Non-alcoholic fatty liver disease is a multifactorial disorder with complicated pathophysiology ranging from simple steatosis to steatohepatitis and liver fibrosis. Trimethylamine-N-oxide (TMAO) production is believed to be correlated with choline deficiency. This study investigated the expression of miRNA-34a, miRNA-122, and miRNA-192 in the fatty liver cell model treated with different concentrations of TMAO. A fatty liver cell model was developed by exposing HepG2 cells to a mixture of palmitate and oleate in a ratio of 1:2 at a final concentration of 1200 μM for 24 h. The confirmed fatty liver cells were treated with 37.5, 75, 150, and 300 μM of TMAO for 24 h. RT-qPCR was used to quantify the expression of microRNAs in a cellular model. The cellular expression of all microRNAs was significantly higher in treated fatty liver cells compared to normal HepG2 cells (P < 0.05). Only 75 and 150 µM of TMAO significantly increased the expression of miRNA-34a and miRNA-122 compared to both fatty and normal control cells (P < 0.05). Our results provided an experimental documentation for the potential effect of TMAO to change the expression of miR-34a and miR-22 as a mechanism for contributing to the pathogenesis of non-alcoholic fatty liver disease.

非酒精性脂肪肝是一种多因素疾病，具有复杂的病理生理学，从简单的脂肪变性到脂肪性肝炎和肝纤维化。三甲胺-N-氧化物（TMAO）的产生被认为与胆碱缺乏有关。本研究探讨了不同浓度TMAO处理的脂肪肝细胞模型中miRNA-34a、miRNA-122和miRNA-192的表达。将 HepG2 细胞暴露于 1:2 比例的棕榈酸酯和油酸酯混合物（终浓度 1200 μM）中 24 小时，建立脂肪肝细胞模型。将确认的脂肪肝细胞用37.5、75、150和300μM的TMAO处理24小时。 RT-qPCR 用于量化细胞模型中 microRNA 的表达。与正常 HepG2 细胞相比，经处理的脂肪肝细胞中所有 microRNA 的细胞表达均显着升高（P  < 0.05）。与脂肪细胞和正常对照细胞相比，仅 75 和 150 µM TMAO 即可显着增加 miRNA-34a 和 miRNA-122 的表达（P  < 0.05）。我们的结果为 TMAO 改变 miR-34a 和 miR-22 表达的潜在作用提供了实验文件，作为非酒精性脂肪肝发病机制的一种机制。