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

Abderrahim Nemmar, Suhail Al-Salam, Shaheen Zia, Fatima Marzouqi, Amna Al-Dhaheri, Deepa Subramaniyan, Subramanian Dhanasekaran, Javed Yasin, Badreldin H. Ali, Elsadig E. Kazzam

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1871-1882
Number of pages12
JournalBritish Journal of Pharmacology
Volume164
Issue number7
DOIs
Publication statusPublished - Dec 2011

Fingerprint

Vehicle Emissions
Cardiovascular System
Lung
Blood Pressure
Pneumonia
Leukocytosis
Platelet Count
Platelet Aggregation
Superoxide Dismutase
Interleukin-6
thymoquinone
Nigella sativa
Air Pollution
Arterioles
Thrombosis
Blood Platelets

Keywords

  • air pollution
  • blood pressure
  • diesel exhaust particles
  • lung inflammation
  • thrombosis
  • thymoquinone

ASJC Scopus subject areas

  • Pharmacology

Cite this

Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone. / Nemmar, Abderrahim; Al-Salam, Suhail; Zia, Shaheen; Marzouqi, Fatima; Al-Dhaheri, Amna; Subramaniyan, Deepa; Dhanasekaran, Subramanian; Yasin, Javed; Ali, Badreldin H.; Kazzam, Elsadig E.

In: British Journal of Pharmacology, Vol. 164, No. 7, 12.2011, p. 1871-1882.

Research output: Contribution to journalArticle

Nemmar, A, Al-Salam, S, Zia, S, Marzouqi, F, Al-Dhaheri, A, Subramaniyan, D, Dhanasekaran, S, Yasin, J, Ali, BH & Kazzam, EE 2011, 'Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone', British Journal of Pharmacology, vol. 164, no. 7, pp. 1871-1882. https://doi.org/10.1111/j.1476-5381.2011.01442.x
Nemmar, Abderrahim ; Al-Salam, Suhail ; Zia, Shaheen ; Marzouqi, Fatima ; Al-Dhaheri, Amna ; Subramaniyan, Deepa ; Dhanasekaran, Subramanian ; Yasin, Javed ; Ali, Badreldin H. ; Kazzam, Elsadig E. / Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone. In: British Journal of Pharmacology. 2011 ; Vol. 164, No. 7. pp. 1871-1882.
@article{83924be63d0d49dd963490858bd836cb,
title = "Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone",
abstract = "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.",
keywords = "air pollution, blood pressure, diesel exhaust particles, lung inflammation, thrombosis, thymoquinone",
author = "Abderrahim Nemmar and Suhail Al-Salam and Shaheen Zia and Fatima Marzouqi and Amna Al-Dhaheri and Deepa Subramaniyan and Subramanian Dhanasekaran and Javed Yasin and Ali, {Badreldin H.} and Kazzam, {Elsadig E.}",
year = "2011",
month = "12",
doi = "10.1111/j.1476-5381.2011.01442.x",
language = "English",
volume = "164",
pages = "1871--1882",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "7",

}

TY - JOUR

T1 - Contrasting actions of diesel exhaust particles on the pulmonary and cardiovascular systems and the effects of thymoquinone

AU - Nemmar, Abderrahim

AU - Al-Salam, Suhail

AU - Zia, Shaheen

AU - Marzouqi, Fatima

AU - Al-Dhaheri, Amna

AU - Subramaniyan, Deepa

AU - Dhanasekaran, Subramanian

AU - Yasin, Javed

AU - Ali, Badreldin H.

AU - Kazzam, Elsadig E.

PY - 2011/12

Y1 - 2011/12

N2 - 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.

AB - 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.

KW - air pollution

KW - blood pressure

KW - diesel exhaust particles

KW - lung inflammation

KW - thrombosis

KW - thymoquinone

UR - http://www.scopus.com/inward/record.url?scp=81355143319&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=81355143319&partnerID=8YFLogxK

U2 - 10.1111/j.1476-5381.2011.01442.x

DO - 10.1111/j.1476-5381.2011.01442.x

M3 - Article

VL - 164

SP - 1871

EP - 1882

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 7

ER -