Stevia: limiting cholesterol synthesis in Hep-G2 cells

Abstract

As of today, no literature has been reported on the efficacy of stevia on lipid regulations conducted in vitro. Thus, the current study was focusing on the potential of Stevia rebaudiana bertoni as an anti-hypercholesterolemia substitute in limiting the de novo cholesterol synthesis in Hep-G2 cell line. The cytotoxicity and lipid internalization effects of stevia on Hep-G2 cells were assessed quantitatively and qualitatively in this study. As evaluated by MTT assay, commercialized stevia (0.5-20.0 mg/ml) and stevioside (1.0-10 µM) inhibited Hep-G2 cells viability in a dose-dependent manner for 24 hours. IC50 was detected at 8.68 mg/ml (commercialized stevia) and 10.91 µM (stevioside). From the assay, suitable concentrations were chosen to study the effect of stevia on cholesterol internalization in Hep-G2 cells supplemented with exogenous lipids. Cholesterol quantification assay revealed that high concentration commercialized stevia and stevioside promoted significant cholesterol internalized in Hep-G2 cells as compared to simvastatin. Finally, immunofluorescent microscopy assessment was done to qualitatively observe the formation of lipid droplets and low-density lipoprotein receptor in relation to total cholesterol extracted. The microphotographs of immunofluorescent microscopy were in parallel to results obtained from the cholesterol quantification assay which further revealed the effect of stevia as a potential anti-hypercholesterolemia agent.

Anti-Cancer Properties of Stevia rebaudiana; More than a Sweetener

“…The MTT assay showed a dose-dependent cytotoxicity for both compounds and the IC 50 was calculated at 8.68 mg/mL for the extract and at 10.91 µM for the glycoside [47]. Regarding lipid regulation, both compounds were able to trigger internalization of cholesterol in HepG2 cells [47]. This observation was confirmed by immunofluorescence imaging of intracellular lipid droplets and of the low-density lipoprotein receptor, suggesting that cholesterol was indeed stored intracellularly.…”

“…The cancer cells were treated with these compounds for 24 h with a wide range of concentrations (extract 0.5-20 mg/mL, stevioside 1-10 µM), which are notably higher for the extract compared to other studies [32,36,37,46]. The MTT assay showed a dose-dependent cytotoxicity for both compounds and the IC 50 was calculated at 8.68 mg/mL for the extract and at 10.91 µM for the glycoside [47]. Regarding lipid regulation, both compounds were able to trigger internalization of cholesterol in HepG2 cells [47].…”

“…The HepG2 hepatocarcinoma cell line was also used to evaluate the lipid regulation efficacy and cytotoxicity of a commercialized stevia extract powder and stevioside [47]. The cancer cells were treated with these compounds for 24 h with a wide range of concentrations (extract 0.5-20 mg/mL, stevioside 1-10 µM), which are notably higher for the extract compared to other studies [32,36,37,46].…”

“…This observation was confirmed by immunofluorescence imaging of intracellular lipid droplets and of the low-density lipoprotein receptor, suggesting that cholesterol was indeed stored intracellularly. It was also proposed that stevia derivatives interfered with the mevalonate pathway, preventing HMG-CoA conversion to mevalonate, a crucial step in cholesterol synthesis [47]. Thus, treatment with stevia derivatives would reduce cholesterol level, which could be linked to their anti-cancer activity, since increased cholesterol synthesis is a hallmark of cancer, responsible for membrane biogenesis, cancer stemness preservation and tumor cell energy needs [55].…”