| Objective:To observe the expression of a1-AT and NE in the lungtissue and bronchoalveolar lavage fluid of rats with COPD.To researchthe changes of lung function, Pathological morphology and theexpression of a1-AT and NE induced by glucocorticoids. To approach theeffect of a1-AT and NE on the occurrence and development of COPD,and the mechanism of glucocorticoid treatment in COPD.Methods:1Preparation of COPD model: SD rats were randomly divided intothree groups: control group, the smoke-exposed group and thebudesonide group. In addition to the control group, the rats in othertwo groups were exposed to secondhand cigarette smoke in the fumebox twice a day for4months. The rats in budesonide group weretreated with budesonide by spraying during the last month. The lungfunction was detected, the number and classification of WBC inbronchoalveolar lavage fluid (BALF) were determined, andpathological morphology of lung tissue was observed.2The expression of a1-AT and NE proteins in rat BALF were detectedwith ELISA. The expression of a1-AT and NE protein in rat lungtissue was detected with immunohistochemistry The expression ofa1-ATand NE mRNAs in rat lung tissue was measured by real-timequantitative PCR.Results:1Compared with the control group, FEV0.3/FVC and Cdy insmoke-exposed group were significantly decreased (P<0.01), and Riand Re significantly increased (P<0.01). The percentage of neutrophils and total white blood cells in BALF of rats insmoke-exposed group were higher than those in control group(P<0.01), but the percentage of lymphocyte was lower (P<0.05). Themean lining interval (MLI) and bronchial wall thickness/diameterwere significantly increased (P<0.01), and the mean alveolar number(MAN) was significantly decreased (P<0.01). Compared with thesmoke-exposed group, budesonide treatment could increaseFEV0.3/FVC (P<0.05), and decrease Re and Cdy (P<0.05).Budesonide had no significant effects on percentage of cells in eachcategory, MAN, MLI and bronchial wall thickness/diameter(P>0.05).2Compared with control group, the protein expression of a1-AT wasdecreased in smoke-exposed group by the way of ELISA(P<0.01). Onthe contrary, the expression of NE protein was significantlyincreased(P<0.01). Compared with the smoke-exposed group,Theexpression of a1-AT was a litter increased, but no statisticalsignificance (P>0.05). The expression of NE protein was significantlydecreased(P <0.01).3Compared with control group, the protein expression of a1-AT wasdecreased in smoke-exposed group by the way ofimmunohistochemistry (P<0.01). On the contrary, the expression ofNE protein was significantly increased(P<0.01). Compared with thesmoke-exposed group,the expression of a1-AT was a litter increased,but no statistical significance (P>0.05),and the expression of NEprotein was significantly decreased(P<0.01).4Compared with control group, the protein expression of a1-AT wasdecreased in smoke-exposed group by the way of real-timequantitative RT-PCR.(P<0.01). The mRNA expression of a1-AT inrat lung tissue in smoke-exposed group was (0.55±0.057) times ofthat in control group. Compared with smoke-exposed group, theprotein expression of a1-AT was increased in budesonide group. The mRNA expression of a1-AT in rat lung tissue in smoke-exposedgroup was (0.69±0.08) times of that in control group. on the contrary,the mRNA expression of NE was significantly increased(P<0.01).The mRNA expression of NE in rat lung tissue in smoke-exposedgroup was (5.18±1.15) times of that in control group. Compared withsmoke-exposed group, mRNA expression of NE and a1-AT wasincreased in budesonide group (P<0.05). The mRNA expression ofNE in rat lung tissue in smoke-exposed group was (2.74±0.90) timesof that in control group.Conclusion:1In this study, COPD rat model was successfully established byinhalation of cigarette smoke for four months. There was significantimprovement on weight, and the number of inflammatory cells inBALF was decreased by budesonide treatment, but there was nosignificant effect on pathological morphology of rat lung.2al-AT and NE play important roles in the appearance andimprovement of COPD. Budesonide treatment could improve theimbalance of al-AT and NE, and that might be a new target forprevention and treatment of COPD. |
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