观察柴油车尾气对小鼠肺脏的氧化应激及气道炎症、病理变化的影响。

将36只6~8周龄的雄性小鼠随机分成三组：A组（对照组）、B组（小排量车尾气污染组）、C组（大排量车尾气污染组），每组12只。柴油车尾气对小鼠染毒4周（B、C组小鼠分别吸入1.4 L、2.8 L排量的尾气），A组正常饲养，观察所有小鼠支气管肺泡灌洗液（BALF）细胞学、肺组织病理学变化，免疫组织化学检测核因子κB（NF-κB）的活化及硝基酪氨酸（3-NT）的表达。

B、C组小鼠BALF中的白细胞总数、淋巴细胞及中性粒细胞分类计数与A组比较，差异均有统计学意义（F=24.25、28.12、18.03，P均< 0.05），且C组BALF中的淋巴细胞和中性粒细胞计数比B组更多（P均< 0. 05）。同样在小鼠肺组织中，B、C组淋巴细胞和中性粒细胞计数与A组相比，差异均有统计学意义（F=20.35、12.61，P均< 0. 05），且C组肺组织中的淋巴细胞和中性粒细胞计数比B组更多（P均< 0.05）；另外B、C组肺组织内出现气道上皮细胞脱落、支气管周围炎性细胞浸润及基底膜纤维化等变化。免疫组织化学结果提示三组肺组织内NF-κB的活化[（6.5 ± 2.4）%、（12.9 ± 4.1）%、（19.4 ± 6.4）%]及3-NT的表达（2.2 ± 0.7、3.7 ± 1.1、5.6 ± 1.6）比较，差异均有统计学意义（F=23.90、24.35，P均< 0. 05），且C组表达都高于B组（P均< 0.05）。进一步相关性分析显示，小鼠肺组织中3-NT蛋白表达与NF-κB的蛋白表达、BALF中淋巴细胞数量都具有正相关性（r=0.659、0.633，P均< 0. 05）。

柴油车尾气可促进小鼠肺组织的氧化应激，产生更多3-NT，从而激活NF-κB，产生更严重的气道炎症和病理改变。

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.