The Effect Of Licorice Consumption By Mice On Ldl Oxidation Macrophage Foam Cell Formation And Atherosclerosis

Dietary supplementation of licorice (200 Ag/day/mouse) to apolipoprotein E-deficient (E j mice for 6 weeks resulted in an 80% reduction in the suscep-

Figure 4 The effect of licorice extract supplementation to hypercholesterol-emic patients on the susceptibility of their LDL to atherogenic modifications: oxidation (a), aggregation (b), or retention (c). LDL was isolated from hypercholesterolemic patients before, after 1 month of licorice extract supplementation, and after an additional 1 month of placebo supplementation. (a) LDL oxidation: LDL (100 mg of protein/L) was incubated with 5 nmol/L CuSO4 for 3 hr at 25°C. The formation of conjugated dienes was kinetically monitored at 234 nm and the lag time was measured. (b) LDL aggregation: The extent of LDL aggregation induced by vortexing was kinetically monitored at 680 nm, and results are given after 60 sec of vortexing. (c) LDL CS binding ability: LDL (200 mg of lipoprotein protein/L) was incubated with chondroitin sulfate (CS, 100 mg/L) for 30 min at 37°C. LDL was then precipitated, and the LDL-asso-ciated glycoseaminoglycan (GAG) content was determined in the precipitate. Results are expressed as mean + SEM. *p < 0.01 (vs. baseline at study entry).

tibility of their LDL to copper-ion-induced oxidation, in comparison to LDL isolated from placebo-treated mice (84).

Administration of purified glabridin to E° mice in their drinking water was followed by analysis of its antioxidative effect against ex vivo LDL oxidation (84). GC-MS analysis of the LDL derived from E° mice after consumption of glabridin revealed that glabridin was absorbed, and bound to the LDL particle. Whereas no glabridin could be detected in LDL from control mice, LDL from mice that consumed glabridin (20 Ag/day/mouse) contained about 2 nmol of glabridin/mg LDL protein. LDL derived from E° mice after consumption of 20 Ag glabridin/day/mouse for 6 weeks was significantly more resistant to copper-ion-induced oxidation (by 22%) than LDL derived from placebo-treated mice. Administration of glabridin (25 Ag/

Figure 5 Effects of glabridin consumption by E0 mice, on the size of their aortic arch atherosclerotic lesion area. Photomicrographs of a typical atherosclerotic lesion of the aortic arch following treatment with placebo (a) or glabridin (b). The sections were stained with alkaline toludine blue. All micrographs are at the same magnification. (c) The lesion area is expressed in square micrometers + SD. *p < 0.01 vs. placebo.

Figure 5 Effects of glabridin consumption by E0 mice, on the size of their aortic arch atherosclerotic lesion area. Photomicrographs of a typical atherosclerotic lesion of the aortic arch following treatment with placebo (a) or glabridin (b). The sections were stained with alkaline toludine blue. All micrographs are at the same magnification. (c) The lesion area is expressed in square micrometers + SD. *p < 0.01 vs. placebo.

day/mouse) to E° mice for 3 months also reduced (by 50%) an additional atherogenic modification of LDL, i.e., its susceptibility to aggregation induced by vortexing (86). Most important, inhibition of atherogenic modifications of LDL (oxidation and aggregation) in E° mice following glabridin consumption was associated with a substantial reduction in macrophage foam cell formation and in the development of the atherosclerotic lesion area (Fig. 5).

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Dieting Dilemma and Skinny Solutions

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