| Objective:To observe the impact of JNK and p38MAPK signaling pathway on the skeletal muscle apoptosis in rats with Chronic obstructive pulmonary disease(COPD).Methods:100 healthy ten-week Wistar rats were randomly divided into two groups:normal control group(n=20)and model group(n=80). The COPD rat model was performed with intratracheal instillation of PEE(20u/100g.Bw)on the 30th day of the modeling and exposed to cigarette smoke for 60 days,30 minutes per day. The control group Was not exposed to smoke but Was intratracheally instilled of the same amount of Physiologic Saline on the 30th day. The model rats were continually raised for another 30 days. Malnutrition was defined when the weight of the rats in the model group was lower than 90% of the mean body weight of the control group. All model rats were re-divided into 3 groups:the control group, the non-malnutrition COPD group, the malnutrition COPD group. Diaphragmatic muscle and long extensor muscle digits from rats were taken to make paraffin section. The rates of muscle apoptosis were measured by TUNEL method, expression of related genes JNK and p38 by immunohistochemical method,and the intensity of the expression of JNK and p38 by Nikon Eclipse 80i system to deal with the pictures. All the data was handled by SPSS 17.0 software through one-factor analysis of variance, t-test and related analysis.Results:1. The rates of muscle apoptosis in both diaphragmatic muscle and long extensor muscle digits of the malnutrition group were significantly higher than those of non-malnutrition group (P<0.01, P<0.01)and the control group(P<0.01, P<0.01). There Were no significant differences between diaphragmatic muscle and long extensor muscle digits in the rates of muscle apoptosis of all three groups(P>0.05).2. The expression of JNK in malnutrition group Were significantly higher than those of non-malnutrition group(P<0.01, P<0.01)and the control group(P<0.01, P<0.01). The expression of p38 in malnutrition group were significantly higher than those of non—malnutrition group(P<0.01, P<0.01) and the control group(P<0.01, P<0.01). There were no significant differences between diaphragmatic muscle and long extensor muscle digits in the expression of JNK and p38 of all three groups(P>0.05).Conclusion:1.Successfully reproduce COPD model rats.2. Skeletal muscle cell apoptosis may be COPD rat models of one of skeletal muscle atrophy mechanism.3. The JNK and P38 might be involved in COPD rat models of skeletal muscle cell apoptosis occur. |