Xie Jingfang, Li Ruijin, Fan Renjun, Meng Ziqiang
Shanxi University, Taiyuan, China.
Inhal Toxicol. 2009 Sep;21(11):952-7. doi: 10.1080/08958370802629602.
Inhibition of cell apoptosis is an increasingly important factor in modulating airway inflammation in asthma, which is related to environmental pollutants. To investigate the effects of sulfur dioxide (SO(2)) on the mRNA and protein expressions of apoptosis-related genes in lungs from asthmatic rats, male Wistar rats were challenged by ovalbumin (OVA) or SO(2) (2 ppm) inhalation alone or together. Examinations were performed 24 h after the last treatment. The mRNA and protein levels of p53, bax, and bcl-2 were analyzed in lungs using real-time reverse transcription-polymerase chain reaction (RT-PCR) assay and Western blot analysis, respectively. The results indicated that increases of bcl-2 or decreases of p53 and bax mRNA and protein levels were not significant in lungs of rats exposed to SO(2) alone, compared with controls, but elevated or reduced levels of these genes appeared in lungs of asthmatic rats exposed to SO(2) plus OVA, compared with controls, suggesting that SO(2) exposure could result in OVA-induced increases or decreases of transcription and translation levels of these apoptosis-related genes in rat lungs, and may have relations to airway inflammation in asthma. The regulation mechanism of apoptosis in asthma disease exposure to SO(2) needs further study.
抑制细胞凋亡是调节哮喘气道炎症中一个日益重要的因素，这与环境污染物有关。为了研究二氧化硫（SO₂）对哮喘大鼠肺组织中凋亡相关基因mRNA和蛋白表达的影响，将雄性Wistar大鼠单独或联合用卵清蛋白（OVA）或吸入SO₂（2 ppm）进行激发。在最后一次处理后24小时进行检测。分别使用实时逆转录-聚合酶链反应（RT-PCR）分析和蛋白质印迹分析来检测肺组织中p53、bax和bcl-2的mRNA和蛋白水平。结果表明，与对照组相比，单独暴露于SO₂的大鼠肺组织中bcl-2增加或p53和bax mRNA及蛋白水平降低并不显著，但与对照组相比，暴露于SO₂加OVA的哮喘大鼠肺组织中这些基因的水平出现升高或降低，这表明暴露于SO₂可导致OVA诱导大鼠肺组织中这些凋亡相关基因转录和翻译水平的增加或降低，并且可能与哮喘气道炎症有关。SO₂暴露在哮喘疾病中凋亡的调节机制需要进一步研究。
