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

Abstract

BACKGROUND AND PURPOSEAcute exposure to particulate air pollution has been linked to acute cardiopulmonary events, but the underlying mechanisms are uncertain. EXPERIMENTAL APPROACHWe 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 mg·per mouse). KEY RESULTSAt 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 mg·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 IMPLICATIONSAt 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.

A review on therapeutic potential of Nigella sativa: A miracle herb

“…Pretreatment of mice with TQ prevented DEP-induced decrease of systolic blood pressure and leucocytosis, increased IL-6 concentration and decreased plasma SOD activity. TQ also prevented the decrease in platelet numbers and the prothrombotic events but not platelet aggregation in vitro [79] .…”

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

“…19,20 Briefly, the trachea was intubated after induction of anesthesia with urethane (1 mg/g body weight, IP), and a 2F venous catheter (Sims Portex Ltd., Hythe, Kent, UK) was inserted in the right jugular vein for the administration of fluorescein (Sigma-Aldrich Co., St Louis, MO, USA). After that, a craniotomy was first performed on the left side, using a microdrill, and the dura was stripped open.…”

The acute pulmonary and thrombotic effects of cerium oxide nanoparticles after intratracheal instillation in mice

“…36 Previous reports showed that pulmonary exposure to pollutant particles and some engineered NPs induce systemic and cardiovascular events. 22,24,37,38 The latter effects were explained by the capacity of NPs to induce lung inflammation, which causes systemic inflammation and oxidative stress, and/or the aptitude of NPs to traverse the air-blood barrier to enter the blood and affect cardiovascular endpoints. 5,18 It has been reported that IV administration of CeO 2 NPs induce liver injury and oxidative stress.…”

“…27,37,45 In this model, the damage to endothelial cells causes the platelets to adhere at the site of endothelial damage and then aggregate. 27,37,45 The data of the present study show that acute IT administration of CeO 2 NPs induced a significant and dose-dependent shortening of the thrombotic occlusion time in pial arterioles and venules, indicating that CeO 2 NPs possess prothrombotic effects. Along with thrombosis in vivo, a dose-dependent and significant increase in the concentrations of the coagulation factor, fibrinogen, and PAI-1 in the plasma following acute exposure to CeO 2 NPs was found.…”

“…42 It has been shown that IT instillation of DEPs induces lung inflammation and oxidative stress responsible for systemic inflammation and oxidative stress at the 18-24-hour time point. 24,37 It has been recently demonstrated that aortic RNA expression of endothelial nitric oxide synthase, tissue factor, and TNFα were significantly increased by 4-week inhalation exposure to whole CeO 2 NPs added to diesel fuel (DECe) or gas-phase components of DECe. 19 However, the latter results are in conflict with the data from another study which implied that the addition of a Ce-based fuel-borne catalyst may decrease the atherosclerotic burden induced by exposure to diesel fuel in atherosclerosis-prone mice.…”