摘要
目的探讨香烟烟雾可吸入微粒对支气管肺组织的氧化损伤作用。方法采集并分析香烟可吸入微粒后,染毒大鼠,观察肺组织病理形态的变化,测定肺泡灌洗液中白细胞总数和分类计数及肺匀浆中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性。结果香烟组的病理改变以炎症为主,各观察指标与对照组比较有差异。结论香烟烟雾可吸入微粒对大鼠气道及肺组织的刺激引发炎性反应,而活性氧介导的炎症反应是其致炎作用机制之一。
Objective To study effect of tobacco smoke on airway oxidative damage in rats. Methods Enironmental tobacco smoke were collected, analyzed and PM10-treat model of rats were established. Lung tissue histopathology was observed. The counts of total leukocyte and neutrophils in bronchoalveoar lavage fluid （BALF） and superoxide dismutase （ SOD ） , glutathion peroxidase （ GSH- Px）, malondiadehyde （MDA） in lung homogenate were measured. Results The counts of total leukocyte, macrophage and neutrophils in PM10 - treat group were increased significantly than those in control group （ P 〈 0. 05 ）. The pathological changes of tobacco smoke group indicated that it can cause airway injury. Conclusion Tobacco smoke particles have ROS activity and cause lung inflammation.
出处
《临床肺科杂志》
2006年第6期703-704,共2页
Journal of Clinical Pulmonary Medicine
关键词
香烟烟雾
可吸入微粒
活性氧
environmental tobacco smoke inhalable particulate ROS
