首页> 中文期刊>山东医药 >COPD患者诱导痰中IL-10、TNF-α、8-iso-PGF2α水平与吸烟及肺功能的关系

COPD患者诱导痰中IL-10、TNF-α、8-iso-PGF2α水平与吸烟及肺功能的关系

     

摘要

目的 探讨慢性阻塞性肺疾病(COPD)稳定期患者诱导痰中白细胞介素10(IL-10)、肿瘤坏死因子(TNF-α)、8-异前列腺素F2α(8-iso-PGF2α)的水平与吸烟及肺功能的关系.方法 选择COPD急性发作频率≥3次/年的患者15例(A组)、COPD急性发作频率≤2次/年的患者15例(B组)、健康吸烟者12例(C组)、健康非吸烟者10例(D组).分别测定4组诱导痰中IL-10、TNF-α、8-iso-PGF2α水平和肺功能指标.结果 ①A组TNF-α、8-iso-PGF2α水平高于B组,但无统计学差异(P>0.05);显著高于C、D组(P<0.05).②A组IL-10水平显著低于B、C、D组(P<0.05).③TNF-α、8-iso-PGF2α水平与第1秒用力呼气容积占预计值百分比(FEV1%)、1秒率(FEV1/FVC)呈负相关(r分别为-0.742、-0.639,P均<0.05);IL-10水平与FEV1%、FEV1/FVC呈正相关(r分别为0.476、0.537,P均<0.05).结论 吸烟可使TNF-α、8-iso-PGF2α水平升高,IL-10水平下降;IL-10、TNF-α、8-iso-PGF2α对患者肺功能有影响,它们参与了COPD气道慢性炎症的过程,对气道重塑可能起重要作用.%Objective To investigate the rlation among the levels of interlenkin-10 (IL-10) , tumor necrosis factor (TNF-α) , prostaglandin ( 8-iso-PGF2α) in induced sputum and lung function and somoking in patients with stable chronic obstructive pulmonary disease ( COPD). Methods Fifteen patients with stable COPD (incidence equal to or greater than third a year, A group) and 15 patients with stable COPD (incidence equal to or less than twice a year, B group) and 12 smokers (C group) and 10 healthy control subjects (D group) were enrolled in the study. Levels of IL-10, TNF-α, 8-iso-PGF2a in sputum supernatant were measured by ELISA and lung function were detected. Results ①The levels of TNF-α, 8-iso-PGF2a in group A were significantly higher than those in group C and D (all P <0. 05) , and were higher than those in group B (all P>0.05). ②The level of IL-10 in group A was significantly lower than that in group group B, C and D (P< 0.05). ③The levels of TNF-α, 8-iso-PGF2α were inversely correlated with FEV, % and FEV/FVC (r = -0. 742, - 0.639, both P < 0.05). The level of IL-10 was positively correlated with FEV, % and FEV, /FVC (r = 0.476, 0.537, both P<0.05). ④It was founded that levels of TNF-α, 8-iso-PGF2α were increased and the level of IL-10 was decreased by smoking. Conclusions The levels of IL-10, TNF-α, 8-iso-PGF2α in the patients with COPD have influence on pulmonary function. It may be involved in the airway inflammatory process and contribute to airway remodeling in COPD.

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