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Effects of SO(2) derivatives on expressions of MUC5AC and IL-13 in human bronchial epithelial cells.

机译:SO(2)衍生物对人支气管上皮细胞中MUC5AC和IL-13表达的影响。

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摘要

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. To investigate the effects of SO(2 )derivatives on the expressions of asthma related genes (MUC5AC and IL-13), the mRNA and protein levels of the two genes in cultured human bronchial epithelial (BEP2D) cells were analyzed using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, immunocytochemistry method and enzyme-linked immunosorbent assay (ELISA), respectively. The results showed that the mRNA expressions of MUC5AC and IL-13 were significantly increased at different concentrations of SO(2) derivatives (0.0001, 0.001, 0.01, 0.1 and 1.0 mM), and the maximum appeared at 0.01 mM for MUC5AC (3.9-fold) or at 0.001 mM for IL-13 (4.7-fold). Meanwhile, SO(2) derivatives significantly increased the mRNA levels at 0, 0.5, 1, 4 and 24 h post-exposure with the maximum at 4 h post-exposure (25-fold for MUC5AC and 41-fold for IL-13). Furthermore, the protein levels of MUC5AC and IL-13 in BEP2D cells were significantly increased at different concentrations and different time courses exposed to SO(2) derivatives, along with the maximum at 4 h post-exposure. These results lead to a conclusion that SO(2) derivatives can increase the expressions of MUC5AC and IL-13 genes on the transcription and translation levels, and it suggests that SO(2) derivatives can induce mucus over-production and inflammation responses in human bronchial epithelial cells and may have relations with asthma diseases. 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)容易在体内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)衍生物对哮喘相关基因(MUC5AC和IL-13)表达的影响,使用实时反向分析了培养的人支气管上皮(BEP2D)细胞中这两个基因的mRNA和蛋白水平。转录聚合酶链反应(实时RT-PCR)测定,免疫细胞化学法和酶联免疫吸附测定(ELISA)。结果显示,在不同浓度的SO(2)衍生物(0.0001、0.001、0.01、0.1和1.0 mM)下,MUC5AC和IL-13的mRNA表达均显着增加,而在MUC5AC(3.9-倍数)或IL-13(0.001倍)的浓度为0.001 mM。同时,SO(2)衍生物在暴露后0、0.5、1、4和24 h显着增加mRNA水平,在暴露后4 h达到最大值(MUC5AC为25倍,IL-13为41倍) 。此外,BEP2D细胞中MUC5AC和IL-13的蛋白质水平在不同浓度和暴露于SO(2)衍生物的不同时间过程中显着增加,以及在暴露后4小时达到最大值。这些结果导致一个结论,即SO(2)衍生物可以增加转录和翻译水平上的MUC5AC和IL-13基因的表达,并且表明SO(2)衍生物可以诱导人类黏液过度产生和炎症反应支气管上皮细胞并可能与哮喘疾病有关。这可能是SO(2)加剧哮喘疾病的可能机制之一。

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