Oxidative stress is an important factor in the occurrence and development of liver disease. Medium-chain fatty acids (MCFAs) have potential antioxidant function, whereas the exact underlying mechanism of MCFA in oxidative injury of hepatocytes remains unclear. In our present study, three different MCFAs, 8-carbon octanoic acid (OA), 10-carbon capric acid (CA), and 12-carbon lauric acid (LA), have been performed to observe their protective action for hepatocyte under the H₂O₂ challenge. The result showed that MCFA treatment significantly increased the cell viability, T-AOC, and expression of antioxidant-related genes in AML12 cells under oxidative stress condition, and reduced reactive oxygen species (ROS) production. Moreover, MCFA treatment significantly increased the protein expression of Nrf2 and the phosphorylation level of ERK1/2; LA treatment significantly promoted the Nrf2 nuclear translocation. With a further test, the rescue ability of MCFA was blocked by treating with the ERK inhibitor U0126. Overall, our data suggested that MCFA treatment has positive impact on protecting AML12 cells against oxidative stress through ERK1/2/Nrf2 pathway.

中文翻译：

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MCFA 通过 ERK1/2/Nrf2 通路缓解 H2O2 诱导的 AML12 细胞氧化应激

氧化应激是肝病发生、发展的重要因素。中链脂肪酸 (MCFA) 具有潜在的抗氧化功能，而 MCFA 在肝细胞氧化损伤中的确切潜在机制仍不清楚。在我们目前的研究中，已经进行了三种不同的 MCFA，即 8 碳辛酸 (OA)、10 碳癸酸 (CA) 和 12 碳月桂酸 (LA)，以观察它们在 H 下对肝细胞的保护作用。₂ O ₂挑战。结果表明，MCFA 处理显着提高了氧化应激条件下 AML12 细胞中的细胞活力、T-AOC 和抗氧化相关基因的表达，并减少了活性氧 (ROS) 的产生。此外，MCFA处理显着增加了Nrf2的蛋白表达和ERK1/2的磷酸化水平；LA治疗显着促进了Nrf2核转位。通过进一步的测试，用 ERK 抑制剂 U0126 治疗阻断了 MCFA 的拯救能力。总体而言，我们的数据表明，MCFA 治疗通过 ERK1/2/Nrf2 通路对保护 AML12 细胞免受氧化应激具有积极影响。