Chronic liver diseases (CLDs) are correlated with oxidative stress induced by the accumulation of intracellular reactive oxygen species (ROS). In this study, we employed HepG2, a human liver carcinoma cell line containing many antioxidant enzymes, to explore the function of delphinidin against oxidative stress induced by H₂O₂ and to provide scientific data of the molecular mechanism. Cells were pretreated with different concentrations of delphinidin (10 μmol/L, 20 μmol/L, and 40 μmol/L) for 2 h before treatment with 750 μM H₂O₂ for 1 h. The results showed that H₂O₂ decreased the survival rate of HepG2 cells and increased the level of ROS, but delphinidin pretreatment could possess the opposite result. At the same time, the expression of Nrf2 was enhanced by the delphinidin pretreatment. This was because delphinidin promoted Nrf2 nuclear translocation and inhibited its degradation, which led to the increase expression of antioxidant protein HO-1 (Nrf2-related phase II enzyme heme oxygenase-1). Besides, we found that delphinidin could significantly alleviate the reduction of Nrf2 protein levels and the accumulation of intracellular ROS levels in Nrf2 knockdown HepG2 cells. In conclusion, our study suggested that delphinidin, as an effective antioxidant, protected HepG2 cells from oxidative stress by regulating the expression of Nrf2/HO-1.

中文翻译：

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Delphinidin对H2O2诱导的HepG2细胞氧化应激的抑制作用

慢性肝病（CLD）与细胞内活性氧（ROS）积累引起的氧化应激相关。在这项研究中，我们采用了含有许多抗氧化酶的人类肝癌细胞系HepG2，来探索飞燕草素对H ₂ O ₂诱导的氧化应激的作用，并提供分子机制的科学数据。将细胞用不同浓度的翠素（10预处理 μ摩尔/ L，20  μ摩尔/ L，和40  μ摩尔/ L）为2小时750处理之前 μ月时₂ ö ₂ 1个小时。结果表明，H ₂ O ₂降低了HepG2细胞的存活率并增加了ROS的水平，但是翠雀素预处理可能具有相反的结果。同时，delphinidin预处理增强了Nrf2的表达。这是因为飞燕草素促进Nrf2核易位并抑制其降解，从而导致抗氧化蛋白HO-1（与Nrf2相关的II期酶血红素加氧酶-1）的表达增加。此外，我们发现delphinidin可以显着减轻Nrf2敲除的HepG2细胞中Nrf2蛋白水平的降低和细胞内ROS水平的积累。总之，我们的研究表明，作为有效的抗氧化剂，飞燕草素可通过调节Nrf2 / HO-1的表达来保护HepG2细胞免受氧化应激。