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Proliferation and migration of VSMCs are initial events in the atherogenesis process. Vascular endothelial growth factor (VEGF) stimulates the proliferation of VSMCs and increases the expression of proinflammatory and prothrombotic molecules in atherosclerotic plaques. Naringin (500 mg · kg−1 · d−1) significantly reduced fatty streak formation and neointimal macrophage infiltration in vessel walls of cholesterol-fed rabbits. Antiatherogenic activity of naringin in hypercholesterolemic rabbits was induced by inhibiting intercellular adhesion molecule 1 (ICAM-1) expression in endothelial cells. Similar antiatherogenic effects of naringin and naringenin were found in high-cholesterol–fed rabbits, downregulating the expression levels of vascular cell adhesion molecule 1 (VCAM-1) and MCP-1 in aortas. A recent study showed the consistent antiatherogenic effect of naringin in wild-type mice fed a high-fat/high-cholesterol diet and in apoE-deficient mice fed a purified diet. Hepatic overproduction of apoB-containing lipoproteins is a characteristic feature of dyslipidemia associated with insulin resistance. In Ldlr−/− mice, the uptake of lipoprotein particles was impaired; thus, the mice became dyslipidemic and insulin resistant and developed atherosclerosis after being fed a high-fat Western-style diet. Naringenin inhibited apoB100 secretion by activating signaling cascades in HepG2 cells. Moreover, naringenin supplementation (3% of diet, wt:wt) reduced the infiltration of MOMA-2–positive leukocytes in lesions and reduced extensive collagen deposition in plaques of Western diet–fed Ldlr−/− mice, suggesting antiatherogenic activity.
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