Expression And Significance Of TNF-α In Diaphragm Of Rat Model Of Chronic Obstructive Pulmonary Disease

ObjectiveTo investigate TNF-αexpression and the influence of recombinant human tumor necrosis factor receptor-Fc in diaphragm of rats of chronic obstructive pulmonary disease.MethodsThirty-six rats were randomly divided into a normal control group,a COPD group and a rhTNFR:Fc-interfered group. Rat models of COPD were established by exposure to cigarette smoking daily for 80 days. rhTNFR:Fc-interfered group were exposed to cigarette and then interfered with rhTNFR:Fc. Lung function was measured in half rats of every group. The levels of Tumor Necrosis Factor alpha(TNF-α)in serum and diaphragm were measured with ELISA . Lung tissure and diaphragm muscle sections were used to study the morphological changes. Mean linear intercept(MLI)and mean alveolar numbers (MAN) were measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were carried out to examined distribution of apoptotic cells in the diaphragm muscle. ResultsComparing with normal control group and rhTNFR:Fc-interfered group, FEV_0.3/FVC and PEF were lower in COPD rats (P< 0.05) ; The levels of TNF-αin serum and diaphragm were higher in COPD group than in the control group (P < 0.05) and rhTNFR:Fc-interfered group (P< 0.05) ; MLI in COPD rats was higher than that in the control group (p< 0.05) , while MAN was lower on the contrary (p < 0.05) comparing with control group and rhTNFR:Fc-interfered group; The number of TUNEL+ cells in diaphragm muscle was significantly increased in COPD group as compared with control group and rhTNFR:Fc-interfered group(P<0.05) ; Compared with control group and rhTNFR:Fc-interfered group, diaphragm muscle atrophy and muscle fiber fragmentation were increased in COPD rats.ConclusionsTNF-αis associated with the pathogenesis of COPD of smoking rats and causes diaphragmatic pathological changes , apoptosis of diaphragm cells and diaphragm muscle atrophy in smoking rats. rhTNFR:Fc may play a certain role in the improvement of diaphragm pathological changes, decrease of diaphragm cells apoptosis in COPD.