In:
Journal of Cellular Biochemistry, Wiley, Vol. 115, No. 8 ( 2014-08), p. 1403-1411
Abstract:
This study investigated the cytoprotective effect of Ecklonia cava ‐derived eckol against H 2 O 2 ‐induced mitochondrial dysfunction in Chang liver cells. While H 2 O 2 augmented levels of mitochondrial reactive oxygen species (ROS), eckol decreased it. Eckol also attenuated high intracellular Ca 2+ levels stimulated by H 2 O 2 and recovered H 2 O 2 ‐diminished ATP levels and succinate dehydrogenase activity. Eckol time‐dependently increased the expression of manganese superoxide dismutase (Mn SOD), a mitochondrial antioxidant enzyme with cytoprotective effect against oxidative stress. Eckol recovered Mn SOD expression and activity that were decreased by H 2 O 2 . Finally, eckol induced Mn SOD through phosphorylated AMP‐activated protein kinase (AMPK) and forkhead box O3a (FoxO3a). Specific silencing RNAs (siRNAs) against FoxO3a and AMPK reduced eckol‐stimulated Mn SOD expression, and diethyldithiocarbamate (Mn SOD inhibitor) and siRNA against Mn SOD reduced the cytoprotective effect of eckol against H 2 O 2 ‐provoked cell death. These results demonstrate that eckol protects cells from mitochondrial oxidative stress by activating AMPK/FoxO3a‐mediated induction of Mn SOD. J. Cell. Biochem. 115: 1403–1411, 2014. © 2014 Wiley Periodicals, Inc.
Type of Medium:
Online Resource
ISSN:
0730-2312
,
1097-4644
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
1479976-5
SSG:
12
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