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目的 探讨红霉素是否对大鼠过敏性气道炎症具有保护作用以及是否通过抑制转录因子NF-κB的活性来达到抗炎效果。方法 用鸡卵清白蛋白 (OVA)腹腔注射一次致敏SD雄性大鼠,同时佐以氢氧化铝和百日咳杆菌, 2周后雾化吸入 1%的OVA进行激发,连续激发 7天,成功制作大鼠过敏性气道炎症模型。治疗干预组动物OVA激发的同时口服红霉素 [180mg/(kg·d) ]。最后一次激发后 24h处死大鼠,留取标本进行检测。用支气管肺泡灌洗液 (BALF)和肺组织病理分析的方法检测肺组织炎症;用免疫组织化学的方法检测核因子 kappaB(nuclearfactorkappaB, NF-κB)亚单位p65在细胞核内的表达;用凝胶电泳迁移改变分析的方法检测肺组织NF κB的结合活性。结果 肺组织病理切片显示红霉素治疗干预组肺组织炎症细胞浸润的范围较模型组明显减小。红霉素干预组BALF中白细胞总数为 (31±22)×108 /L,模型组为 (66±28)×108 /L(P<0.01 )。红霉素干预组主支气管黏膜下层单位面积内细胞核表达NF κB阳性的细胞数为 (1.4±0.4)×103 个 /mm2,模型组为(2.6±0.6)×103 个 /mm2 (P<0.01)。红霉素干预组动物肺组织转录因子NF-κB结合活性(32±14)低于模型组(46±17 ) (P<0.05 )。结论 红霉素干预组BALF中白细胞总数较模型组降低,主支气管黏膜下层单?
Objective To investigate whether erythromycin has protective effect on allergic airway inflammation in rats and whether it can achieve anti-inflammatory effect by inhibiting the activity of transcription factor NF-κB. Methods SD male rats were sensitized intraperitoneally with ovalbumin (OVA), simultaneously with aluminum hydroxide and Bordetella pertussis. After 2 weeks, 1% OVA was inhaled and inhaled to stimulate for 7 days. Successfully produced large Rat allergic airway inflammation model. Oral administration of erythromycin [180 mg / (kg · d)] was given concurrently with OVA challenge in the treatment intervention group. 24h after the last challenge rats were killed, specimens were taken for testing. Lung inflammation was detected by bronchoalveolar lavage fluid (BALF) and lung histopathology. Immunohistochemistry was used to detect the expression of nuclear factor kappaB (NF-κB) subunit p65 in the nucleus. The electrophoretic mobility shift assay was used to detect the binding activity of NF κB in lung tissue. Results The pathological sections of lung tissue showed that the range of infiltration of inflammatory cells in lung tissue of erythromycin treatment group was significantly reduced than that of model group. The total number of leukocytes in BALF in erythromycin intervention group was (31 ± 22) × 108 / L and in model group was (66 ± 28) × 108 / L (P <0.01). The number of NF κB positive cells in the nucleus subunit of erythromycin intervention group was (1.4 ± 0.4) × 103 cells / mm2 and the model group was (2.6 ± 0.6) × 103 cells / mm2 (P <0.01) . The erythromycin intervention group had a lower NF-κB binding activity (32 ± 14) than the model group (46 ± 17) (P <0.05). Conclusion The total number of leukocytes in BALF in erythromycin intervention group is lower than that in model group. The main bronchial submucosa single?