To investigate the effect of diesel engine exhaust on oxidative stress, airway inflammation, and lung pathology in mouse model.

Totally 36 6-8- week male mice were randomly divided into 3 groups (12 each group): group A (control group), group B (low exposure group) and group C (high exposure group). Exposure groups (groups B and C) were inhaled 1.4 liters and 2.8 liters displacement of exhaust gas, respectively. Mice in group A was given normal breeding, without special treatment. Pathological changes of the lungs and bronchoalveolar lavage fluid (BALF) in cytology were observed. Immunohistochemical analysis was used to detect the level of nuclear factor kappa B (NF-κB) activation and the expression of 3-nitrotyrosine (3-NT).

Compared with group A, the numbers of white blood cell, lymphocyte and neutrophil in BALF changed significantly in groups B and C (F=24.25, 28.12, 18.03; all P<0.05); furthermore, the numbers of lymphocyte and neutrophil in BALF of group C were much more than those in group B (all P<0.05). Similarly, the numbers of lymphocyte and neutrophil in lung tissue of these three groups had significant differences (F=20.35, 12.61; all P<0.05); the numbers of lymphocyte and neutrophil in lung tissue of group C were much more than those in group B (all P<0.05). In addition, the exfoliation of airway epithelial cells, the infiltration of inflammatory cells in bronchial surrounding and the basement membrane fibrosis were observed in lung tissue of groups B and C. Immunohistochemical analysis showed the level of NF-κB activation [(6.5 ± 2.4)% vs. (12.9 ± 4.1)% vs. (19.4 ± 6.4)%] and the expression of 3-NT (2.2 ± 0.7 vs. 3.7 ± 1.1 vs. 5.6 ± 1.6) changed significantly in lung tissue of all three groups (F=23.90, 24.35; all P<0. 05); the indices of NF-κB activation and 3-NT in group C were much higher than those in group B (all P<0.05). The further correlation analysis showed the positive correlations in the expression of 3-NT and NF-κB in lung tissue, and the number of lymphocyte in BALF (r=0.659, 0.633; all P<0.05).

Diesel engine exhaust could induce oxidative protein damage, elevate 3-NT expression, stimulate NF-κB activity leading to more severe airway inflammation and pathological changes.