Journal
NEUROCHEMICAL RESEARCH
Volume 34, Issue 8, Pages 1433-1442Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-009-9930-y
Keywords
7-Ketocholesterol; Glycyrrhizin; 18 beta-Glycyrrhetinic acid; PC12 cells; Mitochondria-mediated cell death; Protection
Categories
Ask authors/readers for more resources
Defects in mitochondrial function participate in the induction of neuronal cell injury. In neurodegenerative conditions, oxidative products of cholesterol are elevated and oxysterols seem to be implicated in neuronal cell death. The present work was designed to study the inhibitory effect of licorice compounds glycyrrhizin and 18 beta-glycyrrhetinic acid against the toxicity of 7-ketocholesterol in relation to the mitochondria-mediated cell death process. 7-Ketocholesterol induced the nuclear damage, loss of the mitochondrial transmembrane potential, increase in the cytosolic Bax and cytochrome c levels, caspase-3 activation and cell death in differentiated PC12 cells. Glycyrrhizin and 18 beta-glycyrrhetinic acid prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death. The results obtained show that glycyrrhizin and 18 beta-glycyrrhetinic acid may prevent the 7-ketocholesterol-induced neuronal cell damage by suppressing changes in the mitochondrial membrane permeability.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available