Protection Effect of Cyanidin 3-O-Glucoside Against Oxidative Stress-induced HepG2 Cell Death Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways
- Authors
- Park, Jun Yeon; Kang, Ki Sung; Lee, Hae-Jeung
- Issue Date
- Nov-2017
- Publisher
- WILEY-V C H VERLAG GMBH
- Keywords
- Cyanidin 3-O-glucoside; Tertiary butyl hydroperoxide; Extracellular signal-regulated kinases; Akt
- Citation
- BULLETIN OF THE KOREAN CHEMICAL SOCIETY, v.38, no.11, pp.1316 - 1320
- Journal Title
- BULLETIN OF THE KOREAN CHEMICAL SOCIETY
- Volume
- 38
- Number
- 11
- Start Page
- 1316
- End Page
- 1320
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5538
- DOI
- 10.1002/bkcs.11290
- ISSN
- 1229-5949
- Abstract
- 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.
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