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The Inflammation Response to DEHP through PPARγ in Endometrial Cells

机译:子宫内膜细胞通过PPARγ对DEHP的炎症反应

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Epidemiological studies have shown the possible link between phthalates and endometrium-related gynecological diseases, however the molecular mechanism(s) behind this is/are still unclear. In the study, both primary cultured endometrial cells and an endometrial adenocarcinoma cell line (Ishikawa) were recruited to investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) at human-relevant concentrations. The results showed that DEHP did not affect the viability of either type of cell, which showed different responses to inflammation. Primary cultured cells showed stronger inflammatory reactions than the Ishikawa cell line. The expression of inflammatory factors was induced both at the mRNA and protein levels, however the inflammation did not induce the progress of epithelial-mesenchymal transition (EMT) as the protein levels of EMT markers were not affected after exposure to either cell type. Further study showed that the mRNA levels of peroxisome proliferator-activated receptor gamma (PPARγ) wereup-regulated after exposure. In all, our study showed that human-relevant concentrations of DEHP could elicit the inflammatory response in primary cultured endometrial cells rather than in Ishikawa cell line. PPARγ may act as the mediating receptor in the inflammation reaction.
机译:流行病学研究表明,邻苯二甲酸盐与子宫内膜相关的妇科疾病之间可能存在联系,但是其背后的分子机制仍不清楚。在这项研究中,招募了原代培养的子宫内膜细胞和子宫内膜腺癌细胞系(石川),以研究人相关浓度邻苯二甲酸二(2-乙基己基)酯(DEHP)的作用。结果表明,DEHP不会影响这两种细胞的活力,后者对炎症的反应不同。原代培养细胞比石川细胞系表现出更强的炎症反应。炎症因子的表达在mRNA和蛋白水平上均被诱导,但是炎症并未诱导上皮-间质转化(EMT)的进展,因为暴露于任一细胞类型后EMT标记物的蛋白水平均未受影响。进一步的研究表明,暴露后过氧化物酶体增殖物激活的受体γ(PPARγ)的mRNA水平被上调。总之,我们的研究表明,与人相关的DEHP浓度可以在原代培养的子宫内膜细胞而不是在Ishikawa细胞系中引起炎症反应。 PPARγ可在炎症反应中充当介导受体。

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