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

摘要

Background: Airborne particulate matter, from cooking oil, smoking, engine exhaust and othersources, is associated with the development of atherosclerosis and myocardial infarction. In orderto explore the cellular and molecular events following exposure of rats to lard oil smoke, wemeasured the generation of reactive oxygen species (ROS), substance P, cellular adhesionmolecules, and thrombosis in relation to inhibitors of substance P, the NK-1 receptor, andantioxidants.Methods: Rats were exposed to oil smoke for 120 min with or without 20 min pretreatment withlovastatin (substance P scavenger), L733060 (NK-1 receptor antagonist), vitamin E (antioxidant) orcatechins (antioxidant). The levels of substance P and ROS were measured. Histological studiesobserved ROS damage in the form of HEL adducts. The prothrombotic effects of oil smokeexposure 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 reducedall of these effects of oil smoke exposure; at many time points the reductions were statisticallysignificant.Conclusion: We established a connection between oil smoke exposure and thrombosis whichinvolves substance P and its receptor, the NK-1 receptor, and ROS. This study helps establish amechanistic explanation of how airborne particulate matter can increase the risk of cardiovascularillness