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作 者:王莉[1] 王芬 刘毅[1] 马卫霞[1] 李怀臣[1]
机构地区:[1]山东大学附属省立医院呼吸内科,济南250021 [2]微山县人民医院小儿内科,山东济宁277608
出 处:《山东大学学报(医学版)》2009年第11期42-45,共4页Journal of Shandong University:Health Sciences
基 金:山东省科技攻关计划资助项目(2007GG30002033)
摘 要:目的探讨黄芪对哮喘平滑肌肌动蛋白-α及纤维连接蛋白的影响。方法随机将BALB/C小鼠60只分为对照组(A组)、哮喘组(B组)、黄芪治疗组(C组)各20只。以腹腔注射0.02%鸡卵清蛋白(OVA)和1%OVA雾化吸入建立慢性哮喘模型。治疗组在每次激发前给予黄芪干预。将右肺分离固定,用石蜡包埋切片,并用免疫组化染色技术染色,用LEICAQWINV3分析系统,计算表达阳性结果,把左肺置于液氮中保存,采用逆转录聚合酶链反应(RT-PCR)测定肺组织中平滑肌肌动蛋白-α(α-SMA)及纤维连接蛋白(FN)中信使核糖核酸(mRNA)含量,用Al-phaImager 2 200半定量分析系统分析。结果哮喘组α-SMA及FN阳性表达结果显著高于对照组(P<0.01),α-SMA mRNA及FN mRNA的表达上调(P<0.01);黄芪治疗组的α-SMA及FN的阳性表达、α-SMA mRNA及FN mRNA的表达均显著低于哮喘组(P<0.01)。结论FN及α-SMA为气道重构的重要标志物,黄芪可抑制慢性哮喘模型小鼠肺组织中α-SMA及FN表达,推测抑制α-SMA及FN的表达可能是黄芪抑制哮喘气道重构的重要机制之一。Objective To investigate the inhibition of Radix Astragali′s to expressions of α-SMA and FN in the lung tissues of mice with asthma.Methods The BALB/C mice were divided into three groups: the control group(Group A,n=20),the asthmatic model group(Group B,n=20),and the Radix Astragali managed group(Group C,n=20).A mouse model of asthma was established by exposing the animal to aerosolized ovalbumin(OVA).The managed group was given Radix Astragali before every stimulation.After being sensitized,the mice were subjected to laboratory tests.Expressions of FN mRNA and α-SMA mRNA of the lung tissues were determined by RT-PCR and AlphaImager2200 semi-quantitation analysis system.Masculine expressions of FN and α-SMA were determined by two-step immunohistochemistry and leica QWIN V3 analysis system.Result ①Compared with those in group A,expressions of α-SMA and FN in group B were significantly increased(P〈0.01).Compared with group B,those in group C were significantly decreased(P〈0.01).②Compared with those in group A,expression levels of α-SMA mRNA and FN mRNA in group B had a great increase(P〈0.01).There was a significant decrease of α-SMA mRNA and FN mRNA levels in group C compared with group B(P〈0.01).Conclusion FN and α-SMA are important symbols of airway remodeling.Radix Astragali can inhibit expressions of α-SMA and FN in the lung tissues of mice with chronic asthma,and may inhibit airway remodeling in asthma.
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