Substance P scavenger enhances antioxidant defenses and prevents prothrombotic effects on the rat lung after acute exposure to oil smoke

Li Ping-Chia, Lai I-Ju, Lin Yu-Ching, Chang Li-Ching, Chen Wen-Chung

研究成果: Article

5 引文 (Scopus)

摘要

Background. Airborne particulate matter, from cooking oil, smoking, engine exhaust and other sources, is associated with the development of atherosclerosis and myocardial infarction. In order to explore the cellular and molecular events following exposure of rats to lard oil smoke, we measured the generation of reactive oxygen species (ROS), substance P, cellular adhesion molecules, and thrombosis in relation to inhibitors of substance P, the NK-1 receptor, and antioxidants. Methods. Rats were exposed to oil smoke for 120 min with or without 20 min pretreatment with lovastatin (substance P scavenger), L733060 (NK-1 receptor antagonist), vitamin E (antioxidant) or catechins (antioxidant). The levels of substance P and ROS were measured. Histological studies observed ROS damage in the form of HEL adducts. The prothrombotic effects of oil smoke exposure were measured by experimental induction of thrombosis in vivo. Results. Oil smoke exposure significantly increased substance P levels, ROS levels, ROS damage (HEL adduct levels), and the size of experimentally induced thrombi. The pretreatments reduced all of these effects of oil smoke exposure; at many time points the reductions were statistically significant. Conclusion. We established a connection between oil smoke exposure and thrombosis which involves substance P and its receptor, the NK-1 receptor, and ROS. This study helps establish a mechanistic explanation of how airborne particulate matter can increase the risk of cardiovascular illness.

原文English
文章編號58
期刊Journal of biomedical science
16
發行號1
DOIs
出版狀態Published - 2009 八月 20

指紋

Substance P
Smoke
Neurokinin-1 Receptors
Rats
Reactive Oxygen Species
Oils
Antioxidants
Lung
Thrombosis
Particulate Matter
3-((3,5-bis(trifluoromethyl)phenyl)methyloxy)-2-phenylpiperidine
Vehicle Emissions
Lovastatin
Catechin
Cooking
Vitamin E
Diesel engines
Adhesion
Atherosclerosis
Smoking

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Pharmacology (medical)

引用此文

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abstract = "Background. Airborne particulate matter, from cooking oil, smoking, engine exhaust and other sources, is associated with the development of atherosclerosis and myocardial infarction. In order to explore the cellular and molecular events following exposure of rats to lard oil smoke, we measured the generation of reactive oxygen species (ROS), substance P, cellular adhesion molecules, and thrombosis in relation to inhibitors of substance P, the NK-1 receptor, and antioxidants. Methods. Rats were exposed to oil smoke for 120 min with or without 20 min pretreatment with lovastatin (substance P scavenger), L733060 (NK-1 receptor antagonist), vitamin E (antioxidant) or catechins (antioxidant). The levels of substance P and ROS were measured. Histological studies observed ROS damage in the form of HEL adducts. The prothrombotic effects of oil smoke exposure were measured by experimental induction of thrombosis in vivo. Results. Oil smoke exposure significantly increased substance P levels, ROS levels, ROS damage (HEL adduct levels), and the size of experimentally induced thrombi. The pretreatments reduced all of these effects of oil smoke exposure; at many time points the reductions were statistically significant. Conclusion. We established a connection between oil smoke exposure and thrombosis which involves substance P and its receptor, the NK-1 receptor, and ROS. This study helps establish a mechanistic explanation of how airborne particulate matter can increase the risk of cardiovascular illness.",
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Substance P scavenger enhances antioxidant defenses and prevents prothrombotic effects on the rat lung after acute exposure to oil smoke. / Ping-Chia, Li; I-Ju, Lai; Yu-Ching, Lin; Li-Ching, Chang; Wen-Chung, Chen.

於: Journal of biomedical science, 卷 16, 編號 1, 58, 20.08.2009.

研究成果: Article

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T1 - Substance P scavenger enhances antioxidant defenses and prevents prothrombotic effects on the rat lung after acute exposure to oil smoke

AU - Ping-Chia, Li

AU - I-Ju, Lai

AU - Yu-Ching, Lin

AU - Li-Ching, Chang

AU - Wen-Chung, Chen

PY - 2009/8/20

Y1 - 2009/8/20

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AB - Background. Airborne particulate matter, from cooking oil, smoking, engine exhaust and other sources, is associated with the development of atherosclerosis and myocardial infarction. In order to explore the cellular and molecular events following exposure of rats to lard oil smoke, we measured the generation of reactive oxygen species (ROS), substance P, cellular adhesion molecules, and thrombosis in relation to inhibitors of substance P, the NK-1 receptor, and antioxidants. Methods. Rats were exposed to oil smoke for 120 min with or without 20 min pretreatment with lovastatin (substance P scavenger), L733060 (NK-1 receptor antagonist), vitamin E (antioxidant) or catechins (antioxidant). The levels of substance P and ROS were measured. Histological studies observed ROS damage in the form of HEL adducts. The prothrombotic effects of oil smoke exposure were measured by experimental induction of thrombosis in vivo. Results. Oil smoke exposure significantly increased substance P levels, ROS levels, ROS damage (HEL adduct levels), and the size of experimentally induced thrombi. The pretreatments reduced all of these effects of oil smoke exposure; at many time points the reductions were statistically significant. Conclusion. We established a connection between oil smoke exposure and thrombosis which involves substance P and its receptor, the NK-1 receptor, and ROS. This study helps establish a mechanistic explanation of how airborne particulate matter can increase the risk of cardiovascular illness.

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