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

Abderrahim Nemmar, Suhail Al-Salam, Priya Yuvaraju, Sumaya Beegam, Badreldin H. Ali

Research output: Contribution to journalArticle

27 Citations (Scopus)

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 1. h before and 7. h 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.

Original languageEnglish
Pages (from-to)51-57
Number of pages7
JournalRespiratory Physiology and Neurobiology
Volume215
DOIs
Publication statusPublished - Aug 5 2015

Fingerprint

Emodin
Vehicle Emissions
Airway Resistance
Oxidative Stress
Inflammation
Lung
Pneumonia
Air Pollution
Protective Agents
Bronchoalveolar Lavage Fluid
Interleukin-1
Toxicology
Lipid Peroxidation
Glutathione
Interleukin-6
Reactive Oxygen Species
Neutrophils
Anti-Inflammatory Agents
Tumor Necrosis Factor-alpha
Antioxidants

Keywords

  • Airway resistance
  • Diesel exhaust particles
  • Emodin
  • Inflammation
  • Oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Neuroscience(all)

Cite this

Emodin mitigates diesel exhaust particles-induced increase in airway resistance, inflammation and oxidative stress in mice. / Nemmar, Abderrahim; Al-Salam, Suhail; Yuvaraju, Priya; Beegam, Sumaya; Ali, Badreldin H.

In: Respiratory Physiology and Neurobiology, Vol. 215, 05.08.2015, p. 51-57.

Research output: Contribution to journalArticle

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