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目的探讨N-乙基吗啉挥发气体对肺脏的氧化损伤效应。方法 40只昆明种小鼠按体重随机分为对照组、低剂量组(50mg/m~3)、中剂量组(100mg/m~3)和高剂量组(200mg/m3),每组各10只。采用静式吸入染毒方法,每组染毒2h,连续染毒30d。应用试剂盒检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量,应用流式细胞仪检测肺巨噬细胞凋亡。HE染色检测肺组织病理形态学变化。结果染毒组小鼠肺巨噬细胞凋亡率升高,存活率下降,染毒组与对照组比较,差异均有统计学意义(P<0.05);高剂量组小鼠肺组织MDA含量明显增加,GSH-Px和SOD活性明显下降;高剂量组小鼠肺组织中MDA含量、GSH-Px和SOD活力与对照组比较,差异均有统计学意义(P<0.05);肺组织病理均可见肺泡壁增厚,炎细胞浸润,肺泡扩张,肺泡中度气肿。结论 N-乙基吗啉挥发气体可导致小鼠肺组织氧化损伤和炎症,并发生明显的病理形态学改变。
Objective To investigate the oxidative damage of lungs induced by N-ethylmorpholine volatile gas. Methods Forty Kunming mice were randomly divided into control group, low dose group (50mg / m ~ 3), middle dose group (100mg / m ~ 3) and high dose group (200mg / m3) only. Using static inhalation method, each group exposure 2h, continuous exposure 30d. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) were detected by kit. The apoptosis of lung macrophages was detected by flow cytometry. The pathological changes of lung tissue were detected by HE staining. Results The apoptosis rate of lung macrophages increased and the survival rate decreased in the exposed group. The difference was statistically significant (P <0.05) between the exposed group and the control group. The content of MDA in the lung tissue of the high-dose group was significantly higher The activity of GSH-Px and SOD decreased significantly. The content of MDA, the activity of GSH-Px and SOD in lung tissue of high-dose group were significantly different from those in control group (P <0.05) Alveolar wall thickening, inflammatory cell infiltration, alveolar expansion, moderate alveolar emphysema. Conclusion N-ethylmorpholine volatile gas can cause oxidative damage and inflammation of lung tissue in mice and have obvious pathomorphological changes.