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探讨血红素加氧酶1基因多态性与慢性阻塞性肺疾病的关系

都勇,李玉,姜鹏   

  1. 山东大学齐鲁医院呼吸内科, 山东济南 250012
  • 收稿日期:2005-10-29 修回日期:1900-01-01 出版日期:2006-05-24 发布日期:2006-05-24
  • 通讯作者: 都勇

DU Yong, LI Yu, JIANG Peng   

  1. Department of Respiratory,Qilu Hospital of Shandong University, Jinan 250012, Shandong, China
  • Received:2005-10-29 Revised:1900-01-01 Online:2006-05-24 Published:2006-05-24
  • Contact: DU Yong

摘要: 目的:探讨血红素加氧酶1(HO1)基因启动子区短串连重复序列的等位基因多态性与慢性阻塞性肺疾病(COPD)易感性之间的关系。方法:采用PCR扩增技术和聚丙烯酰胺凝胶电泳方法分析64例COPD患者和56例健康对照者HO1基因启动子区GT二核苷酸重复序列的分布。结果:COPD组和对照组在年龄、性别、吸烟指数等方面差异无统计学意义(P>0.05);COPD患者和健康对照者中HO1基因启动子区L型等位基因频率分别为21.88%和10.72%,两者差异有统计学意义(χ2=7.56,P<0.05);COPD组的1?s用力呼气量(FEV1)和1?s用力呼气量/用力肺活量(FEV1/FVC)分别为(53.56±8.35)%、(49.58±7.02)%,与对照组 [FEV1:(87.56±5.65)%、FEV1/FVC:(84.21±6.50)%]相比差异具有统计学意义(P<0.05);在COPD组内,是否吸烟、不同严重程度的肺功能阻塞(轻、中、重度)以及不同年龄组(<60岁组和>60岁组)等情况对HO1 L等位基因频率分布均无影响(P>0.05)。结论:HO1基因启动子区短串连重复序列多态性与中国北方汉族人COPD的易感性有关。

Abstract: To investigate the relations between the genetic polymorphism of short tandem repeat in human Heme Oxygenase1 promoter region and susceptibility of chronic obstructive pulmonary disease. Method: The genetypes of 64 patients with COPD and 56 healthy control subjects were tested with polymerase chain reaction and polyacrylamide gel electrophoresis to analysis the distribution of GT repeat in human Heme Oxygenase1 promoter region. Result: There was no significant difference between COPD patients and control subjects in age, cigarettes years, et al(P>0.05), whereas there was significant difference between the two groups about lung function(FEV1: 53.56±8.35% vs 87.56±5.65%; FEV1/FVC:49.58±7.02% vs 84.21±6.50%); The L type allele frequencies in promoter region between COPD patients and control subjects were 21.88% and 10.72%, χ2 analysis showed the statistical significance in two groups; In COPD groups, smoking or not, difference of lung function and age (≤60years and >60 years) had no effects on the L type allele frequencies in promoter region.Conclusion: Genetic polymorphism of short tandem repeat in human Heme

Key words: Pulmonary disease, chronic obstructive, Heme oxygenase, Genes, Susceptibilty

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