Consumption In Humans

Evaluation of the protective effect of licorice root extract on the resistance of LDL to ex vivo oxidation was studied in normolipidemic human subjects (84), as well as in hypercholesterolemic patients (85). LDL, which was isolated from the plasma of 10 healthy volunteers after consumption of 100 mg of licorice root ethanolic extract per day, for a period of 2 weeks, was more resistant to copper-ion-induced oxidation, as well as to AAPH-induced oxidation, by 44% and by 36%, respectively, in comparison to LDL isolated prior to licorice supplementation.

Supplementation of licorice root extract (0.1 g/day) to hypercholes-terolemic patients for a period of 1 month was followed by an additional 1 month of placebo consumption (85). Licorice consumption resulted in a

Figure 3 Glabridin inhibits macrophage-mediated oxidation of LDL. (a) Mouse peritoneal macrophages (MPM), harvested from E° mice that consumed placebo (control) or glabridin, were incubated with LDL (100 Ag of protein/mL) for 6 hr under oxidative stress (in the presence of 2 aM CuSO4). The extent of LDL oxidation was measured directly in the medium by the TBARS assay. Results are expressed as mean F SD (n = 3). (b) Superoxide anion release: Glabridin enrichment of macrophages decreases superoxide anion release in response to PMA. MPM from control mice were incubated with ethanol (0.2%, control) or with 20 aM of glabridin (in 0.2% ethanol) for 2 hr at 37°C. Then, the amount of superoxide anion release to the medium in response to 50 ng/mL of PMA was determined. Results are expressed as mean F SD (n = 3). (c) PKC activity: Glabridin inhibits protein kinase C (PKC) in macrophages. Macrophage PKC activity was measured in the cytosolic fraction from macrophages that were enriched with glabridin in comparison to control macrophages. Results are expressed as mean F SD (n = 3). *p < 0.01 (vs. placebo).

Figure 3 Glabridin inhibits macrophage-mediated oxidation of LDL. (a) Mouse peritoneal macrophages (MPM), harvested from E° mice that consumed placebo (control) or glabridin, were incubated with LDL (100 Ag of protein/mL) for 6 hr under oxidative stress (in the presence of 2 aM CuSO4). The extent of LDL oxidation was measured directly in the medium by the TBARS assay. Results are expressed as mean F SD (n = 3). (b) Superoxide anion release: Glabridin enrichment of macrophages decreases superoxide anion release in response to PMA. MPM from control mice were incubated with ethanol (0.2%, control) or with 20 aM of glabridin (in 0.2% ethanol) for 2 hr at 37°C. Then, the amount of superoxide anion release to the medium in response to 50 ng/mL of PMA was determined. Results are expressed as mean F SD (n = 3). (c) PKC activity: Glabridin inhibits protein kinase C (PKC) in macrophages. Macrophage PKC activity was measured in the cytosolic fraction from macrophages that were enriched with glabridin in comparison to control macrophages. Results are expressed as mean F SD (n = 3). *p < 0.01 (vs. placebo).

moderate reduction in the patients' plasma susceptibility to lipid peroxidation (by 19%), and in a marked reduction in the susceptibility of the patients' plasma LDL to oxidation (by 55%), as shown by a prolongation of the lag time required for the initiation of LDL oxidation by 55%, in comparison to the lag time of LDL isolated from plasma derived before licorice extract consumption (Fig. 4a). This effect was even partially sustained after an additional 1 month of placebo supplementation, since LDL derived after this period was still less susceptible to copper-ion-induced lipid peroxidation, as

demonstrated by an 18% increment in the lag time in comparison to the baseline lag time (before licorice administration).

Atherogenicity of LDL is attributed not only to its oxidative modification, but also to its aggregation. Upon analyzing the susceptibility to aggregation of LDL isolated from hypercholesterolemic patients who consumed licorice extract for 1 month, a significant (p < 0.01) reduction of 28% in LDL aggregation was observed (Fig. 4b). After an additional 1 month of placebo consumption, LDL aggregation rates returned toward baseline values.

Retention of LDL, which is an early step in atherogenesis, was measured by analysis of LDL binding to the proteoglycan chondroitin sulfate (CS). Following licorice consumption, LDL CS binding ability was significantly reduced by 25% and this effect was partly sustained for the additional 1 month of placebo consumption (Fig. 4c).

Licorice extract supplementation also resulted in a 10% reduction in the patients' systolic blood pressure, which was sustained for an additional month (during the placebo consumption). Thus, dietary consumption of licorice root extract by hypercholesterolemic patients may act as a moderate hypotensive nutrient and as a potent antioxidant agent, which confer its beneficial health benefit against cardiovascular disease.

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