| Objective:To investigate the apotosis of diaphragmatic muscle and extensor digitorum longus,and analysis the serum levels of malondialdehyde(MDA)in a rat model of chronic obstructive pulmonary disease(COPD).To explore the effect of antioxidative,VitC and N-acetylcysteine,on the proliferation and apotosis of myoblast(C2C12).Methods:One hundred male Wistar rats were randomly divided into groups:normal control group(n=20)and a COPD model group.The methods,which were that exposing to cigarette smoke and intratracheal instillation of PPE(20u/100g),were used to produce the rat model of COPD.While the control group was not exposed to smoke but was intratracheal instilled of the same amount of saline when the model group was accepted to PPE.We presumed,when the weight of the COPD model group was lower than 90%of the mean levels of the control group's, malnutrition with COPD rat occurred.Then the model was succeded comepletly,and re-divided into 3 groups:the control group,the non-malnutrition group with COPD and the malnutrition group.At last, all of the 54 rats were euthanized.We measured:1)the serum levels of MDA by TBA.2)And the apotosis radio in disphragmatic muscle and extensor digitorum longus by terminal-deoxynucleotidyl transferase mediated nick end labeling(TUNEL).3)the effect of antioxidant,VitC and N-acetylcysteine,on the proliferation and apotosis of myoblast(C2C12).Results:(1)Lung function tests showed that FEV0.3,FEV0.3/FVC and PEF values were significantly lower in the COPD group than that of the control(all P<0.01),and pathological changes of the model group consistented with that of COPD in the mankind.(2)And the apotosis radio of disphragmatic muscle and extensor digitorum longus in the malnutrition of COPD model group increased.(3)The serum levels of MDA significantly increased as compared with the others.(4)VitC and N-acetylcysteine,as the effective antioxidant,displayed that the protection for inhibiting the myoblast's apotosis,especially the high concentration of VitC.And VitC could promote the proliferation of myoblast occupying oxdative stress.Conclusion:(1)The production of reactive oxygen species was increased in the malnutrition group with COPD,which maybe induces the apotosis of muscle,such as d;isphragmatic muscle and extensor digitorum longus.(2)Inhibiting the myoblast's apotosis and promoting the proliferation,VitC may be more effective. |