A Study On Changes Of Fas/Apo-1 And TNF-α In The Serum Of Patients Suffering From COPD And Its Clinical Significance With Cell Apoptosis

Objective: apoptosis in the pathogenesis of COPD has played an important role. Apoptosis-soluble Fas on the Fas-induced apoptosis inhibitory regulatory role, as one of the indicators to monitor apoptosis, the incidence of COPD has a unique mechanism of the clinical value. Other scholars believe that the tumor necrosis factor TNF-COPD to participate in the formation of airway inflammation, apoptosis in lung function and the deterioration of COPD, malnutrition, and so on. This study through analysis of chronic obstructive pulmonary disease patients with COPD and control group in serum sFas, TNF-αand peripheral blood Neu / Leu% (neutrophil percentage of the WBC) and the level of relevance, observed in patients with COPD cells Diao The level of death, the initial exploration of apoptosis, inflammation and the relationship between the airflow obstruction.Method: 1, the experimental study 30 patients with COPD patients (acute exacerbation and remission), 25 cases of normal control group of lung function and blood analysis; 2, COPD and ease the acute exacerbation of stable, normal control group were collected Peripheral blood centrifuge, separation frozen, sFas and serum TNF-αwas determined by enzyme-linked immunosorbent assay (ELISA).Results: 1 COPD and control groups FEV1% of lung function indicators were 46.23±25.03,100.28±21.14, FEV1/FVC% Were 47.33±24.70,84.12±6.64, compared two groups of COPD group FEV1% and% FEV1/FVC were significantly lower (P <0.01); 2 COPD patients with acute exacerbation of sFas in the concentration (19.34±2.68ng/ml ) Higher than the stability of the concentration (17.77±4.08 ng / ml), the results are significant differences (P <0.05); COPD exacerbation of acute and stable patients with sFas in the concentration (19.34±2.68ng/ml, 17.77±4.08 ng / ml) higher than the healthy control group of concentration (14.9±4.74ng/ml), the results are significant differences (P <0.05); 3 COPD patients with acute exacerbation of TNF-αin the concentration (128.75±21.75 pg / L) significantly higher than the concentration of stable (100.79±16.11pg / L), the results are significant differences (P <0.01); COPD exacerbation of acute and stable patients with serum concentrations of TNF-α(128.75±21.75 pg / L, 100.79±16.11pg / L) was significantly higher than that of the healthy control group (84.04±10.63pg/ml), the results are significant differences (P <0.01); 4 COPD patients with acute exacerbation of Neu / Leu% (neutrophil percentage of the WBC) values (73.14±11.21%) significantly higher than the stable value (67.67±3.88%), the results are significant differences (P <0.05); 5 COPD patients with acute exacerbation of TNF-α, sFas and Neu / Leu% of the average water increase. Acute exacerbation of COPD patients with serum and stability of TNF-αand peripheral Neu / Leu% positive correlation (r were 0.393 and 0.421, P <0.05); COPD patients with peripheral blood serum sFas Neu / Leu% No (R were 0.135 and 0.071, P> 0.05); 6 COPD and acute exacerbation in patients with stable lung function sFas indicators FEV1% and no correlation (r were 0.202 and 0.228, P> 0.05); COPD acute exacerbation Period and the period of stability in patients with TNF-αand lung function indicators associated with FEV1% (r were 0.174 and 0.131, P> 0.05).Conclusion: (1) COPD group marked not entirely irreversible airflow restricted;(2) COPD exacerbation of acute and stable level of serum sFas significantly higher than the control group, suggesting the existence of apoptosis delay COPD, lung cells can not be in place in time to prevent the removal of the replacement of normal cells;(3) COPD exacerbation of acute and stable levels of TNF-αlevels significantly higher than the control group, suggesting that TNF-αmay be involved in apoptosis, the delay caused apoptosis;(4) COPD exacerbation of acute peripheral Neu / Leu% significantly higher than the level of stable, suggesting that COPD systemic inflammatory response increased, likely to cause abnormal cell lung inflammation invasion, in fulfilling its function of the immune defense immune injury;(5) COPD group TNF-α, sFas and peripheral blood Neu / Leu% of the level of increase, suggesting that inflammatory cells may delay apoptosis, gathered in the airway, the release of a large number of inflammatory cytokines, lysosomal enzyme, such as free radicals Cause airway obstruction. And inflammatory factor (TNF-α, etc.) can inhibit apoptosis phagocytes identification; proteolytic enzymes can be dissolved consumption phagocytes and apoptosis of the cell surface receptor protein apoptosis (sFas increase), to prevent phagocytic uptake apoptosis. Therefore, the delay apoptosis in lung cells gathered from secondary necrosis, the release of more inflammatory cytokines and hydrolysate material, forming a vicious cycle. And may also, and the deterioration of lung function and systemic effects such as weight loss related to the occurrence, and so on.