sumaya Beegam, Badreldin H Ali
• Journal: Respiratory physiology & neurobiology (Respir Physiol Neurobiol) Vol. 215 Pg. 51-7 (Aug 15 2015) ISSN: 1878-1519 [Electronic] Netherlands
• PMID: 26001677 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier B.V. All rights reserved.

Chemical References

• Cytokines
• Muscarinic Agonists
• Particulate Matter
• Protein Kinase Inhibitors
• Reactive Oxygen Species
• Methacholine Chloride
• Glutathione
• Emodin

Topics

• Airway Resistance (drug effects)
• Animals
• Cytokines (metabolism)
• Disease Models, Animal
• Dose-Response Relationship, Drug
• Emodin (pharmacology, therapeutic use)
• Glutathione (metabolism)
• Lipid Peroxidation (drug effects)
• Lung (metabolism)
• Lung Diseases (chemically induced, drug therapy, pathology)
• Methacholine Chloride (toxicity)
• Mice
• Mice, Inbred BALB C
• Muscarinic Agonists (toxicity)
• Oxidative Stress (drug effects)
• Particulate Matter (toxicity)
• Pneumonia (chemically induced, drug therapy)
• Protein Kinase Inhibitors (pharmacology, therapeutic use)
• Reactive Oxygen Species (metabolism)
• Time Factors