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 journalArticlepeer-review

47 Citations (Scopus)


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
Publication statusPublished - Aug 5 2015


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

ASJC Scopus subject areas

  • General Neuroscience
  • Physiology
  • Pulmonary and Respiratory Medicine


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