Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE.
Br J Pharmacol. 2011 Dec;164(7):1871-82. doi: 10.1111/j.1476-5381.2011.01442.x.
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.
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.
急性暴露于颗粒物空气污染与急性心肺事件有关，但潜在机制尚不清楚。
我们研究了柴油废气颗粒（DEP）对小鼠心肺参数的急性（4 和 18 小时）影响，以及百里醌（黑种草的一种成分）的保护作用。小鼠经气管内给予生理盐水（对照）或 DEP（每只小鼠 30 µg）。
在给予 DEP 后 18 小时（而不是 4 小时），肺部发生炎症并丧失肺功能。在 4 小时和 18 小时，DEP 引起全身炎症，表现为白细胞增多、IL-6 浓度增加和收缩压（SBP）降低。只有在 18 小时，超氧化物歧化酶（SOD）活性降低。DEP 减少血小板数量，并加重脑动脉小血管内的体内血栓形成。在体外，将 DEP（0.1-1 µg·mL(-1)）加入未处理的血液中会引起血小板聚集。用百里醌预处理小鼠可预防 DEP 引起的 SBP 和白细胞增多降低、IL-6 浓度增加和血浆 SOD 活性降低。百里醌还可预防血小板数量减少和促血栓形成事件，但不能预防体外血小板聚集。
在暴露于 DEP 后 4 小时，心血管变化似乎不是由肺部炎症引起的，而是可能由 DEP 及其相关成分进入血液引起的。然而，在 18 小时，DEP 引起了显著的肺和心血管功能变化以及肺部炎症。用百里醌预处理可预防 DEP 引起的心血管变化。
