Diesel Exhaust Particles Induce Impairment of Vascular and Cardiac Homeostasis in Mice: Ameliorative Effect of Emodin.

Abstract

BACKGROUND/AIM:

There is strong epidemiological and clinical evidence that components of the cardiovascular system are adversely affected by particulate air pollutants through the generation of inflammation and oxidative stress. Emodin (1,3,8-trihydroxy-6- methylanthraquinone), which is commonly found in the roots of rhubarb plant, has strong antioxidant and anti-inflammatory effects. However, its possible protective effect on the cardiovascular effect of particulate air pollutants has never been reported before.

METHODS:

We tested, in Tuck-Ordinary mice, the possible ameliorative effect of emodin on the acute (24h) cardiovascular effects of diesel exhaust particles (DEP, 1 mg/kg) or saline (control). Emodin (4 mg/kg) was administered intraperitoneally 1h before and 7h after pulmonary exposure to DEP. Twenty four h following DEP exposure, several cardiovascular endpoints were assessed.

RESULTS:

Emodin significantly prevented the increase of leukocyte (n=8, P<0.001) and erythrocyte (n=8, P<0.01) numbers caused by DEP. Likewise, emodin abrogated DEP-induced increase of heart tissue levels of interleukin 1β (n=8, P<0.01) and tumour necrosis factor α (n=8, P<0.05), and significantly mitigated the change of the activities of antioxidant enzymes superoxide dismutase (n=8, P<0.001) and glutathione reductase (n=8, P<0.05). Emodin abolished the in vivo prothrombotic effect of DEP in pial arterioles (n=6, P<0.01) and venules (n=6, P<0.001). Similarly, emodin prevented platelet aggregation in vitro in whole blood (n=4-5, P<0.01), and the shortening of activated partial thromboplastin time (n=4, P<0.001) and prothrombin time (n=4, P<0.01) caused by DEP.

CONCLUSION:

We conclude that emodin treatment has consistently protected against DEP-induced impairment of vascular and cardiac homeostasis in mice. Our study provides experimental evidence that the use of functional food such as emodin, pending further studies, can be considered a useful agent and may have the potential to protect or mitigate the cardiovascular detrimental effects observed in people living in cities with high concentrations of particulate air pollution.

• Authors: Abderrahim Nemmar, Rauda Al Dhaheri, Jawaher Alamiri, Suhaila Al Hefeiti, Hajar Al Saedi, Sumaya Beegam, Priya Yuvaraju, Javed Yasin, Badreldin H Ali
• Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology (Cell Physiol Biochem) Vol. 36 Issue 4 Pg. 1517-26 ( 2015) ISSN: 1421-9778 [Electronic] Germany
• PMID: 26159184 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2015 S. Karger AG, Basel.

Chemical References

• Anti-Inflammatory Agents
• Antioxidants
• Interleukin-1beta
• Particulate Matter
• Tumor Necrosis Factor-alpha
• Vehicle Emissions
• Superoxide Dismutase
• Emodin

Topics

• Animals
• Anti-Inflammatory Agents (therapeutic use)
• Antioxidants (therapeutic use)
• Blood Cell Count
• Blood Coagulation (drug effects)
• Cardiovascular Diseases (blood, drug therapy, pathology)
• Emodin (therapeutic use)
• Heart (drug effects)
• Hematocrit
• Homeostasis (drug effects)
• Interleukin-1beta (analysis)
• Male
• Mice
• Myocardium (pathology)
• Oxidative Stress (drug effects)
• Particulate Matter (toxicity)
• Platelet Aggregation (drug effects)
• Rheum (chemistry)
• Superoxide Dismutase (analysis)
• Thrombosis (blood, drug therapy, pathology)
• Tumor Necrosis Factor-alpha (analysis)
• Vehicle Emissions (toxicity)