To investigate the mechanism and the relationship between fractalkine and oxidative stress of patients with COPD and pulmonary heart disease.

64 patients with AECOPD were divided into the following 8 groups according to whether merger pulmonary heart disease, whether using NAC, Cardiac function and GOLD classification of COPD disease severity. 8 healthy volunteers were selected as control group. Blood samples before and 10 days after treatment were collected to detect the level of all serum indicators, Color Doppler echocardiography, lung function and CAT score were also examined.

Levels of FKN, NF-κB, OX-LDL and hsCRP in different groups of AECOPD patients were higher than healthy control (P<0.05) and all of them were higher in severe group than mild group (P<0.05). Also, before and after treatment, those in pulmonary heart disease group were higher than COPD group, but decreased significantly in COPD+ NAC group and mild cases of pulmonary heart disease + NAC group (P<0.05). SOD, on the contrary. Administration of NAC resulted in elevated FEV₁ in mild cases of COPD group and pulmonary heart disease group (P<0.05). Pulmonary arterial pressure changed strikingly in the mild cases of pulmonary heart disease + NAC group after treatment (P<0.05), Compared to mild cases of pulmonary heart disease patients, higher pulmonary arterial pressure existed in severe cases. Compared with COPD group, the pulmonary artery pressure of pulmonary heart disease group was significantly higher (P<0.05). Besides, in severe cases of pulmonary heart disease group, CAT score in other groups altered significantly before and after treatment (P<0.05). Also, marked difference was seen between COPD group and pulmonary heart disease group(P<0.05); The level of FKN was positively correlated with CAT score, NF-κB, OX-LDL, hsCRP and pulmonary artery pressure (r=0.417, 0.521, 0.401, 0.456, 0.395, P<0.05), and negatively correlated with SOD(r=-0.387, P<0.05), while had no obvious correlation with FEV₁ (r=0.215, P>0.05).

Oxidative stress in patients with COPD and cor pulmonale is closely related to FKN, Hypoxemia causes an increase in ROS, which activates the NF-κB and promotes FKN to generate and release. NAC could inhibit ROS generation, which prevents the activation of NF-κB and reduces the production of FKN. Our results show that NAC may be helpful for prevention of COPD and pulmonary heart disease in early stage.