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周林福,殷凯生.三氧化二砷对哮喘豚鼠肺内嗜酸性粒细胞凋亡的影响[J].,2002,(4):292-294
三氧化二砷对哮喘豚鼠肺内嗜酸性粒细胞凋亡的影响
Effect of Arsenic Trioxide on Apoptosis of Pulmonary Eosinophile in Asthmatic Guinea-Pigs
  
DOI:
中文关键词:  三氧化二砷  支气管哮喘  嗜酸性粒细胞  细胞凋亡
英文关键词:arsenic trioxide  bronchial asthma  eosinophile  cell apoptosis
基金项目:江苏省中医管理局基金资助项目 (No .9974)
Author NameAffiliation
ZHOU Lin fu 南京医科大学第一附属医院呼吸内科 南京210029 
YIN Kai sheng 南京医科大学第一附属医院呼吸内科 南京210029 
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中文摘要:
      目的 :研究三氧化二砷 (As2 O3)对哮喘豚鼠肺内嗜酸性粒细胞 (EOS)凋亡的影响及其作用机制。方法 :豚鼠 30只随机分为 3组 ,即对照组、哮喘组和As2 O3(2mg/kg)治疗组。采用末端脱氧核苷酸转移酶介导的脱氧三磷酸尿嘧啶缺口末端标记 (TdT mediateddUTPnickendlabelling ,TUNEL)技术原位标记细胞凋亡 ;计算机图像分析技术对气道壁EOS浸润和EOS凋亡进行定量测定。结果 :对照组豚鼠气道壁EOS计数 (4 4± 2 5 )个 /HP ,EOS凋亡指数为 (0 4 2± 0 0 8) % ;与对照组比较 ,哮喘组豚鼠气道壁EOS浸润显著增加 (P <0 0 1) ,EOS凋亡指数显著下降 (P <0 0 1) ;As2 O3治疗组 ,气道壁EOS浸润显著下降 (P <0 0 1) ,EOS凋亡指数显著增加 (P <0 0 1) ,并且气道壁EOS浸润数量与EOS凋亡指数之间呈显著性负相关 (r =- 0 94 9,P <0 0 1)。结论 :EOS凋亡异常是支气管哮喘的一个重要的发病机制 ;As2 O3通过促进肺内EOS凋亡 ,下调EOS浸润数量 ,从而减轻了哮喘气道炎症 ;小剂量As2 O3治疗哮喘既有效又相对安全 ,具有潜在的应用价值。
英文摘要:
      Objective: To study the effect and mechanism of arsenic trioxide (As 2O 3) on apoptosis of pulmonary eosinophiles (PE) in asthmatic guinea pigs. Methods: Thirty guinea pigs were divided into 3 groups at random, the control group, the asthmatic group and the As 2O 3 group. The dosage of As 2O 3 used was 2 mg/kg. The apoptotic PE were labelled by TdT mediated dUTP nick end labelling technique, and the PE infiltration and apoptosis were detected quantitatively using computerized image analysis technique. Results: In the control group, the amount of infiltrating PE was 4.4±2.5 cells/HP and the PE apoptotic index (AI) was 0.42± 0.08%. In the asthmatic group, the amount increased (P<0 01) and AI decreased significantly (P<0 01). After the asthmatic animals had been treated with As 2O 3, the two parameters changed reversedly significantly (P<0 01), and there was a significantly negative correlation between them (r=-0 949,P<0 01). Conclusion: The PE apoptosis abnormality is one of the important mechanisms that cause bronchial asthma, As 2O 3 could alleviate the airway inflammation through promoting PE apoptosis and lower PE infiltration. Low dose of As 2O 3 is proved to be effective with relative safety, it also has potential value in treating asthma.
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