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Objective: To evaluate diesel exhaust particles (diesel exhaust particle DEP) rats inhaled asthma late-phase reaction. Methods: 60 male Wistar rats were randomly divided into six groups, each group 10. Group B asthma model group, using freshly prepared 100mg ovalbumin (ovalbumin OVA) 100mg 1ml of aluminum hydroxide complexes in section 1,8,15 days to do was injected intraperitoneally, the first 22 days start giving 3% ovalbumin nebulized saline solution once a day, every 30min, 7 consecutive days. A group of normal control group with saline instead of OVA attack, step with the B group. Observation component C, D, E, F groups, each group were given OVA attacks step with the B group. After the attack OVA inhalation DEP200μg/ml each group were saline solution of 1,2,3,4 weeks. DEP inhalation after over one week and then 3% OVA inhalation 30min stimulate physiological saline solution. After challenge with OVA, after 24 hours, and then each group of methacholine (Methacholine MCH) for bronchial provocation test. Each rat was measured airway resistance (RL) changes were observed whether an airway hyperresponsiveness: To observe the bronchoalveolar lavage fluid (BALF) of eosinophils (EOS) count; using enzyme-linked immunosorbent assay (ELISA) method for the determination of IgE in serum and lung tissue concentrations of cytokines (IL-5, IFN-γ) levels change; observe pathological changes of lung tissue. Results: ① A group did not occur airway hyperresponsiveness B, C, D, E, F group after group of bronchial provocation test line airway resistance (RL) ratio higher than the normal control group, the difference was statistically significant (F = 104.472, P <0.01), E, ??F and B group rats airway resistance ratio of the difference was statistically significant (P <0.01), and the time of DEP inhalation airway resistance ratio was positively correlated (r = 0.886, P <0.01). ② B, C, D, E, F group in bronchoalveolar lavage fluid eosinophils (EOS) the percentage of total cells was significantly higher in group A, the difference was statistically significant (F = 54.411, P <0.01). Inhalation one week from the DEP (C group) started eosinophil infiltration gradually increased, E, F and B group difference was statistically significant (P <0.01). ③ serum IgE levels in the B, C, D, E, F group was significantly higher than that in group A, the difference was statistically significant (F = 6.071, P <0.01), C, D, E, F compared with group B IgE levels had no significant difference (P> 0.05) ④ B, C, D, E, F lung tissue levels of IL-5 compared with group A was significantly higher. The difference was statistically significant (F = 23.667, P <0.01), D, E, F and B group difference was statistically significant (P <0.01), and DEP inhalation time and IL-5 levels were positively correlated ( r = 0.583, P <0.01); B, C, D, E, F lung tissue IFN-γ levels decreased significantly compared with group A, the difference was statistically significant (F = 33.229, P <0.01), E, F group and B group difference was statistically significant (P <0.01), and DEP inhalation time and IFN-γ levels were negatively correlated (r = -0.550, P <0.01). ⑤ lung tissue biopsy can be seen in group A complete epithelial cells, airway inflammatory cell infiltration seen around to ciliated columnar epithelial cells in the main, only a small number of goblet cells, basement membrane no fibrosis. With DEP, 1,2,3,4-week inhalation, the gradual emergence of epithelial cell necrosis, interruption, loss, goblet cell hyperplasia, airway inflammatory cell infiltration around and the basement membrane fibrosis and other changes. Conclusion: Diesel exhaust particles (DEP) can aggravate asthmatic rat inhalation late-phase reaction.
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