Glycyrrhizin Prevents 7-Ketocholesterol Toxicity Against Differentiated PC12 Cells by Suppressing Mitochondrial Membrane Permeability Change |
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Authors: | Doo Eung Kim Young Chul Youn Young KI Kim Ki Moo Hong Chung Soo Lee |
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Affiliation: | (1) Department of Neurology, Seoul Veterans Hospital, Seoul, 134-791, South Korea;(2) Department of Neurology, Chung-Ang University Hospital, Chung-Ang University, Seoul, 156-755, South Korea;(3) Department of Anesthesiology and Pain Medicine, GangNeung Asan Hospital, College of Medicine, University of Ulsan, Gangwon-do, 210-711, South Korea;(4) Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, 156-756, South Korea |
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Abstract: | 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 18β-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 18β-glycyrrhetinic acid prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death. The results obtained show that glycyrrhizin and 18β-glycyrrhetinic acid may prevent the 7-ketocholesterol-induced neuronal cell damage by suppressing changes in the mitochondrial membrane permeability. |
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Keywords: | 7-Ketocholesterol Glycyrrhizin 18β -Glycyrrhetinic acid PC12 cells Mitochondria-mediated cell death Protection |
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