The Function Of Atrogin-1Protein In The Skeletal Muscle In Chronic Obstructive Pulmonary Disease And Its Relationship With IGF-1

Objective To investigate the function of Atrogin-1protein in chronic obstructive pulmonary disease in the skeletal muscle and its relationship with IGF-1.Methods70Wistar male rats were randomly divided into two groups: COPD model group(n=35); normal control group(n=35). The COPD rats model were established by intratracheal instillation of PPE(20u/100g. Bw) and being exposed to cigarettes smoke for104days,30minutes per day. The normal control group was not exposed to cigarettes smoke but was in intratracheal instilled of the same amount of Saline on the same day. Two groups of rats were both carried out ordinary observation.104days later, Two groups of rats were examined the lung function, then we took the rats’middle lobe of the right lung, the extensor digitorum longus muscle and the midriff muscle to fixing, pathological section and protein extraction. All the tissues were HE stained to be observed the pathological changes by light microscopy. And the extensor digitorum longus and diaphragm muscle were further tested by immunohistochemical method and Western bolt method for the detection to quantitative expression of Atrogin-1protein and IGF-1protein and their correlation study. All results are applied SPSS17.0software for statistical analysis. Results (1) The lung function test find that FEV0.3/FVC (%) and FEV0.3of the model COPD group were significantly lower than the control group, RI of the model COPD group was significantly higher, there were significant difference (all P<0.05), reaching for chronic obstructive pulmonary disease standard. Lung function of the normal control group showed no significant abnormality.(2) HE staining observation in rat lung and bronchial tissue showed:the levels of lung tissue destruction, proliferation and inflammation in COPD model rats were significantly greater than in the control group, bullas and chronic inflammation were formed. the control group with normal alveolar structure, no inflammatory cell infiltration.(3) The extensor digitorum longus diameter and nuclear number in unit area of COPD model group rats were lower than the normal control group.(4) Protein expression in extensor digitorum longus and diaphragm was measured quantificationally by immunohistochemistry and western bolt. In COPD group, Atrogin-1expression was significantly higher and IGF-1expression was significantly lower than the expression in normal control group.(5) The protein expression amount of Atrogin-1and IGF-1in skeletal muscle of COPD rats was negatively correlated.Conclusions (1) The skeletal muscle cell of COPD model rats was atrophied, while the skeletal muscle atrophy of control group was not obvious.(2) One reason of skeletal muscle atrophy in COPD may be that expression of Atrogin-1protein is increased and expression of IGF-1is decline in COPD rats’skeletal muscle.(3) In COPD, skeletal muscle IGF-1protein content and Atrogin-1protein content was negatively correlated.