Abstract
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.
Highlights
The death toll of chronic liver disease (CLDs) associated with cirrhosis, liver cancer, hepatitis, etc. is on the rise worldwide [1]
HepG2 cells were treated with different concentrations (0~200 μM) of delphinidin for 24 h to test the cytotoxicity, and the growth inhibition rate was measured by MTT assays
According to the results of the above MTT experiments, 10 μM, 20 μM, and 40 μM delphinidin were used to pretreat the cells and the cell viability of HepG2 cells treated with H2O2 (750 μM) was examined
Summary
The death toll of chronic liver disease (CLDs) associated with cirrhosis, liver cancer, hepatitis, etc. is on the rise worldwide [1]. Increasing evidences confirmed the contributory role of oxidative stress in the pathogenesis of CLDs. As the common cause of oxidative stress [2, 3], reactive oxygen species (ROS) are a collective name for molecules containing oxidative reactions, including superoxide anions (O2-), hydroxyl radicals (OH), hypochlorous acid (HOCl), ozone (O3), and hydrogen peroxide (H2O2) [4]. Antioxidants, antioxidant enzymes, and phase II detoxifying enzymes are included in this system. The antioxidant response element (ARE), a common nucleotide sequence in the promoter regions of phase II detoxifying enzymes, could be effectively activated by nuclear factor erythroid 2-related factor 2 (Nrf2) and could regulate the expression of its downstream genes [6]
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