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作 者:王琼艳[1] 李孟荣[1] 王玥[1] 姜晗丹[1] 李迎春[1]
机构地区:[1]温州医学院附属第二医院育英儿童医院呼吸科哮喘及变态反应免疫治疗中心,325027
出 处:《医学研究杂志》2013年第7期121-125,共5页Journal of Medical Research
基 金:温州市科技局对外科技合作交流项目(H20090021)
摘 要:目的观察CpGODN干预对哮喘小鼠肺组织GITR及GITRL表达的影响。方法 48只SPF级雄性BALB/c小鼠随机分为正常对照组(简称对照组),哮喘模型组(简称模型组),地塞米松治疗组,CpGODN治疗组。以卵清白蛋白(OVA)致敏和激发建立小鼠哮喘模型。观察肺组织病理;对支气管肺泡灌洗液(BALF)进行细胞分类及计数;反转录-聚合酶链反应(RT-PCR)、免疫组化检测肺组织中GITR、GITRL的表达。结果 BALF中嗜酸性粒细胞平均(x±s,下同)计数:CpGODN组为(2.76±0.25)×107/L,地塞米松组为(1.05±1.72)×107/L,均低于模型组的(12.09±2.62)×107/L,差异有统计学意义(P<0.01),CpGODN组与地塞米松组比较差异无统计学意义(P>0.05)。RT-PCR、免疫组化结果:CpGODN组与地塞米松组GITR、GITRL表达高于模型组,差异有统计学意义(P均<0.05),CpGODN组GITRL mRNA、GITR蛋白表达高于地塞米松组,差异有统计学意义(P<0.05)。相关分析:肺组织GITR与GITRL表达呈正相关(P<0.01,n=40)。结论 CpGODN能改善哮喘小鼠气道炎症,显著增强哮喘小鼠模型中GITR及GITRL在肺组织中的表达。Objective To investigate the offect of CpGODN on the expression of GITR and GITRL in lung tissue in asthmatic murine models. Methods Totally 48 male BALB/e mice were randomly divided into control group, asthma group, Dexamethasone group (DEM group ) and CpGODN group. Asthma model mouse were sensitized with ovabumin(OVA) ,and repeatedly exposed to OVA. The histologi- cal changes of the lungs were observed by light microscope and transmission electron . The bronehoalveolar lavage fluid (BALF) of lung was collected and the cells counting as well as differentiation were performed. The expression of GITR and GITRL were detected by reverse transeriptase polymerase chain reaction ( RT - PCR) , and immunohistoehemistry. Results In the BALF, the mean numbers of EOS were (2.76± 0.25)×10^7/L in the CpGODN group and ( 1.05± 1.72)×10^7/L in the DEM group, respectively ,and were both significantly lower than the asthma group,which was (12.09 ±2.62) ×10^7/L (P 〈0.01 ). The expression of GITR and GITRL in the CpGODN group and DEM group were significantly higher than asthma group (P 〈 0.05). GITRL mRNA,GITR of CpGODN group were both significantly. higher than DEM group( P 〈 0.05 ). In correlative analysis,the expression of GITRL was positively correlated with GITR ( P 〈 0.01, n = 40). Conclusion CpGODN can markedly augment the expression of GITR and GITRL in lung tissue, and thereby improve airway inflam- mation.
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