Membrane cholesterol delays cellular apoptosis induced by ginsenoside Rh2, a steroid saponin

Toxicology and Applied Pharmacology
Sandrine L VerstraetenMarie-Paule Mingeot-Leclercq

Abstract

Saponins exhibit several biological and pharmacological activities, such as antibacterial, anti-inflammatory and anticancer effects. Many studies attribute their activities to their interactions with cholesterol. In this study, we focus on the steroid saponin ginsenoside Rh2, one of the active principles of Panax ginseng root. Some evidence suggests that lipid rafts, defined as nanodomains enriched in cholesterol and sphingolipids, could be involved in the Rh2-induced apoptosis. However, the role of membrane lipids, especially cholesterol, in this process is still poorly understood. Here, we demonstrate that (i) A549, THP-1 and U937 cells are all susceptible to the Rh2-induced apoptosis but to a differential extent and (ii) the cytotoxic effect inversely correlates with the cell membrane cholesterol content. Upon cholesterol depletion via methyl-β-cyclodextrin, those three cells lines become more sensitive to Rh2-induced apoptosis. Then, focusing on the cholesterol-auxotroph U937 cell line, we showed that Rh2 alters plasma membrane fluidity by compacting the hydrophobic core of lipid bilayer (DPH anisotropy) and relaxing the interfacial packaging of the polar head of phospholipids (TMA-DPH anisotropy). The treatment with Rh2 co...Continue Reading

Citations

Sep 19, 2018·Biomolecules·Hélène PolletDonatienne Tyteca
Oct 13, 2020·Frontiers in Pharmacology·Sandrine L VerstraetenMarie-Paule Mingeot-Leclercq
Aug 18, 2020·Seminars in Cancer Biology·Carmen Garcia-RuizJose C Fernandez-Checa
Oct 28, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Jules César BayihaMarie-Paule Mingeot-Leclercq
Nov 25, 2020·International Journal of Molecular Sciences·Wendy S SmithDavid J Flavell

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis