ABSTRACT
OBJECTIVE：To study the effects of methylprednisolone sodium succinate on oxidative stress and anti-endothelial cell antibody （AECA）of autoimmune emphysema model rats. METHODS ：Male SD rats were randomly divided into control group，model group and intervention group ，with 8 rats in each group. Except that control group was given same volume of complete Freund ’s adjuvant intraperitoneally ，model group and intervention group were given the mixture of human umbilical vein endothelial cells and complete Freund ’s adjuvant intraperitoneally to establish the model of autoimmune emphysema. On 2nd day after modeling ，intervention group was intraperitoneally injected with 10 mg/（kg·d）methylprednisolone sodium succinate. Control group and model group were intraperitoneally injected the same volume of normal saline ，once a day ，for consecutive 21 days. After last medication ，the right lung tissue of rats were taken for paraffin section and HE staining in each group ，and the pathological changes of lung tissue were observed. The mean alveolar number （MAN）and mean linear intercept （MLI）were measured. The contents of MDA and GSH ，the activities of SOD and glutathione peroxidase （GSH-Px）in bronchial alveolar lavage fluid（BALF）of left lung were determined ；the contents of AECA in BALF and serum were also determined. The correlation of AECA with MDA ，GSH，SOD and GSH-Px were determined in model group by Pearson analysis. RESULTS ：Compared with control group ，the pathological changes of pulmonary emphysema were obvious in model group ，MAN decreased significantly ，and MLI prolonged significantly （P＜0.01）； GSH content ， GSH-Px and SOD activities in BALF were decreased 1100，1195） significantly，the contents of AECA in BALF and serum were increased significantly （P＜0.01）. Compared with modelgroup，the pathological changes of pulmonary emphysema was improved significantly in the intervention group ， increased significantly ，while MLI shortened significantly （P＜ ·1208；GSH content ，SOD and GSH-Px activities were increased significantly，while the contents of AECA in BALF and serum were decreased significantly （P＜0.01）. AECA in BALF of rats in model group was positively correlated with MDA （r＝0.710， P＜0.05），and the AECA were negatively correlated with GSH ，SOD and GSH-Px （r＝－0.754，－0.781，－0.736，P＜0.05）. CONCLUSIONS：Methylprednisolone sodium succinate may achieve the purpose of the prevention of autoimmune emphysema through reducing oxidative stress and inhibiting the expression of AECA.
ABSTRACT
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.