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

摘要

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 3a??Oa??glucoside, on tertiary butyl hydroperoxide (tBHP)a??induced oxidative damage in HepG2 cells. L. caerulea extract and its active compound, cyanidin 3a??Oa??glucoside, showed a dosea??dependent hepatoprotective effect on tBHPa??induced HepG2 cell damage. In addition, L. caerulea and cyanidin 3a??Oa??glucoside inhibited the production of intracellular ROS in tBHPa??treated HepG2 cells. The protein expression of phosphorylateda??extracellular signala??regulated kinases and Akt, which are responsible for cell protection against ROS, were increased after treatment with cyanidin 3a??Oa??glucoside (50 and 100 ??M) in a dosea??dependent manner. Therefore, cyanidin 3a??Oa??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.