Effect of sulforaphane on antioxidant capacity and mitochondrial function of hepatocytes in vitro and in rats with hepatic oxidative stress

Objective To investigate the effect of sulforaphane (SFN) on oxidative stress and mitochondrial injury in hepatocytes. Methods We examined malondialdehyde (MDA) content by ELISA in the liver tissues and the protein expression of the antioxidant enzymes including hemeoxygenase-1 (HO-1), NADH dehydrogenase quinone 1 (NQO1) and glutathione S-transferase (GST) using Western blotting in the liver tissues from a rat model of hepatic oxidative stress established by high-fat diet. We also assessed the level of reactive oxygen species (ROS) and mitochondrial membrane protential by fluorescence microscopy, tested glutathione (GSH) and superoxide dismutase (SOD) levels using ELISA, and detected mitochondrial DNA (mtDNA) content using real-time quantitative PCR in cultured hepatocytes (HHL-5 cells) under fatty acid-induced oxidative stress. Results In the rat model of hepatic oxidative stress, SFN significantly reduced high-fat diet-induced elevation of MDA level (P < 0.05) and up-regulated the protein expression of the antioxidant enzymes in the liver tissues (P < 0.05). In cultured HHL-5 cells, SFN obviously reduced free fatty acid-induced elevation of ROS level (P < 0.05) and increased GSH content (P < 0.05), SOD level (P < 0.05), mitochondrial membrane potential (P < 0.05), and the content of mtDNA (P < 0.05). Conclusion SFN can enhance the antioxidant capacity of hepatocytes to improve high-fat diet-induced hepatic oxidative stress in rats and provide protection of mitochondrial function in the hepatocytes.