Objective To investigate the effects of methyprednislone on the expression of tumor alveolar septal cell apoptosis in autoimmune emphysema rats,in order to provide a theoretical basis for Chronic obstructive pulmonary disease(COPD)pathogenesis and it’s treatment.Methods 24 rats were randomly divided into three groups:normal control group (n=8 ),model group (n=8 )and intervention group (methylprednisolone sodium succinate,n=8).Intraperitoneal injection of primary cultured human umbilical vein endothelial cells were given to establish the autoimmune emphysema models,intervention group was injected with methylprednisolone at the meantime,and normal control group was received adjuvant only.Pathological changes were observed in lung tissues stained by hematoxylin eosin,mean liner intercept(MLI)and mean alveolar numbers(MAN)were measured.The localization of VEGF and VEGFR-2 in lung tissues were detected by immunohistochemical analysis.Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)technique was carried out to detect the alveolar septal cells apoptosis. Results The MLI in model group was higher than that in normal control group,while MAN was lower(P<0.05 );MLI in intervention group was lower than that in model group,but the MAN was higher (P<0.05 ).The localization of VEGF and VEGFR-2 in lung tissues in model group were lower than that in normal control group,and those in intervention group were higher than that in model group,the difference were all statistically significant(P<0.05 ).AI of alveolar septal cell in model group was higher than that in normal control group,which in intervention group was higher than that in model group,the difference were all statistically significant(P<0.05).Conclusion The decreasing of VEGF and VEGFR-2 in lung tissues may cause alveolar septal cell apoptosis and contribute to the pathogenesis of autoimmune emphysema of rats.Methyprednislone can alleviate the form of autoimmune emphysema in rats,which may be ralated to the regulation of VEGF and VEGFR-2 expression and inhibition of alveolar septal cell apoptosis.