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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells.
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Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells.

机译:二氧化硫衍生物对人支气管上皮细胞中四种哮喘相关基因表达的影响。

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Sulfur dioxide (SO(2)) is a common air pollutant, and inhaled SO(2) in airway epithelium easily forms its soluble derivatives in vivo (bisulfite and sulfite), which are toxic to the respiratory system and related to the exacerbation of asthma. In order to study the possible asthmatic molecular mechanism of SO(2) and its derivatives, the dose-response and time-response relationships of SO(2) derivatives on gene expressions of some asthma-related genes in human bronchial epithelial cells (BEP2D) were investigated. The mRNA and protein levels of EGF, EGFR, ICAM-1 and COX-2 were analyzed in BEP2D cells using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, radio-immunoassay (RIA) method and Western blot analysis, respectively. The results showed that SO(2) derivatives caused the dose-dependent inductive expressions of four gene mRNA and protein in BEP2D cells. Moreover, SO(2) derivatives significantly increased the mRNA and protein levels at 0, 0.5, 1, 4 and 24h post-exposure, along with the highest inductions at 0.5h post-exposure for EGFR and COX-2 and at 4h post-exposure for EGF and ICAM-1. It was suggested that SO(2) derivatives could increase the expressions of EGF, EGFR, ICAM-1 and COX-2 on the transcription and translation levels in BEP2D cells, and result in mucus over-production and inflammation responses. This might be one of the possible mechanisms that SO(2) aggravates asthma disease.
机译:二氧化硫(SO(2))是一种常见的空气污染物,在气道上皮中吸入的SO(2)在体内容易形成其可溶性衍生物(亚硫酸氢盐和亚硫酸盐),这对呼吸系统有毒并与哮喘发作有关。为了研究SO(2)及其衍生物可能的哮喘分子机制,SO(2)衍生物对人支气管上皮细胞(BEP2D)某些哮喘相关基因的基因表达的剂量反应和时间反应关系被调查了。使用实时逆转录-聚合酶链反应(实时RT-PCR)测定,放射免疫测定(RIA)方法和BEP2D细胞分析EGF,EGFR,ICAM-1和COX-2的mRNA和蛋白水平分别进行蛋白质印迹分析。结果表明,SO(2)衍生物引起BEP2D细胞中四个基因mRNA和蛋白质的剂量依赖性诱导表达。此外,SO(2)衍生物在暴露后0、0.5、1、4和24h显着增加了mRNA和蛋白质水平,在EGFR和COX-2暴露后0.5h以及暴露后4h的诱导率最高。 EGF和ICAM-1的暴露。有人建议SO(2)衍生物可能会增加BEP2D细胞转录和翻译水平上EGF,EGFR,ICAM-1和COX-2的表达,并导致粘液过度产生和炎症反应。这可能是SO(2)加剧哮喘疾病的可能机制之一。

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