• 关键词：二氧化硫  哮喘大鼠  实时定量RT-PCR  Western Blot  p53  bax  bcl-2

• 基金项目：国家自然科学基金项目(No.20677035,30740037)

• 解静芳
• 1. 山西大学环境与资源学院, 太原 030006; 2. 山西大学环境医学与毒理学研究所, 太原 030006

• 金国文
• 山西大学环境医学与毒理学研究所, 太原 030006

• 李瑞金
• 山西大学环境医学与毒理学研究所, 太原 030006

• 王学峰
• 山西大学环境医学与毒理学研究所, 太原 030006

• 刘丽娜
• 山西大学环境医学与毒理学研究所, 太原 030006

• 孟紫强
• 山西大学环境医学与毒理学研究所, 太原 030006

• 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WesternBlot方法研究吸入SO₂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:SO₂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.

• Abstract：The effects of sulfur dioxide on the mRNAand 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⁺OVAgroup,and ④ control group.The mRNAand protein levels of apoptosis-related genes(p53,bax and bc1-2) were analyzed in lungs using real-time reverse transcription-polymerase chain reaction(real-time RT-PCR) assay and Western blot analysis,respectively.The results indicated that the increases of both bc1-2 and the ratio of bc1-2/bax or decreases of p53,bax mRNAand protein levels were not significant in lungs of rats exposed to SO₂ alone compared with the control,but OVAexposure significantly changed the mRNAand protein expressions of p53,bax and bc1-2 compared with the control.However,altered levels of these genes appeared in lungs of rats exposed to SO₂ plus OVAcompared with the control or with the OVAgroup.These results lead to the conclusion that SO₂ can change the expressions of p53,bax and bc1-2 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.

• Key words：sulfur dioxide  asthma rats  RT-PCR  Western Blot  p53  bax  bcl-2

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