Glycyrrhizin prevents 7-ketocholesterol toxicity against differentiated PC12 cells by suppressing mitochondrial membrane permeability change.

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 18beta-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 18beta-glycyrrhetinic acid prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death. The results obtained show that glycyrrhizin and 18beta-glycyrrhetinic acid may prevent the 7-ketocholesterol-induced neuronal cell damage by suppressing changes in the mitochondrial membrane permeability.

Mild encephalopathy with reversible lesion in the splenium of the corpus callosum and bilateral frontal white matter.

A 59-year-old man visited an emergency room due to the sudden onset of severe dysarthria with a drowsy mental status. MRI demonstrated T2 prolongation and restricted diffusion involving the splenium of the corpus callosum and bilateral frontal white matter neurological signs and symptoms were mild, and the recovery was complete within a week. Follow-up MRI performed one month later revealed complete resolution of the lesions. The clinical and radiological courses were consistent with previously reported reversible isolated splenial lesions in mild encephalitis/encephalopathy except for the presence of frontal lesions. This case suggests that such reversible lesions can occur outside the splenium.