中文摘要：

为了研究SO2对哮喘大鼠肺细胞凋亡相关基因mRNA和蛋白表达的影响．对健康雄性Wistar大鼠随机分为正常组、SO2暴露组、卵蛋白（OVA）致敏哮喘组、SO2和OVA联合作用组，采用荧光实时定量RT—PCR和Western Blot方法研究吸入S02对哮喘大鼠肺细胞p53、bax、bcl-2三种细胞凋亡相关基因mRNA和蛋白表达的影响．结果表明，SO2暴露组肺中p53和baxmRNA和蛋白水平降低，bcl-2表达和bcl-2／bax比值均有升高，但与对照组相比无显著性差异．与对照组相比，哮喘组肺中p53和baxmRNA和蛋白的表达水平呈现不同程度的降低；bcl-2的表达和bcl-2／bax比值显著升高．SO2和OVA联合作用后，与哮喘组相比，肺中p53和bax蛋白表达显著下降，而bcl-2蛋白表达显著升高．结论：S02可加剧哮喘大鼠的哮喘症状，其机制可能是通过影响哮喘大鼠肺组织凋亡相关基因（p53、bax、bcl-2）的表达水平，抑制气道炎性细胞的凋亡来实现的．这些机制的阐明有助于对SO2毒作用机制的理解和所致疾病的治疗．

英文摘要：

The effects of sulfur dioxide on the mRNA and protein expressions of apoptosis-related genes were studied in lungs from asthmatic rats. The rats were challenged by ovalbumin （OVA） or SO2 inhalation alone or together. Male Wistar rats were divided randomly into 4 equal groups of 6 animals each ： ① SO2 group, ② ovalbumin （OVA） group （asthma group） , ③ SO2 ＋ OVA group, and ④ control group. The mRNA and protein levels of apoptosis- related genes （p53, bax and bcl-2） were analyzed in lungs using real-time reverse transcrlption-polymerase chain reaction （real-time RT-PCR） assay and Western blot analysis, respectively. The results indicated that the increases of both he1-2 and the ratio of be1-2/bax or decreases of p53, bax mRNA and protein levels were not significant in lungs of rats exposed to SO2 alone compared with the control, but OVA exposure significantly changed the mRNA and protein expressions of p53 ,bax and bcl-2 compared with the control. However, altered levels of these genes appeared in lungs of rats exposed to SO2 plus OVA compared with the control or with the OVA group. These results lead to the conclusion that SO2 can change the expressions of p53, bax and bcl-2 in the lungs from asthmatic rats at the transcription and translation levels, and it suggests that SO2 exposure can suppress apoptosis in inflammation and induce inflammation reactions in the lungs from asthmatic rats, which might be one of the mechanisms by which SO2 pollution aggravates asthma. Elucidating the expression patterns of those genes due to SO2 inhalation is critical to our understanding the mechanisms of SO2 effects and helpful for therapeutic intervention.