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Effects of SO2 derivatives on expressions of MUC5AC and IL-13 in human bronchial epithelial cells

机译:SO2 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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Sulfur dioxide (SO2) is a common air pollutant, and inhaled SO2 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 SO2 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 SO2 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, SO2 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 SO2 derivatives, along with the maximum at 4 h post-exposure. These results lead to a conclusion that SO2 derivatives can increase the expressions of MUC5AC and IL-13 genes on the transcription and translation levels, and it suggests that SO2 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 SO2 aggravates asthma disease.
机译:二氧化硫是一种常见的空气污染物,吸入气道上皮的二氧化硫在体内容易形成其可溶性衍生物(亚硫酸氢盐和亚硫酸盐),对呼吸系统有毒并与病情加重有关。哮喘。为了研究SO2衍生物对哮喘相关基因(MUC5AC和IL-13)表达的影响,实时分析了人类支气管上皮细胞(BEP2D)中这两个基因的mRNA和蛋白质水平。逆转录聚合酶链反应(实时RT-PCR)测定,免疫细胞化学法和酶联免疫吸附测定(ELISA)。结果表明,在不同浓度的SO2 衍生物(0.0001、0.001、0.01、0.1和1.0 mM)下,MUC5AC和IL-13的mRNA表达显着增加,而在MUC5AC(3.9时,最大值为0.01 mM) -倍数)或IL-13的0.001 mM(4.7倍)。同时,SO2 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,暴露于SO2 衍生物的不同浓度和时间段,BEP2D细胞中MUC5AC和IL-13的蛋白质水平显着升高,并且暴露后4 h达到最大值。这些结果得出结论:SO2 衍生物可以增加MUC5AC和IL-13基因在转录和翻译水平上的表达,这表明SO2 衍生物可以诱导粘液过度产生和炎症反应。在人支气管上皮细胞中可能与哮喘疾病有关。这可能是SO2加重哮喘病的可能机制之一。

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