探讨吸烟对慢性阻塞性肺疾病(COPD)患者，体内血清氧化应激及炎症因子的影响。

选取茂名城区40～79岁男性居民行肺功能检查，根据肺功能及吸烟情况分四组：COPD吸烟组、COPD非吸烟组、非COPD吸烟组以及非COPD非吸烟组，每组各40例，检测四组人群血清中的氧化应激指标(MDA、SOD)及炎症因子(IL-8、TNF-α)情况，对比其氧化应激失调及炎症因子情况，并进行统计学分析，了解其差异及相关性。

与轻度COPD非吸烟组相比较，轻度COPD吸烟组患者的MDA、IL-8、TNF-α水平偏高、SOD水平偏低，除TNF-α差异显著(P<0.05)外，MDA、IL-8和SOD差异不显著(P>0.05)；与非COPD吸烟组比较，轻度COPD吸烟组的IL-8、TNF-α水平偏高(P<0.05)，SOD水平偏低(P<0.05)，MDA偏高但差异不显著(P>0.05)，但是SOD水平偏低(P<0.05)，IL-8、TNF-α水平偏高(P<0.05)；轻度COPD吸烟组的MDA、IL-8、TNF-α水平显著高于非COPD非吸烟组(P<0.05)，而SOD偏低(P<0.05)。IL-8、TNF-α与MDA呈正相关(相关系数r分别为0.487、0.468，P值均<0.01)；IL-8、TNF-α与SOD呈负相关(相关系数r分别为－0.463、－0.457，P值均<0.01)；IL-8、TNF-α与FEV₁%pred呈负相关(相关系数r、P值分别为－0.492、P<0.01，－0.697、P<0.01)。

在非COPD患者中，与非吸烟人群相比，吸烟人群MDA、IL-8、TNF-α偏高，SOD偏低，而COPD人群上述差异更明显。在轻度COPD患者中，IL-8、TNF-α与MDA呈正相关，而与SOD、FEV₁%pred呈负相关。提示吸烟所致氧化应激失调可能是由抗氧化剂减少引起，氧化应激失调会导致炎症因子升高，而炎症因子升高会加速肺功能下降，从而导致COPD的发生。

To investigate the effects of smoking on serum oxidative stress and inflammatory factors in patients with chronic obstructive pulmonary disease (COPD).

The male residents age ranged from 40 year old to 79 year-old of Maoming city were divided into four groups according to their lung function and smoking status including COPD smoke group, COPD non-smoke group, non-COPD smoke group , and non-COPD non-smoke group, 40 cases in each group. Oxidative stress indicators of serum (MDA, SOD) and inflammatory factors (IL-8, TNF-α) in the serum of the four groups were measured and analysis to understand their differences and relevance.

COPD: with mild non smoking group, smoking group of patients with mild COPD MDA, IL-8, TNF-α, SOD alpha level high level is low, in addition to TNF-α significant difference (P<0.05), MDA, IL-8 and SOD have no significant difference (P>0.05); compared with the non COPD smoking group, mild smoking group COPD IL-8 the high level of TNF-α, alpha (P<0.05), SOD (P<0.05), the low level of MDA is higher but the difference was not significant (P>0.05), but low levels of SOD (P<0.05), IL-8, TNF-α high level (P<0.05); mild COPD smoking group of MDA, IL-8, TNF-levels were significantly higher than non COPD group (non smoking P<0.05), and SOD (P<0.05). IL-8 and TNF-alpha were positively correlated with MDA (correlation coefficient r=0.487, 0.468, P<0.01); IL-8 was negatively correlated, TNF-alpha and SOD (correlation coefficient r=-0.463, -0.457, P all <0.01); was negatively related to IL-8, TNF-alpha and FEV₁%pred (correlation coefficient r, P the values were -0.492, P<0.01, -0.697, P<0.01). COPD: with mild non smoking group, smoking group of patients with mild COPD MDA, IL-8, TNF-α, SOD alpha level high level is low, in addition to TNF-α significant difference (P<0.05), MDA, IL-8 and SOD have no significant difference (P>0.05); compared with the non COPD smoking group, mild smoking group COPD IL-8 the high level of TNF-α, alpha (P<0.05), SOD (P<0.05), the low level of MDA is higher but the difference was not significant (P>0.05), but low levels of SOD (P<0.05), IL-8, TNF-α high level (P<0.05); mild COPD smoking group of MDA, IL-8, TNF-levels were significantly higher than non COPD group (non smoking P<0.05), and SOD (P<0.05). IL-8 and TNF-alpha were positively correlated with MDA (correlation coefficient r=0.487, 0.468, P<0.01); IL-8 was negatively correlated, TNF-alpha and SOD (correlation coefficient r=-0.463, -0.457, Pall<0.01); was negatively related to IL-8, TNF-alpha and FEV₁%pred (correlation coefficient r, P the values were -0.492, P<0.01, -0.697, P<0.01).

In non-COPD group, compared with non-smokers, MDA, IL-8, TNF-αand SOD were higher in smokers and the differences were more obvious in COPD patients. Among patients with mild COPD, IL-8 and TNF-α were positively correlated with MDA, but negatively correlated with SOD and FEV₁% pred. It suggested that the imbalance of oxidative stress caused by smoking may be caused by the reduction of antioxidants and oxidative stress imbalance can lead to increased inflammatory factors, and inflammatory factors will accelerate the decline in lung function, therefore leading to COPD.