Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone

BACKGROUND AND PURPOSE Acute exposure to particulate air pollution has been linked to acute cardiopulmonary events, but the underlying mechanisms are uncertain. EXPERIMENTAL APPROACH We investigated the acute (at 4 and 18 h) effects of diesel exhaust particles (DEP) on cardiopulmonary parameters in...

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Published in:British journal of pharmacology 2011-12, Vol.164 (7), p.1871-1882
Main Authors: Nemmar, Abderrahim, Al‐Salam, Suhail, Zia, Shaheen, Marzouqi, Fatima, Al‐Dhaheri, Amna, Subramaniyan, Deepa, Dhanasekaran, Subramanian, Yasin, Javed, Ali, Badreldin H, Kazzam, Elsadig E
Format: Article
Language:English
Subjects:
air pollution
Airway Resistance - drug effects
Animals
Anti-Inflammatory Agents - therapeutic use
Arterioles - drug effects
Arterioles - physiopathology
Benzoquinones - therapeutic use
Biological and medical sciences
blood pressure
Blood Pressure - drug effects
Cerebrovascular Disorders - drug therapy
Cerebrovascular Disorders - physiopathology
Cerebrum - blood supply
Cerebrum - physiopathology
diesel exhaust particles
Interleukin-6 - blood
Leukocyte Count
Lung - drug effects
Lung - pathology
lung inflammation
Male
Medical sciences
Mice
Nigella sativa
Particulate Matter - toxicity
Pharmacology. Drug treatments
Platelet Aggregation - drug effects
Pneumonia - blood
Pneumonia - chemically induced
Pneumonia - drug therapy
Pneumonia - pathology
Research Papers
Superoxide Dismutase - blood
thrombosis
Thrombosis - drug therapy
Thrombosis - physiopathology
thymoquinone
Vehicle Emissions - toxicity
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Summary:BACKGROUND AND PURPOSE Acute exposure to particulate air pollution has been linked to acute cardiopulmonary events, but the underlying mechanisms are uncertain. EXPERIMENTAL APPROACH We investigated the acute (at 4 and 18 h) effects of diesel exhaust particles (DEP) on cardiopulmonary parameters in mice and the protective effect of thymoquinone, a constituent of Nigella sativa. Mice were given, intratracheally, either saline (control) or DEP (30 µg·per mouse). KEY RESULTS At 18 h (but not 4 h) after giving DEP, there was lung inflammation and loss of lung function. At both 4 and 18 h, DEP caused systemic inflammation characterized by leucocytosis, increased IL‐6 concentrations and reduced systolic blood pressure (SBP). Superoxide dismutase (SOD) activity was decreased only at 18 h. DEP reduced platelet numbers and aggravated in vivo thrombosis in pial arterioles. In vitro, addition of DEP (0.1–1 µg·mL−1) to untreated blood‐induced platelet aggregation. Pretreatment of mice with thymoquinone prevented DEP‐induced decrease of SBP and leucocytosis, increased IL‐6 concentration and decreased plasma SOD activity. Thymoquinone also prevented the decrease in platelet numbers and the prothrombotic events but not platelet aggregation in vitro. CONCLUSIONS AND IMPLICATIONS At 4 h after DEP exposure, the cardiovascular changes did not appear to result from pulmonary inflammation but possibly from the entry of DEP and/or their associated components into blood. However, at 18 h, DEP induced significant changes in pulmonary and cardiovascular functions along with lung inflammation. Pretreatment with thymoquinone prevented DEP‐induced cardiovascular changes.
ISSN:0007-1188
1476-5381
1476-5381
DOI:10.1111/j.1476-5381.2011.01442.x