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Title 

The novel resveratrol derivative 3,5-diethoxy-3',4'-dihydroxy-trans-stilbene induces mitochondrial ROS-mediated ER stress and cell death in human hepatoma cells in vitro

 

신규한 resveratrol 유도체에 의한 mitochondria 활성산소 및 ER stress 유도

Authors 

J W ParkW G ChoiP J LeeS W ChungB S KimH T ChungSungchan ChoJ H KimB H KangH KimH P KimS H Back

Publisher 

Nature Publishing Group

Issue Date 

2017

Citation 

Acta Pharmacologica Sinica

Keywords 

4-phenylbutyrateApoptosisEndoplasmic reticulum stressHepG2 human hepatoma cellsMito-TEMPOMitochondriaNACResveratrolResveratrol-006ROS

Abstract 

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a well-known polyphenol that is present in grapes, peanuts, pine seeds, and several other plants. Resveratrol exerts deleterious effects on various types of human cancer cells. Here, we analyzed the cell death-inducing mechanisms of resveratrol-006 (Res-006), a novel resveratrol derivative in human liver cancer cells in vitro. Res-006 suppressed the viability of HepG2 human hepatoma cells more effectively than resveratrol (the IC50 values were 67.2 and 354.8 μmol/L, respectively). Co-treatment with the ER stress regulator 4-phenylbutyrate (0.5 mmol/L) or the ROS inhibitor N-acetyl-L-cysteine (NAC, 1 mmol/L) significantly attenuated Res-006-induced HepG2 cell death, suggesting that pro-apoptotic ER stress and/or ROS may govern the Res- 006-induced HepG2 cell death. We further revealed that treatment of HepG2 cells with Res-006 (65 μmol/L) immediately elicited the dysregulation of mitochondrial dynamics and the accumulation of mitochondrial ROS. It also collapsed the mitochondrial membrane potential and further induced ER stress and cell death. These events, except for the change in mitochondrial morphology, were prevented by the exposure of the HepG2 cells to the mitochondrial ROS scavenger, Mito-TEMPO (300-1000 μmol/L). The results suggest that Res-006 may kill HepG2 cells through cell death pathways, including the ER stress initiated by mitochondrial ROS accumulation. The cell death induced by this novel resveratrol derivative involves crosstalk between the mitochondria and ER stress mechanisms

ISSN 

1671-4083

Link 

http://dx.doi.org/10.1038/aps.2017.106

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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