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目的 研究三氧化二砷 (As2 O3 )对哮喘豚鼠气道嗜酸性粒细胞 (EOS)凋亡和核因子 κB(NF κB)表达的影响作用 ,探讨As2 O3 对哮喘可能的治疗机制。方法 豚鼠 2 0只建立哮喘模型后随机分为对照组和As2 O3 (2mg/kg)治疗组。每组 10只 ,采用TUNEL技术原位标记细胞凋亡 ;免疫组织化学染色技术检测豚鼠气道壁NF κB ;计算机图像分析技术对气道壁EOS凋亡和NF κB表达进行定量检测。结果 对照组豚鼠支气管壁EOS凋亡指数为 (0 2 3± 0 0 5 ) % ,整个肺组织包括气管、支气管、肺泡和脏层胸膜构成了一个NF κB+ 细胞网络 ,其中支气管壁胞核NF κB+ 细胞密度为 (12 6 1± 190 )个 /mm2 上皮面积 ;哮喘豚鼠经As2 O3 处理后 ,支气管壁EOS凋亡指数显著增加 (P <0 0 1) ,胞核NF κB+ 细胞密度显著下降 (P <0 0 1) ,并且气道壁EOS凋亡指数与胞核NF κB+ 细胞密度之间呈显著性负相关 (r =- 0 91,P <0 0 1)。结论 抑制气道NF κB激活 ,促进EOS凋亡 ,可能是As2 O3 治疗哮喘的重要机制之一。
Objective To investigate the effects of arsenic trioxide (As2 O3) on the airway eosinophil (EOS) apoptosis and the expression of nuclear factor kappa B (NF κB) in asthmatic guinea pigs and to explore the possible therapeutic mechanism of As2 O3 on asthma. Methods Twenty guinea pigs were randomly divided into control group and As2O3 (2mg / kg) group. TUNEL technique was used to label the apoptotic cells in situ. The NF-κB in guinea-pig airway was detected by immunohistochemical staining. The apoptosis of EOS and the expression of NF-κB were detected by computer image analysis. Results The apoptosis index of EOS in the bronchial wall of guinea pigs in the control group was (0 2 3 ± 0 0 5)%. The whole lung tissue including the trachea, bronchus, alveoli and visceral pleura formed a NF κB + cell network in which the nuclear NF κB + The cell density was (12 6 1 ± 190) / mm 2 epithelial area. The apoptosis index of bronchial wall in asthmatic guinea pigs treated with As 2 O 3 was significantly increased (P 0 01) <0 01), and there was a significant negative correlation between the apoptosis index of EOS in the airway wall and the nuclear NFκB + cell density (r = - 0 91, P 0 01). Conclusion Inhibition of airway NF κB activation and promotion of EOS apoptosis may be one of the important mechanisms of As 2 O 3 in the treatment of asthma.