【摘要】 目的　研究PM2 5的急性毒效应 ,探讨免疫损伤和氧化损伤在PM2 5对肺损伤过程中的作用。方法　以昆明小鼠为试验对象 ,随机分成空白对照组 ,生理盐水对照组和低剂量、中剂量、高剂量PM2 5组共 5组 ,除空白对照组外 ,其他各组气管滴注染毒 2 4小时后 ,分析支气管肺灌洗液中乳酸脱氢酶 (LDH)、碱性磷酸酶(AKP)、酸性磷酸酶 (ACP)、白蛋白 (ALB)、一氧化氮 (NO)、一氧化氮合酶 (NOS)、丙二醛 (MDA)、超氧化物歧化酶 (SOD)等含量和细胞因子肿瘤坏死因子α(TNF α)、白细胞介素 1(IL - 1)活性 ,以及测定肺巨噬细胞的吞噬功能 ,并观察肺组织病理学改变。结果　空白对照组和生理盐水对照组比较 ,各指标未见明显差异 ;试验组和生理盐水对照组比较 ,肺灌洗液中LDH、AKP、ACP、ALB、NO、NOS、MDA等含量和TNF α、IL 1活性有显著性增高 (P <0 0 5 ) ,SOD含量和肺巨嗜细胞的吞噬功能明显下降 (P <0 0 5 ) ,均呈现出剂量依赖性关系。结论　PM2 5的吸入引起机体的免疫反应和氧化应激反应 ,从而造成对小鼠肺实质细胞和膜性组织的毒作用。更多还原

【Abstract】 Objective In order to study the acute toxicity of PM 2.5 and to explore the role of immunoreaction and oxidative stress in mouse pulmonary acute injury induced by PM 2.5.Methods Kunming mice were randomly divided into five groups including blank control group, saline control group, three level PM 2.5 (low, middle and high)groups. Three level PM 2.5 groups were inoculated with suspensions of PM 2.5 via trachea for 24 hours and saline control group were inoculated saline, Pulmonary pathological injury and bronchoalveolar lavage fluid (BALF) of all mice were later examined, including the level of LDH, AKP, ACP, ALB, NO, NOS, MDA, SOD, activities of TNF-α,IL-1 and phagocytosis of Alveolar macrophages (AM). Results The amount of LDH, AKP, ACP, ALB, NO, NOS, MDA and activities of TNF-α,IL-1 in exposed groups were significantly higher than those in control(P<0.05), and at the same time the amount of SOD and phagocytosis of AM decreased significantly (P<0.05). Dose-response relationships were observed in all indexes. Conclusion Air-borne PM 2.5 could have acute toxic effects on mouse pulmonary cells and membrane tissues via immunotoxicity and oxidative stress injury.更多还原