Effects of sulfur dioxide on expressions of p53, bax and bcl-2 in lungs of asthmatic rats
文献类型: 外文期刊
作者: Xie, Jingfang 1 ; Li, Ruijin 1 ; Fan, Renjun 3 ; Meng, Ziqiang 1 ;
作者机构: 1.Shanxi Univ, Inst Environm Med & Toxicol, Taiyuan 030006, Peoples R China
2.Shanxi Univ, Coll Environm & Resource, Taiyuan 030006, Peoples R China
3.Shanxi Acad Agr Sci, Inst Plant Protect, Taiyuan, Peoples R China
关键词: sulfur dioxide;asthmatic rats;lungs;bax;bcl-2;p53
期刊名称:INHALATION TOXICOLOGY ( 影响因子:2.724; 五年影响因子:2.55 )
ISSN: 0895-8378
年卷期: 2009 年 21 卷 8-11 期
页码:
收录情况: SCI
摘要: 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 (SO2) on the mRNA and protein expressions of apoptosis-related genes in lungs from asthmatic rats, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (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 (RTPCR) 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 SO2 alone, compared with controls, but elevated or reduced levels of these genes appeared in lungs of asthmatic rats exposed to SO2 plus OVA, compared with controls, suggesting that SO2 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 SO2 needs further study.
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