Curcumin inhibits ROS formation and apoptosis in methylglyoxal-treated human hepatoma G2 cells

被引:88
作者
Chan, WH [1 ]
Wu, HJ
Hsuuw, YD
机构
[1] Chung Yuan Christian Univ, Dept Biosci Technol, Chungli 32023, Taiwan
[2] Chung Yuan Christian Univ, Ctr Nanotechnol, Chungli 32023, Taiwan
[3] Fooyin Univ, Dept Nutr & Hlth Sci, Kaohsiung, Taiwan
来源
ROLE OF THE MITOCHONDRIA IN HUMAN AGING AND DISEASE: FROM GENES TO CELL SIGNALING | 2005年 / 1042卷
关键词
curcumin; methylglyoxal; oxidative stress; apoptosis; cytochrome c;
D O I
10.1196/annals.1338.057
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Methylglyoxal (MG) is a reactive dicarbonyl compound endogenously produced mainly from glycolytic intermediates. Elevated MG levels in diabetes patients are believed to contribute to diabetic complications. MG is cytotoxic through induction of apoptosis. Curcumin, the yellow pigment of Curcuma longa, is known to have antioxidant and anti-inflammatory properties. In the present study, we investigated the effect of curcumin on MG-induced apoptotic events in human hepatoma G2 cells. We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase). Using the cell permeable dye 2',7'-dichlorofluorescein diacetate (DCF-DA) as an indicator of reactive oxygen species (ROS) generation, we found that curcumin abolished MG-stimulated intracellular oxidative stress. The results demonstrate that curcumin significantly attenuates MG-induced ROS formation, and suggest that ROS triggers cytochrome c release, caspase activation, and subsequent apoptotic biochemical changes.
引用
收藏
页码:372 / 378
页数:7
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