IL-13对小鼠哮喘模型气道黏蛋白基因Muc5ac及Bcl02、Bax表达的作用

Effects of interleukin 13 on airway Muc5ac gene and Bcl-2,Bax expression in murine asthmatic model

目的 研究白细胞介素 1 3(IL 1 3)处理小鼠支气管哮喘 (哮喘 )模型前后肺组织黏蛋白基因Muc5ac、凋亡相关蛋白Bcl 2和Bax表达的作用 ,探讨气道黏液过度分泌的机制。方法 4 5只雄性BALB c小鼠随机分为对照组、哮喘组和IL 1 3组 ,每组 1 5只。用逆转录 聚合酶链反应 (RT PCR)方法和免疫组化法分别检测Muc5acmRNA、Muc5ac蛋白、Bcl 2蛋白以及Bax蛋白在肺组织的表达。结果哮喘组和对照组肺组织Muc5acmRNA分别为 (0 .1 5 5 2± 0 .0 0 5 7)和 (0 .0 6 33± 0 .0 0 1 3) ,Muc5ac蛋白分别为 (0 .884 9± 0 .0 2 5 7)和 (0 .1 1 6 6± 0 .0 0 6 4 ) ,两组比较差异均有统计学意义 (P <0 .0 1 ) ;IL 1 3组肺组织Muc5acmRNA和蛋白分别为 (0 .2 80 7± 0 .0 0 2 7)和 (1 .6 1 38± 0 .0 4 83) ,与哮喘组、对照组比较差异也均有统计学意义 (P均 <0 .0 1 )。与对照组Bcl 2蛋白 (0 .32 79± 0 .0 1 36 )、Bax蛋白 (1 .72 84± 0 .0 2 6 3)相比 ,哮喘组分别增加和降低 (分别为 0 .8383± 0 .0 31 0和 0 .8987± 0 .0 1 0 6 ) ,两组差异均有统计学意义 (P均 <0 .0 1 ) ;IL 1 3处理后可分别促进Bcl 2和Bax蛋白增加和降低 (分别为 1 .6 934± 0 .0 2 2 9和 0 .35 2 2±0 .0 1 5 2 ) 。

Objective To study the influence of interleukin 13(IL-13)on the airway mucin gene Muc5ac, apoptosis related protein Bcl-2 and Bax expression in murine asthmatic model, and to investigate the mechanism of airway mucus overproduction. Methods Forty-five male BALB/c mice were randomly divided into control group, asthmatic group and IL-13 group,15 mice per group. Expression of Muc5ac mRNA , Muc5ac protein, Bcl-2 protein and Bax protein were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical assay respectively. Results The Muc5ac mRNA in asthmatic group and control group were 0.1552±0.0057 and 0.0633±0.0013 respectively, there was significant difference between two groups(P<0.01). The Muc5ac protein were 0.8849±0.0257 and 0.1166±0.0064 respectively, there was also significant difference between two groups(P<0.01). In IL-13 group, the Muc5ac mRNA and protein in lung were 0.2807±0.0027 and 1.6138±0.0483 respectively,there were also significant differences compared with asthmatic group and control group(all P<0.01). The Bcl-2 protein 0.3279±0.0136 and Bax protein 1.7284±0.0263 in asthmatic group elevated and decreased respectively compared with control group(both P<0.01), IL-13 could induce the increase and reduction of Bcl-2 protein 1.6934±0.0229 and Bax protein 0.3522±0.0152 respectively, there were obvious differences compared with asthmatic group(both P<0.01). There were positive relationship between Muc5ac mRNA, protein expression and Bcl-2 protein expression, negative relationship between Muc5ac mRNA, protein expression and Bax protein expression in both asthmatic group and IL-13 group(all P< 0.05). Conclusion IL-13 is a critical cytokine induced airways mucus overproduction of asthma and may causes above changes through altering Bcl-2 and Bax expression.