title: 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.affiliation: Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab Emirates. Electronic address: anemmar@uaeu.ac.ae.
authors.forename: Abderrahim
authors.initials: A
authors.lastname: Nemmar
authors.affiliation: Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab Emirates.
authors.forename: Suhail
authors.initials: S
authors.lastname: Al-Salam
authors.affiliation: Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab Emirates.
authors.forename: Priya
authors.initials: P
authors.lastname: Yuvaraju
authors.affiliation: Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab Emirates.
authors.forename: Sumaya
authors.initials: S
authors.lastname: Beegam
authors.affiliation: Department of Pharmacology and Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University, P.O. Box 35, Muscat 123, Al-Khod, Oman.
authors.forename: Badreldin H
authors.initials: BH
authors.lastname: Ali
mesh_terms: D000403:Airway Resistance / Q000187:drug effects*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004642:Emodin / Q000494:pharmacology* / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008168:Lung / Q000378:metabolism; D008171:Lung Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D016210:Methacholine Chloride / Q000633:toxicity; D051379:Mice; D008807:Mice, Inbred BALB C; D018721:Muscarinic Agonists / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects*; D052638:Particulate Matter / Q000633:toxicity; D011014:Pneumonia / Q000139:chemically induced / Q000188:drug therapy*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors
chemical_list: D016207:Cytokines; D018721:Muscarinic Agonists; D052638:Particulate Matter; D047428:Protein Kinase Inhibitors; D017382:Reactive Oxygen Species; D016210:Methacholine Chloride; D005978:Glutathione; D004642:Emodin
keywords: Airway resistance; Diesel exhaust particles; Emodin; Inflammation; Oxidative stress