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, Wen-Chung Chen

Description

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.

Informations

• Publié par: biomed
• Publié le: 01 janvier 2009
• Nombre de lectures: 11
• Langue: English
• Poids de l'ouvrage: 1 Mo

Extrait

Journal of Biomedical Science

BioMedCentral

Open Access Research Substance P scavenger enhances antioxidant defenses and prevents prothrombotic effects on the rat lung after acute exposure to oil smoke 1 23 1 Li PingChia*, Lai IJu, Lin YuChing, Chang LiChingand Chen Wen 4 Chung

1 Address: Departmentof Occupational Therapy, IShou University, No. 8 EDa Road, JiauShu Tsuen, YanChau Shiang, Kaohsiung County 824, 2 Taiwan, R.O.C,Department of Medical Nutrition, IShou University, No. 8 EDa Road, JiauShu Tsuen, YanChau Shiang, Kaohsiung County 824, 3 Taiwan, R.O.C,Department of Physical Medicine and Rehabilitation, EDA Hospital, No. 1 EDa Road, JiauShu Tsuen, YanChau Shiang, 4 Kaohsiung County 824, Taiwan, R.O.C andDepartment of Pathology, National Cheng Kung Univeristy Hospital, No. 138 ShengLi Rd., Tainan City, Taiwan R.O.C Email: Li PingChia*  [e-mail]; Lai IJu  [e-mail]; Lin YuChing  [e-mail]; Chang Li Ching  [e-mail]; Chen WenChung  [e-mail] * Corresponding author

Published: 6 July 2009Received: 28 November 2008 Accepted: 6 July 2009 Journal of Biomedical Science2009,16:58 doi:10.1186/1423-0127-16-58 This article is available from: http://www.jbiomedsci.com/content/16/1/58 © 2009 Ping-Chia et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.

The cost of publication inJournal of Biomedical Science is bourne by the National Science Council,Taiwan.

Page 1 of 10 (page number not for citation purposes)