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作 者:霍建民[1] 陈晶莹[1] 孔英君[1] 石玉枝[1]
机构地区:[1]哈尔滨医科大学第一临床医学院呼吸内科,150001
出 处:《中华结核和呼吸杂志》2007年第8期573-576,共4页Chinese Journal of Tuberculosis and Respiratory Diseases
基 金:黑龙江省自然科学基金资助项目(D200535);黑龙江省"十五"攻关课题基金资助项目(GC02C151)
摘 要:目的探讨慢性阻塞性肺疾病(COPD)患者肺组织中血管内皮生长因子(VEGF)、诱生型一氧化氮合酶(iNOS)的表达情况及吸烟对二者表达的影响。方法取46例因肺癌行肺叶切除患者的癌旁组织,依据吸烟及肺功能情况分成:(1)吸烟伴 COPD 组19例;(2)吸烟不伴 COPD 组12例;(3)不吸烟不伴 COPD 组15例。用免疫组化法检测肺组织 VEGF 及 iNOS 的表达。结果吸烟不伴COPD 组(1.50±0.39,1.45±0.41)与不吸烟不伴 COPD 组(1.18±0.33,1.09±0.41)比较,肺组织VEGF、iNOS 表达增强;吸烟伴 COPD 组(2.19±0.51,2.39±0.45)与不吸烟不伴 COPD 组比较表达明显增强。肺组织 VEGF 表达与 iNOS 表达呈明显正相关(r=0.78,P<0,01)。肺组织 VEGF 表达与FEV_1呈明显负相关(r=-0.67,P<0.01)。结论吸烟以及轻度 COPD 患者肺组织 VEGF、iNOS 表达上调,iNOS、VEGF 的过度表达可能参与 COPD 患者气道与血管重建和气流受限的过程。Objective To investigate the expressions of and the effect of smoking on vascular endothelial growth factor (VEGF) and induced nitric oxide synthase (iNOS) in lung tissues of chronic obstructive pulmonary disease (COPD) patients. Methods The peripheral lung tissues were obtained from 46 patients with lung carcinoma. They were divided into three groups according to their habit of smoking and lung function, 19 smokers with moderate COPD, 12 smokers and 15 nonsmokers with normal lung function. The expression of VEGF and iNOS was detected by immunohistochemistry. Results Expressions of VEGF and iNOS were increased in lung tissues of smokers without COPD ( 1.50 ± 0. 39,1.45 ± 0. 41 ) compared with nonsmokers without COPD ( 1.18 ± 0. 33, 1.09 ± 0. 41 ) ( each P 〈 0. 05 ), and were significantly increased in lung tissues of smokers with moderate COPD ( 2. 19 ± 0. 51,2. 39 ± 0. 45 ) compared with nonsmokers without COPD ( each P 〈 0. 01 ). The expression of VEGF in lung tissues was significantly correlated with the expression of iNOS ( r = 0.78, P 〈 0.01 ) , but was inversely correlated with FEV1 ( r = -0. 67 ,P 〈 0. 01 ). Conclusions Expressions of VEGF and iNOS were upregulated in lung tissues of smokers and patients with moderate COPD. Overexpression of iNOS and VEGF may participate in the mechanism of airway and vascular remodeling,and airflow limitation in COPD.
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