Protection Effect of Cyanidin 3-O-Glucoside Against Oxidative Stress-induced HepG2 Cell Death Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways

The attack of reactive oxygen species (ROS) on unsaturated fatty acids causes peroxidation. The membranes of liver cells are rich in unsaturated fatty acids, which are a target of lipid peroxidation by free radicals. The purpose of the present study was to identify the hepatoprotective potential of Lonicera caerulea and its active compound, cyanidin 3-O-glucoside, on tertiary butyl hydroperoxide (tBHP)-induced oxidative damage in HepG2 cells. L. caerulea extract and its active compound, cyanidin 3-O-glucoside, showed a dose-dependent hepatoprotective effect on tBHP-induced HepG2 cell damage. In addition, L. caerulea and cyanidin 3-O-glucoside inhibited the production of intracellular ROS in tBHP-treated HepG2 cells. The protein expression of phosphorylated-extracellular signal-regulated kinases and Akt, which are responsible for cell protection against ROS, were increased after treatment with cyanidin 3-O-glucoside (50 and 100 mu M) in a dose-dependent manner. Therefore, cyanidin 3-O-glucoside is the active compound in L. caerulea, which is responsible for the hepatoprotective effects through the inhibition of ROS and the activation of antioxidant mechanisms.