Summary

The beneficial health effects attributed to the consumption of fruits and vegetables are related, at least in part, to their antioxidant activity. Of special

Figure 6 Major pathways by which licorice flavonoids inhibit LDL cholesterol oxidation and atherosclerosis. Licorice-derived flavonoids affect LDL directly by interacting with the lipoprotein and inhibiting LDL oxidation. Licorice flavonoids can also protect LDL indirectly, by their accumulation in the arteries and protection of arterial macrophages against oxidative stress. The latter effect is associated with inhibition of the formation of ''oxidized macrophages'' and reduction in the capacity of macrophages to oxidize LDL. In addition, licorice-derived glabridin preserves paraoxonase activity, thereby increasing the hydrolysis of lipid peroxides in lipopoteins and in atherosclerotic lesion, leading to attenuation in the progression of atherosclerosis.

Figure 6 Major pathways by which licorice flavonoids inhibit LDL cholesterol oxidation and atherosclerosis. Licorice-derived flavonoids affect LDL directly by interacting with the lipoprotein and inhibiting LDL oxidation. Licorice flavonoids can also protect LDL indirectly, by their accumulation in the arteries and protection of arterial macrophages against oxidative stress. The latter effect is associated with inhibition of the formation of ''oxidized macrophages'' and reduction in the capacity of macrophages to oxidize LDL. In addition, licorice-derived glabridin preserves paraoxonase activity, thereby increasing the hydrolysis of lipid peroxides in lipopoteins and in atherosclerotic lesion, leading to attenuation in the progression of atherosclerosis.

interest is the inverse relationship between intake of dietary nutrients rich in polyphenols and cardiovascular diseases. This effect is attributed to the polyphenols' capability to inhibit LDL oxidation, macrophage foam cell formation, and atherosclerosis. Our current view on the major pathways by which licorice flavonoids protect LDL against oxidative modifications, and thereby reduce macrophage foam cell formation and the development of advanced atherosclerosis, are summarized in Figure 6. Licorice-derived glabridin can protect LDL against cell-mediated oxidation via two major pathways, including a direct interaction with the lipoprotein and/or an indirect effect through accumulation in arterial macrophages. Licorice-derived glabridin was shown to reduce the capacity of macrophages to oxidize LDL, owing to its binding to LDL and inhibition of its oxidation [by scavenging reactive oxygen species (ROS) and reactive nitrogen species (RNS)], also owing to its accumulation in arterial macrophages, followed by inhibition of macrophage lipid peroxidation and the formation of lipid-peroxide-rich macrophages. Furthermore, licorice-derived glabridin was shown to preserve serum paraoxonase (PON1) activity, resulting in PON1-induced hydrolysis of lipid peroxides in oxidized lipoproteins and in atherosclerotic lesion.

All these antioxidative and antiatherosclerotic effects of licorice-derived glabridin were demonstrated in vitro, as well as in vivo (in humans and in the atherosclerotic apolipoprotein E-deficient mice). We conclude that licorice is a source of some potent nutrients, which can attenuate the development of atherosclerosis secondary to its antioxidatie properties against lipid peroxidation in cells and in lipoproteins (87-89).

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