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

Bulletin of the Korean Chemical Society

Jun Yeon Park¹  Ki Sung Kang¹  Hae‐² 

[1] College of Korean Medicine Gachon University Seongnam 13120 Korea;Department of Food and Nutrition, College of BioNano Technology Gachon University Seongnam 13120 Korea

关键词: Cyanidin 3‐;    O‐;    glucoside;    Tertiary butyl hydroperoxide;    Extracellular signal‐;    regulated kinases;    Akt;   

DOI  :  10.1002/bkcs.11290

学科分类：化学（综合）

来源: Korean Chemical Society

【 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 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 μM) 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.

【 授权许可】

Unknown