The Journal of pharmacy and pharmacology · 2018
Co-administrating apigenin in a high-cholesterol diet prevents hypercholesterolaemia in golden hamsters.
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Wong Tsz Yan, Tan Yan Qin, Lin Shu-Mei, Leung Lai K
Аннотация
OBJECTIVES: Hypercholesterolaemia is a major risk factor for developing atherosclerosis. Increased consumption of fruits and vegetables is recommended to hypercholesterolaemic patients. In this study, the hypocholesterolaemic effect of apigenin and luteolin was evaluated in a hamster model.
METHODS: Hamsters were put on a high-cholesterol diet for 9 weeks, and apigenin or luteolin was administered in the diet at 60 and 300 ppm.
KEY FINDINGS: Both apigenin and luteolin supplementations could attenuate the aorta plaque formation by 30% and 20%, respectively. Apigenin-fed hamsters at both dosages displayed a 1.5-fold increase in hepatic Ldlr expression and a 40% reduction in non-HDL cholesterol level as compared with those in the control fed a high-cholesterol (HC) diet. Besides, faecal elimination of cholesterol was facilitated by 20% in the hamsters with high apigenin consumption. Suppressing the expression of the cholesterol transporter ncp1l1 in the intestinal mucosa could block the cholesterol absorption and promote its elimination. The differential regulations of ncp1l1 and Ldlr appeared to be the underlying hypocholesterolaemic mechanism of apigenin in this model system. Luteolin supplementation, on the other hand, had no effect on the blood cholesterol.
CONCLUSIONS: This study illustrated that dietary administration of apigenin attenuated HC feeding-induced hypercholesterolemia in hamsters.
METHODS: Hamsters were put on a high-cholesterol diet for 9 weeks, and apigenin or luteolin was administered in the diet at 60 and 300 ppm.
KEY FINDINGS: Both apigenin and luteolin supplementations could attenuate the aorta plaque formation by 30% and 20%, respectively. Apigenin-fed hamsters at both dosages displayed a 1.5-fold increase in hepatic Ldlr expression and a 40% reduction in non-HDL cholesterol level as compared with those in the control fed a high-cholesterol (HC) diet. Besides, faecal elimination of cholesterol was facilitated by 20% in the hamsters with high apigenin consumption. Suppressing the expression of the cholesterol transporter ncp1l1 in the intestinal mucosa could block the cholesterol absorption and promote its elimination. The differential regulations of ncp1l1 and Ldlr appeared to be the underlying hypocholesterolaemic mechanism of apigenin in this model system. Luteolin supplementation, on the other hand, had no effect on the blood cholesterol.
CONCLUSIONS: This study illustrated that dietary administration of apigenin attenuated HC feeding-induced hypercholesterolemia in hamsters.