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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Inhibition of intestinal ascorbic acid uptake by lipopolysaccharide is mediated via transcriptional mechanisms
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Inhibition of intestinal ascorbic acid uptake by lipopolysaccharide is mediated via transcriptional mechanisms

机译：通过转录机制介导脂多糖的抑制肠抗坏血酸摄取

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Abstract Ascorbic acid (AA) accumulation in intestinal epithelial cells is an active transport process mainly mediated by two sodium-dependent vitamin C transporters (SVCT-1 and SVCT-2). To date, little is known about the effect of gut microbiota generated lipopolysaccharide (LPS) on intestinal absorption of water-soluble vitamins. Therefore, the objective of this study was to investigate the effects of bacterially-derived LPS on AA homeostasis in enterocytes using Caco-2 cells, mouse intestine and intestinal enteroids models. Pre-treating Caco-2 cells and mice with LPS led to a significant decrease in carrier-mediated AA uptake. This inhibition was associated with a significant reduction in SVCT-1 and SVCT-2 protein, mRNA, and hnRNA expression. Furthermore, pre-treating enteroids with LPS also led to a marked decrease in SVCT-1 and SVCT-2 protein and mRNA expression. Inhibition of SVCT-1 and SVCT-2 occurred at least in part at the transcriptional level as promoter activity of SLC23A1 and SLC23A2 was attenuated following LPS treatment. Subsequently, we examined the protein and mRNA expression levels of HNF1α and Sp1 transcription factors, which are needed for basal SLC23A1 and SLC23A2 promoter activity, and found that they were significantly decreased in the LPS treated Caco-2 cells and mouse jejunum; this was reflected on level of the observed reduction in the interaction of these transcription factors with their respective promoters in Caco-2 cells treated with LPS. Our findings indicate that LPS inhibits intestinal carrier- mediated AA uptake by down regulating the expression of both vitamin C transporters and transcriptional regulation of SLC23A1 and SLC23A2 genes. Graphical abstract Display Omitted Highlights ? LPS inhibits intestinal ascorbic acid uptake. ? LPS down regulates SVCT-1 and SVCT-2 expression. ? LPS reduced expression of nuclear factors HNF1α and SP1. ? These factors affect SLC23A1 and SLC23A2 promoter activity on LPS treatment.
机译：摘要抗坏血酸（AA）肠上皮细胞的积累是主要由两种依赖性维生素C转运蛋白（SVCT-1和SVCT-2）介导的主动运输过程。迄今为止，关于肠道微生物生成的脂多糖（LPS）对水溶性维生素的肠道吸收的影响很少。因此，本研究的目的是探讨使用Caco-2细胞，小鼠肠和肠道进入液模型的肠细胞对肠溶细胞的细胞衍生的LPS对AA稳态的影响。用LPS预处理CaCO-2细胞和小鼠导致载体介导的AA摄取的显着降低。该抑制与SVCT-1和SVCT-2蛋白，mRNA和HNRNA表达的显着降低有关。此外，预处理LPS的肠外病毒也导致SVCT-1和SVCT-2蛋白和mRNA表达的显着降低。由于在LPS处理后，作为SLC23A1和SLC23A2的启动子活性，对转录水平至少部分地发生SVCT-1和SVCT-2的抑制。随后，我们研究了基底SLC23A1和SLC23A2启动子活性所需的HNF1α和SP1转录因子的蛋白质和mRNA表达水平，并发现它们在LPS处理的CaCO-2细胞和小鼠Jejunum中显着降低;这反映在用LPS处理的CaCO-2细胞中，观察到这些转录因子与其各自的启动子相互作用的水平。我们的研究结果表明，LPS抑制肠载体介导的AA吸收通过降低维生素C转运蛋白的表达和SLC23A1和SLC23A2基因的转录调节。图形抽象显示省略了亮点？ LPS抑制肠道抗坏血酸摄取。还LPS下调调节SVCT-1和SVCT-2表达。还LPS减少了核因子HNF1α和SP1的表达。还这些因素影响LPS处理的SLC23A1和SLC23A2启动子活性。

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